Sleep & MemoryReviewSleep, dreams, and memory consolidati.docx

Sleep & Memory/Review
Sleep, dreams, and memory consolidation:
The role of the stress hormone cortisol
Jessica D. Payne and Lynn Nadel1
The University of Arizona, Department of Psychology, Tucson,
Arizona 85721, USA
We discuss the relationship between sleep, dreams, and
memory, proposing that the content of dreams reflects
aspects of memory consolidation taking place during the
different stages of sleep. Although we acknowledge the
likely involvement of various neuromodulators in these
phenomena, we focus on the hormone cortisol, which is
known to exert influence on many of the brain systems involved
in memory. The concentration of cortisol escalates
over the course of the night’s sleep, in ways that we propose
can help explain the changing nature of dreams across
the sleep cycle.
There is currently no convincing explanation for why we dream
or what we dream about. In this article we propose an approach
to dreaming that focuses on the relationship between sleep and
memory. We suggest that dreams reflect a biological process of
long-term memory consolidation, serving to strengthen the
neural
traces of recent events, to integrate these new traces with older
memories and previously stored knowledge, and to maintain the
stability of existing memory representations in the face of
subse-
quent experience (Winson 1985, 2002, 2004; Kali and Dayan

2004).
It is generally assumed that long-term memory consolida-
tion involves interactions among multiple brain systems, modu-
lated by various neurotransmitters and neurohormones. We pro-
pose that the characteristics of dreams are best understood in
the
context of this neuromodulatory impact on the brain systems
involved in memory consolidation. Although a number of neu-
rotransmitters and neurohormones are likely involved, we focus
our attention in particular on the stress hormone cortisol, which
has widespread effects on memory during waking life through
its
impact on many of the critical brain structures implicated in
memory function.
Our hypothesis, briefly stated, is that variations in cortisol
(and other neurotransmitters) determine the functional status of
hippocampal ↔ neocortical circuits, thereby influencing the
memory consolidation processes that transpire during sleep. The
status of these circuits largely determines the phenomenology of
dreams, providing an explanation for why we dream and of
what. As a corollary, dreams can be thought of as windows onto
the inner workings of our memory systems, at least those of
which we can become conscious.
In addition to exploring these ideas in more detail, we pro-
vide some background concerning (1) the states of sleep and the
role of various neurotransmitters in switching from one sleep
state to another, (2) how the characteristics of dreams vary as a
function of sleep state, (3) the memory content typically associ-
ated with dreaming in different dream states, and (4) the role of
sleep in the consolidation of memory.
Background to the hypothesis

Stages of sleep
There are two major types of sleep. The first, rapid eye
movement
or REM sleep, occurs in ∼90-min cycles and alternates with
four
additional stages known collectively as NREM sleep—the
second
type of sleep. Slow wave sleep (SWS) is the deepest of the
NREM
phases and is the phase from which people have the most diffi-
culty being awakened. REM sleep is characterized by low-
amplitude, fast electroencephalographic (EEG) oscillations,
rapid
eye movements (Aserinsky and Kleitman 1953), and decreased
muscle tone, whereas SWS is characterized by large-amplitude,
low-frequency EEG oscillations (Maquet 2001). More than 80%
of SWS is concentrated in the first half of the typical 8-h night,
whereas the second half of the night contains roughly twice as
much REM sleep as does the first half. This domination of early
sleep by SWS, and of late sleep by REM, likely has important
functional consequences but also makes it difficult at this time
to
know which distinction is critical: NREM sleep versus REM
sleep
or early sleep versus late sleep. We will use the terms
NREM/early
sleep and REM/late sleep, where necessary, to reflect this
current
ambiguity.
Neurotransmitters, particularly the monoamines (largely se-
rotonin [5-HT] and norepinephrine [NE]) and acetylcholine,
play
a critical role in switching the brain from one sleep stage to
another. REM sleep occurs when activity in the aminergic

system
has decreased enough to allow the reticular system to escape its
inhibitory influence (Hobson et al. 1975, 1998). The release
from
aminergic inhibition stimulates cholinergic reticular neurons in
the brainstem and switches the sleeping brain into the highly
active REM state, in which acetylcholine levels are as high as in
the waking state. 5-HT and NE, on the other hand, are virtually
absent during REM. SWS, conversely, is associated with an ab-
sence of acetylcholine and nearly normal levels of 5-HT and NE
(Hobson and Pace-Schott 2002).
The distribution of dreams
In the study of dreams, a major distinction has been drawn be-
tween REM and NREM sleep. Until recently, virtually all dream
research focused on REM sleep, and indeed, dreams are
prevalent
during REM. In a recent review of 29 REM and 33 NREM recall
studies, Nielsen (2000) reported an average REM dream recall
rate
of 81.8%. Importantly, however, he also reported an average
NREM recall rate of ∼50%. Some NREM dreams are similar in
content to REM dreams; the majority of these come from those
few NREM periods occurring early in the morning, during the
peak phase of the diurnal rhythm, when cortisol levels are at
their zenith (Kondo et al. 1989). Foulkes (1985) has argued for
the existence of NREM dreaming and against a simple “REM
sleep = dreaming” view. By simply changing the question asked
of awakened subjects from “Did you dream?” to “Did you expe-
1Corresponding author.
E-mail [email protected]; fax (520) 621-9306.
Article and publication are at
http://www.learnmem.org/cgi/doi/10.1101/
lm.77104.

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rience any mental content?,” Foulkes was able to show a far
higher percentage of dream reports from NREM stages than
origi-
nal studies had suggested. These dream reports after NREM
awak-
enings led Foulkes and others to conclude that the stream of
consciousness never ceases during sleep and that the brain en-
gages in cognitive activity of some sort during all sleep stages
(Antrobus 1990).
Dreams and episodic memory content
Typical REM and NREM dreams are quite distinct, particularly
with respect to episodic memory content. Episodic memory re-
fers to knowledge about the past that incorporates information
about where and when particular events occurred. It is typically
contrasted with semantic memory, which consists of knowledge
(e.g., facts, word meanings) that has been uncoupled from place
and time, existing on its own (Tulving 1983). When examining
REM sleep dreams for memory content, one finds that episodic
memories are rare (see Baylor and Cavallero 2001) and
typically
emerge as disconnected fragments that are often difficult to re-
late to waking life events (see Schwartz 2003). These
fragmented

REM dreams often have bizarre content (Stickgold et al. 2001;
Hobson 2002). For example, the normal rules of space and time
can be ignored or disobeyed, so that in REM dreams it is
possible
to walk through walls, fly, interact with an entirely unknown
person as if she was your mother, or stroll through Paris past
the
Empire State Building. NREM dreams, however, are quite
differ-
ent (Cavallero et al. 1992). Here, episodic memories do appear
in
dream content (see Foulkes 1962; Cicogna et al. 1986, 1991;
Ca-
vallero et al. 1992; Baylor and Cavallero 2001). Recent
episodes
are predominant, but remote memories occasionally appear as
well. This pattern of results suggests to us that the memory sys-
tems needed to generate complete episodic retrieval are func-
tional in NREM sleep but not in REM sleep. Although we do
not
fully understand how nightly neurochemical fluctuations ac-
count for this difference, some clues are available.
Sleep and memory consolidation
One important clue is that different types of memory (e.g., pro-
cedural, episodic) appear to be best consolidated during specific
stages of sleep. REM sleep may be preferentially important for
the
consolidation of procedural memories and some types of emo-
tional information (see Karni et al. 1994; Plihal and Born
1999a;
Kuriyama et al. 2004; Smith et al. 2004), whereas NREM, espe-
cially SWS, appears to be critical for explicit, episodic memory
consolidation (Plihal and Born 1997, 1999a,b; Rubin et al.
1999;
also see Peigneux et al. 2001). This role for SWS appears to

apply
both to verbal tasks (e.g., list learning, paired-associated
learning
tasks; Plihal and Born 1997) and spatial tasks (e.g., spatial rota-
tion; Plihal and Born 1999a). For example, Plihal and Born
(1997)
tested both episodic and procedural memory after retention in-
tervals defined over early sleep (dominated by SWS) and late
sleep (dominated by REM). Subjects were trained to criterion in
the recall of a paired-associate word list (episodic) and a
mirror-
tracing task (procedural) and were retested after 3-h retention
intervals, during either early or late nocturnal sleep. Recall of
paired associates improved significantly more after a 3-h sleep
period rich in SWS than after a 3-h sleep period rich in REM or
after a 3-h period of wake. Mirror tracing, on the other hand,
improved significantly more after a 3-h sleep period rich in
REM
than after 3 h spent either in SWS or awake. The fact that
memo-
ries for personal episodes only undergo effective consolidation
early in the night, when NREM (SWS) is particularly
prominent,
provides another indication that episodic memory systems are
functional during NREM sleep.
Summary of background
This brief review highlights several points:
1. Sleep stages vary across the night: Early sleep is rich in
NREM,
but late sleep is rich in REM. These stage changes relate to, and
are caused by, neurochemical fluctuations during sleep.
2. Dream content varies as a function of sleep stage or time of
night: There is considerable episodic content in dreams during

NREM/early sleep, but little episodic content in dreams during
REM/late sleep.
3. Sleep affects memory consolidation, but in a complex way:
Procedural memory benefits from both REM/late sleep and
NREM/early sleep, but episodic memory only benefits from
NREM/early sleep.
These points raise two critical questions:
1. What can account for the differences in dream content and
effectiveness of memory consolidation as an apparent func-
tion of NREM/early sleep versus REM/late sleep?
2. What underlying concomitants of this difference actually pro-
duce the variations in dream content and memory consolida-
tion?
Are neurotransmitters the key, as some have suggested (see
Hob-
son 1988)? Is it strictly the REM/NREM distinction, or alterna-
tively, could it be fundamental differences in early versus late
sleep? It is important to note that Plihal and Born’s studies
(1997,
1999a) used late versus early sleep as the manipulation, not
REM
versus NREM per se. Moreover, late night NREM dreams are
more
“dream-like” and are thus often indistinguishable from REM
dreams (Kondo et al. 1989), so perhaps something about late
night sleep accounts for differences in dream content and
memory consolidation. These are just some of the issues that
arise within the framework we propose.
The hypothesis in brief
Our hypothesis focuses on how cortisol influences the hippo-

campal formation. In doing so we do not seek to minimize the
role of neurotransmitters such as acetylcholine, NE, and 5-HT,
all
of which play important roles in controlling sleep (see Hobson
and Pace-Schott 2002), dreams (see Hobson 1988; Stickgold et
al.
2001), and memory function (see Cahill and McGaugh 1998;
Hasselmo 1999). Each of these neurotransmitters, in addition to
having independent effects on memory, likely interacts with
cor-
tisol in important ways that may affect memory consolidation
and dreaming. In this article we limit our focus to cortisol be-
cause it is known that high levels of cortisol can disrupt hippo-
campal function, interfering with interactions between the hip-
pocampal system and its neocortical neighbors (Kim and Dia-
mond 2002). These effects on hippocampal function thus
provide a possible basis for understanding the interplay among
sleep, dreams, and memory.
Assumptions
1. Sleep has multiple purposes, including analysis of the “resi-
due” of recent experiences, and integration of the outcome of
that analysis with previously stored “knowledge.”
2. Dreams reflect activity in brain structures concerned with (1)
processing, storing and/or representing recent experiences;
and (2) the knowledge an individual has built up over a life-
time of experiences.
3. Dream content reflects which of these brain structures are
active. Variations in activity over the course of the night re-
flect processing, or “memory consolidating,” occurring within
different neural systems.
4. Over the course of the night, the brain oscillates between a

Payne and Nadel
672 Learning & Memory
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state that is more conducive to the consolidation of episodic
memories, and a state or states that may be more conducive to
the consolidation of procedural memories.
5. Because cortisol levels exert control over hippocampal func-
tion, they may be able to switch the brain from one memory
consolidating state to the other.
These assumptions lead to several testable hypotheses:
1. First, because cortisol levels rise over the course of a night’s
sleep, episodic memories should be better consolidated early
in the night, when a modest cortisol level allows the hippo-
campus to function properly in memory consolidation. Pro-
cedural memories should be effectively consolidated through-
out the night, as high cortisol levels are not known to disrupt
the brain systems critical to these kinds of memories.
2. Second, dreams reported early in the night, largely during
SWS, should reflect normal episodic content; dreams reported
late at night, largely during REM sleep, should reflect dis-
rupted hippocampal → neocortical communication and hence
should seem fragmented and often bizarre.

We claim that differences in dream content and memory con-
solidation between NREM/early sleep and REM/late sleep
reflect
different levels of critical modulatory factors in these states. In
particular, high levels of cortisol during REM interfere with
hip-
pocampal—neocortical interactions, disrupting consolidation of
episodic material and altering the episodic coherence of dreams.
We now discuss some of these points at greater length, starting
with a discussion about memory and memory processing that
should help ground our ideas.
What is memory consolidation?
The phrase “memory consolidation” gets used frequently, and in
rather different contexts, but is rarely clearly defined, except in
the most abstract sense of postencoding processes that contrib-
ute to the stabilization of long-term memory. There has been
much focus on molecular and cellular level events taking place
during consolidation, and knowing about these is of both intrin-
sic and practical interest. But there is also a psychological
dimen-
sion to memory consolidation that we believe speaks to the con-
tent and nature of dreams. So, what is memory consolidation all
about?
We assume that during consolidation specific neural circuits
are strengthened. But which ones, and what part of memory are
they? What information do they represent? We believe that
memory consolidation involves both the strengthening of traces
representing the episodic details of experience, and the parallel
integration of information extracted from experience with pre-
viously acquired semantic knowledge. In this view, episodic and
semantic knowledge are processed in parallel interacting
systems,
and much of what happens during memory consolidation in-

volves these parallel processors communicating with each other
and sharing aspects of their knowledge.
A framework for thinking about this neural interaction
builds on the idea that the hippocampal formation and neocor-
tical structures use different computational strategies for storing
information (O’Keefe and Nadel 1978; McClelland et al. 1992,
1995; Kali and Dayan 2004). The hippocampal formation is spe-
cialized to store unique representations, and its circuitry
permits
both the separation of similar input patterns and the completion
of a pattern from partial inputs. Many parts of the neocortex, by
contrast, are specialized to store overlapping representations, in
which the extent of similarity determines the overlap. Thus,
these two systems are well suited for episodic and semantic
memory representations, respectively. McClelland et al. (1995)
argued that because of the superpositional nature of representa-
tion within neocortical networks, it is critical for changes in
these
networks to be accomplished incrementally. Fast change would
destabilize previously stored representations. Slow change per-
mits the integration of old with new in a fashion that does not
lead to “catastrophic interference.” They argued that one way to
accomplish incremental change in neocortical circuits was to
provide multiple iterations of the input, and that replay of an
episodic representation from hippocampal formation to neocor-
tical circuits during certain phases of sleep could accomplish
this
goal.
The functions of memory consolidation and memory replay
Building on these insights, we see replay within the episodic
and
semantic systems during sleep as an example of the communi-
cation between the systems referred to above. This communica-

tion has a number of consequences for memory consolidation.
First, representations within neocortical sites are slowly
strength-
ened, capturing feature information about the objects, actors,
and events of experience. The information being captured con-
cerns similarity relations and statistical regularities—not unique
occurrences (cf. taxon systems; O’Keefe and Nadel 1978).
Second,
representations within the hippocampal formation are strength-
ened, as suggested in the “multiple trace theory” (see Nadel and
Moscovitch 1997). These representations are about particular
ex-
periences, their contexts of occurrence, and unique relations be-
tween objects and actors in those experiences. Third, connec-
tions between hippocampal “episode” traces and neocortical
“feature” traces are strengthened, making it easier for the
former
to activate the latter, enhancing retrieval of properly detailed
memories. This aspect of memory consolidation is particularly
important in maintaining links between the hippocampal epi-
sode trace and the neocortical feature traces because the latter
are
subject to continual “drift” as new information is acquired. This
drift would eventually sever the connections between an episode
and its details unless constant adjustments were made. Replay
provides the basis for these adjustments (Kali and Dayan 2004).
Finally, fourth, neocortical—neocortical connections are en-
hanced, allowing for strengthening of links between loosely re-
lated concepts and distant-but-related experiences, a process
that
eventually results in “semantic” or schematized versions of
some
(but certainly not all) episodic memories (Nadel and Moscovitch
1998). These semantic memories, in the absence of any hippo-
campal contribution, have lost much of their context and detail
but have gained associations with similar knowledge and expe-

rience. Thus, the individual episode is lost, but a stronger
schema
for similar experience is gained.
All these consequences of replay reflect what happens when
hippocampal and neocortical systems are communicating prop-
erly, for example, during SWS sleep early in the night. Matters
change later when cortisol levels rise, and as a consequence,
there
is a disruption of the processing of episodes as coherent units
because high cortisol levels can disrupt the function of the hip-
pocampal formation (Plihal and Born 1999a; Kim and Diamond
2002). This loss of coherence leads to “inefficient
consolidation”
as measured by memory testing (Plihal and Born 1997, 1999a),
but also to the activation of memory fragments in isolation. We
think it is these memory fragments that compose the discon-
nected sounds and images and the bizarre plot lines that con-
stitute many REM sleep dreams. More specifically, hippocam-
pal → neocortical communication is disrupted because high cor-
tisol levels exert a negative influence on the primary output
field
of the hippocampus, the CA1 region (for more detail, see
below).
As a result, disconnected fragments, stored in dispersed neocor-
tical regions, become activated in the absence of the spatial and
temporal contexts that situate them as episodic memories.
Sleep, dreaming, and memory
Learning & Memory 673
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Dreams can be extremely fragmented, but they are rarely
experienced as random sequences of associated images. Rather,
they exhibit varying degrees of narrative and thematic
coherence
(see Foulkes 1999). We have argued that when the waking brain
is confronted with fragmented information, it attempts to syn-
thesize these fragments into narrative themes (Jacobs and Nadel
1998), even if the themes make little sense (Holden and French
2002), and we believe the same principle holds for the sleeping
brain. Activated memory fragments and internally constructed
narrative themes constitute dreams. In addition to being de-
scribed as “fragmented and bizarre,” dreams are often described
as creative, and perhaps this is why we find them so intriguing.
In the absence of hippocampal input during most of REM sleep,
neocortical–neocortical communication proceeds normally.
Thus, disrupted hippocampal communication during REM may
actually aid the linking of loosely related concepts (Stickgold et
al. 1999; Stickgold and Walker 2004), perhaps inspiring new
ideas, the ability to see relationships between previously unre-
lated concepts, and the often noted creative insight inspired by
dreams (see Wagner et al. 2004).
Potential mechanisms
We have suggested that because high cortisol levels disrupt hip-
pocampal–neocortical interactions they can alter dream content.
To understand better the ways in which this alteration occurs,
and the form it takes, we need to look more closely at the actual
mechanisms proposed to cause it. How, for example, do fluctua-
tions in neuromodulators control patterns of neural interaction
during the various stages of sleep?
The functionality of hippocampal ↔ neocortical interaction

varies across the sleep cycles, as we have already observed.
Buzsaki (1996) suggested that hippocampal → neocortical com-
munication is reduced in REM sleep compared with NREM
sleep
or wake. During wake, information about the external world
first
activates the neocortex and then reaches the hippocampus via
the entorhinal cortex. A similar pattern of communication is
seen during REM sleep, when information largely flows out of
neocortex and into hippocampus (neocortex → hippocampus).
Hasselmo (1999) attributes this directionality to acetylcholine,
contending that because acetylcholine is linked to encoding
processes in the awake brain, it follows that in REM sleep,
when acetylcholine levels are as high as during wake, the direc-
tionality of hippocampal–neocortical interaction should mimic
that of initial information processing in the waking state (neo-
cortex → hippocampus).
During SWS the direction of information flow could be re-
versed, reflecting hippocampal neuronal bursts called “sharp
waves” (Buzsaki 1998). These bursts, the most prominent
hippo-
campal pattern during SWS, reflect transient activation of CA3-
CA1 pyramidal cells associated with a sharp wave in stratum
radiatum and fast field oscillation (140- to 200-Hz ripple) in the
CA1 pyramidal layer (Buzsaki et al. 1992; Chrobak and Buzsaki
1996). Thus, in SWS, information is likely reactivated in the
hip-
pocampus and then flows back to neocortex. A recent article
(Sirota et al. 2003), however, suggests that information might
flow in both directions (hippocampus ↔ neocortex) during
SWS.
These investigators demonstrated temporal coupling of neuronal
activity between the neocortex and hippocampus on both slow
and fine time scales during SWS. Neocortical neuronal dis-
charges, associated with the delta wave and spindle events of

NREM sleep, may “select” via the entorhinal input which hippo-
campal neurons will participate in the triggered ripple events.
These specific inputs can select burst initiators of the
hippocam-
pal sharp wave events, and in turn, the sharp wave/ripple-
related
discharge of neurons in the hippocampus will provide a
synchro-
nous output preferably to those neocortical cell assemblies that
continue to participate in the spindle event. Thus, the hippo-
campal output likely coexists with the postsynaptic discharge of
a specific group of neocortical cells (Sirota et al. 2003). In
contrast
to the situation during REM sleep, in which hippocampal output
to the neocortex is severely diminished, the neocortical–
hippocampal–neocortical circuit may remain functionally intact
during SWS. The coupling between neocortical and
hippocampal
networks demonstrated by Sirota et al. (2003) may provide the
temporal framework for coordinated information exchange be-
tween the two structures during SWS.
How can these differences in the directionality of hippo-
campal–neocortical communication across the two main stages
of sleep be accounted for? Why are hippocampal outputs to neo-
cortex disrupted during REM sleep, whereas the entire neocorti-
cal–hippocampal–neocortical circuit seems to remain intact dur-
ing SWS? The above discussion about the functional relation-
ships between hippocampus and neocortex is based on rodent
data. Thus, it is important to remain cautious when using these
results to speculate about human sleep and memory consolida-
tion.
The role of cortisol
We suggest that nightly variations in cortisol, and interactions

between cortisol and other neurotransmitters that fluctuate dur-
ing sleep (acetylcholine, 5-HT, NE), play a critical role in these
phenomena. Cortisol level varies over the course of the night’s
sleep; it begins to rise in the middle of the sleep period and
slowly
escalates with a series of pulses that tend to coincide with REM
sleep until peaking in the early morning hours (Weitzman et al.
1971). Cortisol has both quick and delayed effects on neural
function. The former, nongenomic, effects involve increases in
excitatory amino acids (Venero and Borrell 1999). The latter,
ge-
nomic, effects are mediated by receptors located within the cell
nuclei (McEwen 1991). Within the central nervous system
(CNS),
two kinds of receptors are activated by cortisol: so-called gluco-
corticoid receptors (GRs; type II), and mineralocorticoid recep-
tors (MRs; type I). When a neuron contains receptors of both
types, as many within the hippocampus do, cortisol level affects
the function of the hippocampus in an inverted U-shaped fash-
ion (see Diamond et al. 1992; Pavlides and McEwen 2000). For
example, Diamond et al. (1992) demonstrated that glucocortid-
coids facilitate LTP at low levels but impair it at high levels.
The mechanisms producing this complex interaction are in-
teresting. Type I (MR) receptors have a considerably higher
affin-
ity for cortisol than do type II (GR) receptors. Until all or
virtually
all the MRs are occupied, there is little occupancy of GRs. With
extensive activation of the MR receptors, and the possibility of
activation of GRs, the falling limb of the inverted U emerges.
Thus, impairment of hippocampal function by high levels of
cortisol depends upon the colocalization of MRs and GRs.
Recent work (Han et al. 2002; Patel and Bulloch 2003) has
confirmed that MRs and GRs are colocalized in the dentate

gyrus
and the CA1 field, but much less so in the CA2 and CA3 fields,
where concentrations of GR are much diminished. This differ-
ence has potentially critical functional implications. Most
promi-
nently, it means that at high levels of cortisol, communication
between the hippocampus and the neocortex, which is mediated
by CA1 → subiculum → rhinal cortex connectivity, will be al-
tered or disrupted. At the same time, communication within
parts of the hippocampus itself, most prominently CA3, could
remain intact2. Thus, as the night progresses and cortisol levels
2This observation seems, at first glance, to conflict with the
fact that CA3 is
highly susceptible to the toxic effects of chronic stress
(Sapolsky, 2000). How-
ever, the impact of acute and chronic stress clearly differs in a
number of ways,
and this conflict may be more apparent than real.
Payne and Nadel
www.learnmem.org
increase, hippocampal–neocortical communication will eventu-
ally be altered. Note that levels between 10 and 30 µg/dL are
associated with memory impairment during wake (see Kirsch-
baum 1996; de Quervain et al. 2000), and early in the morning

(prior to waking), cortisol levels vary between 15 and 20 µg/dL.
However, neither cortical–cortical activity itself nor activity
within the CA3 circuits of the hippocampal formation will nec-
essarily be disrupted. This interruption of hippocampal–
neocortical communication would halt the consolidation of as-
pects of memory requiring it, for example, episodic memory (cf.
Plihal and Born, 1997, 1999a), but not the neuronal replay in
CA3 seen in recent experiments (see Battaglia et al. 2004), or
consolidation within procedural memory circuits.
High levels of cortisol during late night REM sleep could do
more than interfere with episodic memory consolidation. By vir-
tue of the same mechanisms, high cortisol levels could affect
the
nature of dreams. It is generally assumed that episodes consist
of
events involving actors, actions, and consequences, all playing
out in settings composed of various objects bound to a specific
spatial and temporal context (see Paller and Voss 2004). The
hip-
pocampal system, as noted earlier, is critical to this binding
pro-
cess, perhaps by contributing the spatial context to which the
bits and pieces of an episode are attached and woven into a
cohesive whole (Nadel and Moscovitch, 1998; Nadel and Payne,
2002; Nadel et al. 2002). When this binding context is absent,
neocortical circuits can generate only semantic knowledge, or
“episode-like” fragments that can be rather bizarre. It is worth
noting the similarities between the nature of dreams and the
kind of memories created during stress or trauma. Clinical evi-
dence suggests that memory for stressful experience lacks
coher-
ence, context, and episodic detail and thus is experienced as
“fragmented” (Golier et al. 1997; Bremner 1999; Gray and Lom-
bardo 2001; van der Kolk et al. 2001). For example, fragmenta-
tion is an important feature of posttraumatic stress disorder

(PTSD), in which patients sometimes describe gaps in recalled
experiences, not only of trauma but of other personal experi-
ences as well (Bremner 1999).
It seems likely that in dreams, as in waking life, retrieved
fragments are subject to narrative smoothing, in which educated
guesses are made about what might have occurred. This process
may begin during the dream and likely continues upon awaken-
ing as cortisol continues to rise. Constructing narratives is a
nor-
mal function of memory. The hippocampal system works to-
gether with the neocortex to recreate episodic memories from
representations of the various attributes or features of the event.
We have suggested that high levels of cortisol undermine this
normal process, leading to false memories (see Payne et al.
2002,
2004) and, in the case of dreams, fragmentation that leads to the
bizarre narratives we attempt to make sense of upon awakening.
In addition to clinical evidence, there is experimental evi-
dence that high levels of cortisol alter memory function. Patient
populations with chronically elevated levels of cortisol, such as
Cushing’s syndrome, major depression, and schizophrenia, as
well as asthmatic patients treated with the glucocorticoid pred-
nisone are characterized by impaired memory function (Stark-
man et al. 1992; Mauri et al. 1993; Keenan et al. 1995; Sheline
et
al. 1999; Sapolsky 2000; Rasmusson et al. 2001). As might be
expected given our discussion thus far, patients with Cushing’s
syndrome and major depression not only have memory impair-
ments associated with high cortisol levels but also have differ-
ences in their ratios of SWS and REM sleep. Because these
disor-
ders are associated with high levels of cortisol, it follows that
SWS
should be diminished in the sleep of these patients. Indeed,

Friedman et al. (1994) demonstrated that patients with
Cushing’s
syndrome spent much less time in SWS than did healthy con-
trols. REM sleep, however, was not significantly different be-
tween groups in this study. Not surprisingly, however, REM
sleep
in patients with Cushing’s syndrome is strikingly similar to the
sleep of patients with major depression, with REM latency
being
shortened and REM density being increased (see Shipley et al.
1992).
In addition to the clinical evidence, experimental studies of
acute stress and memory have been carried out in animals (for
reviews, see Lupien and McEwen 1997; Lupien and LaPage
2001;
Kim and Diamond 2002), and several well-controlled studies
have recently been conducted in humans. For example, Kirsch-
baum et al. (1996) demonstrated that a single, low dose of hy-
drocortisone (10 mg) led to a deficit in verbal episodic memory.
In this study, subjects who received hydrocortisone recalled
fewer words (via a cued recall test) from a previously learned
word list than did control subjects when recall occurred 60 min
after receiving the drug. Further, Lupien et al. (1998) demon-
strated that prolonged cortisol elevations in older adults are as-
sociated with reduced hippocampal volume and impairments in
hippocampally dependent memory tasks. Aging is another con-
dition that is associated not only with elevated levels of cortisol
and memory impairments but also with sleep deficits. As might
be expected, the sleep deficits occur primarily in SWS (see
Kern et
al. 1996; Van Cauter et al. 2000), perhaps helping to explain the
episodic memory impairments often associated with aging. Al-
though a complete review of this growing literature is beyond
the

scope of this article, many other studies have shown a relation-
ship between high levels of glucocorticoids and episodic
memory
deficits (see Wolkowitz et al. 1990, 1993; Newcomer et al.
1994,
1999; de Quervain et al. 2000, 2003; Payne et al. 2002; E.D.
Jack-
son, J.D. Payne, L. Nadel, and W.J. Jacobs, in prep.; J.D.
Payne,
E.D. Jackson, S. Hoscheidt, W.J. Jacobs, and L. Nadel, in
prep.)3.
Because high cortisol levels produce memory deficits during
the waking state, they likely also prevent episodic memory con-
solidation late in the night when REM sleep is abundant (as
shown by Plihal and Born 1997, 1999a). This idea, central to
our
proposal, is supported by several recent studies. Plihal and Born
(1999b), for example, using the early versus late sleep
procedure
(Plihal and Born 1997, 1999a), showed that increasing plasma
cortisol concentrations during early sleep eradicated the benefit
SWS sleep typically bestows on episodic memory. Recall that
sub-
jects who study a list of paired-associates before retiring to bed
typically show great improvement after 3 h of sleep dominated
by SWS, but not after 3 h of REM. Plihal and Born (1999b)
showed that infusing cortisol during the 3-h SWS retention in-
terval undercuts the facilitation of episodic memory that would
otherwise be observed during this time. However, cortisol infu-
sion failed to disrupt retrieval of the procedural memory task.
Gais and Born (2004) have recently shown precisely the same
effect with injection of an anticholinesterase agent that
increases
acetylcholine levels. Whether acetylcholine triggers the rise in
cortisol, which then alters hippocampal function is not known at

this time4 but is a fit topic for future study.
3Not all glucocorticoid effects on memory are negative. For
example, there is
ample evidence that glucocorticoids released during or after
emotionally
arousing experiences play a critical role in the formation of
lasting memo-
ries (Roozendaal 2003), and memory for emotional materials is
actually facili-
tated by cortisol (see Buchanan and Lovallo 2001; J.D. Payne,
E.D. Jackson, S.
Hoscheidt, W.J. Jacob, and L. Nadel, in prep.). Memory for
emotionally neutral
experiences, by contrast, is typically negatively affected by
acute stressors or
administration of cortisol (for a review, see Payne et al. 2004).
Along these lines
it is interesting to note that many dreams are distinctly
emotional, often in-
volving intense fear, and that emotional dreams are among the
most well-
remembered.
4Although Gais and Born (2004) failed to show a corresponding
increase in
cortisol after administration of a small dose of the acetylcholine
agonist phy-
sostigmine (0.75 mg), it remains possible that higher levels of
acetylcholine
may trigger a concomitant rise in cortisol.
www.learnmem.org

It is worth noting that cortisol in the Plihal and Born
(1999b) study was elevated just enough to mimic the late night
peak of circadian HPA activity (15.2 + 0.68 mg/dL). This is
similar
to cortisol levels observed in response to a mild to moderate
stressor (∼10 to 30 mg/dL) and, as mentioned, is a sufficient
dose
to disrupt episodic memory function (see Kirschbaum et al.
1996;
de Quervain et al. 2000). Thus, cortisol levels, not sleep stage
or
time of night per se, could determine both the nature of dreams
and episodic memory consolidation effects. To repeat, elevated
cortisol leads to binding problems and fragmentation. When the
brain is confronted with decontextualized fragments, it imposes
a narrative upon them, leading to distorted memories or, in the
case of dreams, to bizarre reconstructions.
Two caveats
We have argued that diurnal elevations in cortisol may help ex-
plain the nature of dreams. We do not mean to suggest that
cortisol is the only factor affecting the structure and content of
dreams. Several of the neurotransmitters that fluctuate across
the
sleep cycle are also known to affect memory function during
wake (e.g., acetylcholine, see Hasselmo 1999; NE, see Cahill
and
McGaugh 1998), and there has been much speculation about
their influence on memory processing during sleep (Hobson

1988; Solms 2000). Moreover, these neurotransmitters likely in-
teract with cortisol during sleep. For example, acetylcholine and
cortisol are both diminished during SWS (they are also both el-
evated during REM sleep). Levels of cholinergic activity and
cor-
tisol production during SWS are both quite low, and this
appears
necessary for episodic memories to undergo effective consolida-
tion; experimentally elevating either substance impairs perfor-
mance on verbal episodic memory tasks (Plihal and Born 1999b;
Gais and Born 2004). In addition to cortisol then, acetylcholine
is another candidate modulator of dreams; a thorough consider-
ation of this possibility is beyond the scope of the present
paper.
Recent neuroimaging evidence demonstrates a selective in-
activation of portions of the frontal cortex during REM sleep
(see
Braun et al. 1997; Nofzinger et al. 1997). These studies demon-
strated a prominent decrease in activity of the dorsolateral pre-
frontal cortex, and disruption in this region has been associated
with confabulatory syndromes that are in some ways similar to
dreaming. Moreover, as the prefrontal cortex is thought to play
a
role, along with the hippocampus, in binding the elements of a
memory together (Mitchell et al. 2000), deactivation seen in this
region could be related to the fragmented nature of dreams. In-
terestingly, frontal deactivation may also underlie our tendency
to blithely accept dream fragments and bizarre themes as
common-
place and normal. This notion is consistent with evidence that
the
frontal lobes contribute to reality monitoring (Johnson 1991),
working memory (Goldman-Rakic 1992), and other executive
func-
tions (Smith and Jonides 1999) during the waking state.

Conclusions
We have proposed that the hormone cortisol plays an important
role in controlling the state of memory systems during sleep.
High levels of cortisol, as are observed late at night and,
typically
in the context of REM sleep, disrupt normal hippocampal →
neo-
cortical communication, thereby interfering with forms of
memory consolidation dependent upon this communication. At
the same time, the content of dreams is also affected. In SWS
dream content reflects the normal interaction between hippo-
campal and neocortical circuits, allowing for typical episodic
memories to emerge. In REM sleep, however, dream content re-
flects only neocortical activation, which we assume accounts for
the fragmented, often bizarre, nature of these dreams.
The fact that normal episodic memories are only retrieved
during SWS when hippocampal–neocortical communication is
functional has interesting implications for a current debate
about
the storage of remote episode memories. Some (see Alvarez and
Squire 1994) believe that remote episode memories are ulti-
mately stored in the neocortex, after consolidation has been
completed. Others (see Nadel and Moscovitch 1997) have
argued
that the hippocampal complex is always involved in the
retrieval
of fully elaborated episode memories. The absence of proper
epi-
sodic retrieval in dreams during REM sleep, when
hippocampal–
neocortical communication is disrupted, but neocortical–
neocortical communication is preserved, is consistent with the
latter position. If fully consolidated episode memories could be

elaborated in the neocortex, we should expect to observe their
retrieval during REM dreams—but this does not appear to be the
case, at least in the few studies reported to date. Closer
examina-
tion of the nature of dreams in REM sleep, and the presence, or
absence, of remote memories in these dreams, would provide
important clues in this ongoing debate about the nature of
memory storage in the brain.
In addition to telling us something about the contributions
hippocampal and neocortical circuits make to episodic memory,
to the consolidation of episodic and semantic memory, and to
the content of dreams, our proposal suggests some intriguing
possibilities about creativity and the generation of novel
thoughts. One stage of consolidation likely involves the integra-
tion of information with pre-existing knowledge and the linking
of distant but related concepts. We dream when we become
aware of these activated traces, which are often fragmented im-
ages and sounds coupled with motor activity. Similar to memo-
ries created under stress, these fragments are immediately sub-
jected to a process of narrative smoothing, and the result is
typi-
cally a story that is often confabulatory, quite bizarre, but
possibly also creative.
Although it is true that accurate recall is adaptive in many
cases, there may nonetheless be a positive side to a process that
produces fragmentation—both during wake and during sleep.
All
new ideas are based upon previously stored information. These
fragments, or pieces and patches of knowledge, are bound into
representations that we use to recall information about personal
experience and to help us understand and act in the world. When
these bonds are weakened, this information can be recombined,
either in dreams or misremembered episodes—perhaps resulting
in a process leading us down unusual paths to creative insights

and new ideas.
Dreams are but interludes which fancy makes
When monarch reason sleeps, this mimic wakes.
Compounds a medley of disjointed things
A mob of cobblers and a court of Kings.
John Dryden (1700)
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References
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“The Effect of Temperature on Amylase Activity”
Methods
The objective of this experiment was to determine the effect of
temperatures (0 °C, 25 °C, 55 °C, and 85 °C) on fungal
(Aspergillus oryzae,) and bacterial amylase’s ability to break
down starch. Our team monitored starch catalysis using the
Iodine test. Iodine turns the most catalyzed starch yellow, and
the least catalyzed blue. When the reaction turns blue-black or
dark brown, it means that starch is present and, therefore, not
catalyzed.
Each member of team four had a temperature assigned to work
with. Each individual monitored the activity of amylase (fungal
and bacterial.) Time also varied respectively ( 0 mins, 2 mins, 4
mins, 6 mins, 8 mins, and 10 mins.) The group marked the spot
plates with time (on the side) and temperatures (across the top.)
The team labeled 4 test tubes with different temperatures, the
enzyme source (B or F) and the group’s number (4.) The group
also marked the pipette for each temperature. Test tubes were
placed into the respective temperatures. Finally, the team
carefully carried out the two trials.
Without removing the test tubes from the water bath at different
temperatures, the team added 2 drops of starch from each
temperature to the first row of the spot plate (at 0 minutes)
containing iodine. The team poured the same amount of iodine
before each trial. The team proceeded, transferring the starch
into the amylase (fungal and bacterial) at their respective water
bath and mix these two without removing the test tubes from the
water bath. Then, the team added two drops of this new mixture
(starch-amylase) at their respective temperatures to the second
row of the spot plate. The other rows were filled with the same
mixture at the temperatures assigned with two minutes interval
between each trial.
Results
The following tables and pictures show the results group four
(first) and all groups (last) obtained.

Group 4 Result
Data Collected for all Groups
Fungal Amylase vs. starch
Bacterial Amylase vs. starch
After conducting the whole experiment, the team collected the
data for the results. The group observed that the least amount of
starch was present at 55 °C at any time, for bacterial amylase
and 25°C to 55 °C for fungal amylase (for most students.) The
reasoning behind this statement might be that the mixtures at 55
°C turned light yellow in the presence of iodine (at all times
except time 0) for bacterial amylase. The mixture became dark
yellow (at all times except time 0) at temperatures 25 °C to 55
°C for fungal amylase, which could indicate that amylase
activity was not affected. The team also noticed that the enzyme
amylase denatures at higher temperatures (85 °C) for both types
of amylase. The group made that assumption because the
solution turned dark blue brown at 85 °C at all times. According
to The Iodine test, dark color indicates the starch is present and
not catalyzed.
The average of starch concentration of all groups at each
temperature for fungal amylase demonstrates that there are no
outsiders in our data and that the results’ standard deviation is
not significantly big for the experiment concluded. The results
obtained for all the trials suggest that amylases (bacterial or
fungal) have a respective optimum temperature. It is also
evident that if these amylases are not placed on their ideal
temperature, it loses their ability to break starch down.
Guerra 2
Guerra 2

“The Effect of Temperature on Amylase Activity”
Methods
The objective of this experiment was to determine the effect of
temperatures (0 °C, 25 °C, 55 °C, and 85 °C) on fungal
(Aspergillus oryzae,) and bacterial amylase’s ability to break
down starch. Our team monitored starch catalysis using the
Iodine test. Iodine turns the most catalyzed starch yellow, and
the least catalyzed blue. When the reaction turns blue-black or
dark brown, it means that starch is present and, therefore, not
catalyzed.
Each member of team four had a temperature assigned to work
with. Each individual monitored the activity of amylase (fungal
and bacterial.) Time also varied respectively ( 0 mins, 2 mins, 4
mins, 6 mins, 8 mins, and 10 mins.) The group marked the spot
plates with time (on the side) and temperatures (across the top.)
The team labeled 4 test tubes with different temperatures, the
enzyme source (B or F) and the group’s number (4.) The group
also marked the pipette for each temperature. Test tubes were
placed into the respective temperatures. Finally, the team
carefully carried out the two trials.
Without removing the test tubes from the water bath at different
temperatures, the team added 2 drops of starch from each
temperature to the first row of the spot plate (at 0 minutes)
containing iodine. The team poured the same amount of iodine
before each trial. The team proceeded, transferring the starch
into the amylase (fungal and bacterial) at their respective water
bath and mix these two without removing the test tubes from the
water bath. Then, the team added two drops of this new mixture
(starch-amylase) at their respective temperatures to the second
row of the spot plate. The other rows were filled with the same
mixture at the temperatures assigned with two minutes interval
between each trial.
Results
The following tables and pictures show the results group four

(first) and all groups (last) obtained.
Group 4 Result
Data Collected for all Groups
Fungal Amylase vs. starch
Bacterial Amylase vs. starch
After conducting the whole experiment, the team collected the
data for the results. The group observed that the least amount of
starch was present at 55 °C at any time, for bacterial amylase
and 25°C to 55 °C for fungal amylase (for most students.) The
reasoning behind this statement might be that the mixtures at 55
°C turned light yellow in the presence of iodine (at all times
except time 0) for bacterial amylase. The mixture became dark
yellow (at all times except time 0) at temperatures 25 °C to 55
°C for fungal amylase, which could indicate that amylase
activity was not affected. The team also noticed that the enzyme
amylase denatures at higher temperatures (85 °C) for both types
of amylase. The group made that assumption because the
solution turned dark blue brown at 85 °C at all times. According
to The Iodine test, dark color indicates the starch is present and
not catalyzed.
The average of starch concentration of all groups at each
temperature for fungal amylase demonstrates that there are no
outsiders in our data and that the results’ standard deviation is
not significantly big for the experiment concluded. The results
obtained for all the trials suggest that amylases (bacterial or
fungal) have a respective optimum temperature. It is also
evident that if these amylases are not placed on their ideal
temperature, it loses their ability to break starch down.
Guerra 2
Guerra 2

Writing a Scientific Report or Paper
Results of careful laboratory work are not useful unless they
can be presented in a clear, concise manner to others
for comment and evaluation. Such presentations are usually in
the form of a scientific paper published in a reputable
scientific journal. Scientific communications have many things
in common, which leads to a rather standard style of
writing that allow the results and meaning of experimentation to
be quickly grasped by the reader. Scientists do not
expect to read attractive, stimulating prose to obtain
information from technical scientific papers. The experimental
design, results and explanation of results are what are attractive
and stimulating not the cleverness of the prose. The
following discussion should be useful in helping you prepare
your laboratory reports, which are scientific reports.
Read it carefully before beginning your reports. Your laboratory
instructor may make additional comments. The
specific format of a scientific paper varies among journals.
However, the format presented below is the most
commonly used. It is the format you must use in your scientific
writing for this course.

Part I: Format of a Scientific Report
The scientific report will be composed of seven sections. Each
section will have a heading immediately followed by
the text, figures or graphs. The order of the sections is: title,
abstract, introduction, methods, results, discussion and
literature cited.
A) Format regulations:
• typed
• double spaced
• 10-12 font, Times New Roman
• 1 inch margins
• pages numbered
• titled sections
• untitled hypothesis
• Quotes are NOT allowed. Everything must be properly
paraphrased.
• No website references are permitted as sources. No
exceptions.
• Everything must be properly cited. It is considered plagiarism
if it is not.
• Write in third person, past tense

The overall presentation/grammar/spelling will be evaluated.
Although this is not an English class, these elements
are important to the proper communication of science. Before
you turn in your final version, use the spell check
function and reread your report. You should also take the time
to visit the Center for Academic Success to
participate in the Read, Write, and Cite Workshop series for
additional help on writing your reports.
Note: Never write statements like the following: “My lab report
is about…”, “My hypothesis is…”,
or any version of this type of statement.
(1) Title Section
Create a title that briefly conveys to the reader the purpose of
the paper. The title of your report must be informative.
Many readers scan journal article titles and the decision whether
or not to pursue an article is based on the
information in the title. Generally, this information includes:
primary factor(s) manipulated or studied; outcome of
manipulation (the response or effects); and organism studied, if
relevant. An example of an informative title would
be: "The Effect of Varying Serotonin Concentrations on
Calcium Release at Synaptic Membrane in Motor Neurons
of Aplysia."

The title page must contain your name, Panther ID, lab partners’
names, title, and lab section.
(2) Abstract Section
The Abstract should be an autonomous summary of the entire
report. It serves to help readers determine how
relevant the report is to their own interests. This section is
brief, only one paragraph, in which the author indicates
what was done, the reasoning behind it, the results and the
conclusions. It must highlight only the most important
elements of each major sections of the report (Introduction,
Methods, Results, and Discussion). The scientific report
can be summarized into an abstract with four types of
statements: purpose statements that are general in describing
the importance and/or goals of the research; methods statements
that explain what was done and how it was done;
results statements that describe what information or data was
acquired; and discussion/conclusion statements that
explain what the information or data probably means and what
conclusions are drawn. Only the most important
aspects of the report should make it to the abstract.
This section should be between 200 and 250 words in length.
This section should contain a clear summary of what

was demonstrated, how each part of the lab was carried out and
how conclusions were reached. This section should
contain one or two purpose statements (without saying "The
purpose of this experiment is..."), a complete summary
of each experiment (method statements) in a few sentences, and
brief, accurate explanations of the results. The final
sentences should be the concluding statements.
(3) Introduction Section
This section should indicate why the study was done and give
the reader sufficient background to understand the
report. The "why" of the study will include historical
information that leads to your study and the significance of the
study to a specific discipline (such as developmental
neurobiology) to which the study belongs. The reader, after
perusing the introduction, should know precisely the importance
of the problem being addressed. You should write
about the questions you will be answering in this experiment.
Although, the content of the introduction should start
broad and narrow in scope as the introduction proceeds, be
careful not to start too broad. This could lead to
problems with the scope of the paper. Note: any historical
background (that is, previous studies) must be properly
cited. This section must include 4 peer reviewed outside sources

(outside of lab book and text book), of which 2
should be primary literature.
This section contains the basic background information for the
lab report. Be sure to comment on what is the
significance of this study and its relation to the larger field.
Give an example of why the study is significant. Your
hypothesis is used to make the prediction(s). The predictions
are based on the background information that was
gathered. You should have a clear statement of the reason for
performing the lab along with including the rationale
for each technique used.
• What was the purpose of each experiment? For each
experiment, include questions that will be answered
and the expected predictions of the results for each question.
Try to include a hypothesis. (without saying
"My predictions are..." or "My hypothesis is...")
• Note: Just because you are writing a report about a lab
exercise does not mean you are basing the entire
report on one hypothesis. You are more than likely going to
need to discuss more than one set of variables,
which would lead to more than one hypothesis or prediction.
• This section should be between 450-700 words long and
smoothly flow from one topic to the next.
(4) Methods Section

A reader can evaluate the results of your study only if he or she
understands the experimental design, the materials
used and the reasoning behind them. Thus, it is important to
carefully outline procedures and techniques used.
Complicated procedures might be graphically outlined. Besides
procedures, this section should include models or
equipment used (this should not be written like a laundry list of
materials), source of chemicals (if relevant),
numbers and types of organisms used, including sex and strain
sample sizes, number of times experimental
procedure was performed, and other pertinent factors. Please
note: There should NEVER be a list of materials in this
or any section.
• This section is 200-350 words and is a narrative. No credit
will be given for a methods section written in a
bulleted format.
• Include a brief description of how each experiment was
performed. There should be enough detail so the
reader (experienced researcher) could repeat the experiment.
This does not mean having an extensive
section on how you labeled a test tube. That is not important for
the replication of the experiment. You
need to include the aspects of the methods which are crucial for

replication.
• You should explain the procedural steps taken (summarize)
and not create a duplicate of the instructions
from the lab manual. You must write the procedures in your
own words, not the manual’s or anyone else’s.
• Again, NO list of materials is permitted.
(5) Results Section
It is crucial that the outcomes of experiments are carefully
organized and clearly presented. This is best
accomplished by presenting data in clearly labeled graphs and
tables. What the tables and/or graphs are meant to
indicate should be clear without reference to text. However,
references to each graph and table MUST be made in
the text of the Results section. Graphs and tables should be
numbered in the order in which they are mentioned in
the text; that is, tables should be labeled as consecutive series
(Table 1, Table 2, etc.). Each figure should have a
figure title, number, and brief caption. The section text should
elaborate on the information presented on the table as
well as, summarize information presented in tables and/or
graphs that will be pertinent to the discussion section.
You cannot turn in a lab report with a results section that does
not have associated text explaining the incorporated
figures. Analyses must be performed on class data. Thus, the

data represented in your report should be
representative of the class data, not just your group’s data.
Included in this section should be sample data in the form
of a picture. This can be a picture of your groups data as
representative of the type of data collected.
• All graphs and tables should be your own work! Graphs and
tables should not be identical to anyone else's
in the lab, including your lab partner's.
• Also include a concise detailed description, which clearly
summarizes the graph or table. Include
comments about the results for each experiment and control.
This text is a verbal description of what the
table/graph/picture is illustrating (enough detail to be on its
own).
• The text should be between 250-450 words long
• Do not interpret the results in this section. This section
focuses on what you observed quantitatively and
qualitatively throughout the collection of data. The discussion
section will include why things happened the
way this did.
(6) Discussion Section
In brief, the Discussion section is where results are interpreted
and conclusions are drawn. The significance and
interpretation of the study should be explained in this section.
Specific points made in the Results section should be

discussed in light of previous studies and hypotheses. This
means there needs to be cited literature in this section.
Often, new hypotheses are put forth, based on the experimental
outcome. This may be included in your discussion.
The most important part of the Discussion section is
establishing what the results indicate, both for the ongoing
study and for future studies. For each point made in the results,
you need to discuss why things happened the way
they did. If there were errors made, then this needs to be
included and in context with the interpretation of the
results. Were the questions you included in the Introduction
section, answered by this study? If not, how could the
study be redesigned? Some questions that can be answered in
interpreting the results in the Discussions section are:
Why are these results the same as (or different from) previously
published studies? What parameters of the
experimental design were important in the expected (or
unexpected) results? Are some of the results due to artifacts?
How do you know? How might the experimental design be
altered to diminish artifacts? What are limitations of the
experimental design? Why are these results important in a
broader context?
• This section should be approximately 500-700 words long.

• This section should include a clear discussion in relation to
each hypothesis and/or prediction and should
discuss what is known about the topic (reported by other
researchers).
• Include a brief summary of your results with reference points
to your results, and explain how you
interpreted your results (why did things turn out the way they
did?). Be sure to refer to the specific
illustration whenever discussing the results.
• Remember nothing is EVER proven. So the results either
support or refute your original
hypotheses/predictions.
• Also, explain why the control and experimental outcomes were
what you expected or were not what you
expected.
• Comments should also be made about problems and/or
improvements for the next time. This is where you
can discuss the experimental design and follow-up studies.
• This section is where you are essentially asking "why"
everything/anything happened during the
experiment.
(7) Literature Cited Section
This section includes the alphabetical listing of all sources of
fact or theory mentioned in your paper that were not
generated by you. This will primarily include research articles,

but may include review articles and texts as well.
The citations should be written using APA (6th edition) format.
• You MUST include at least six references. There should be at
least 2 primary sources, 2 secondary sources,
and you must include the general biology textbook, and lab
manual (don’t forget to cite the methods).
• You must include 4 peer reviewed outside sources (outside of
lab book and text book), of which 2 should
be primary literature.
• No website references or any encyclopedia references are
allowed.
• YOU MUST HAVE IN-TEXT CITATIONS!!!
• Any citation in the body of the report is put at the end of a
sentence and should be done like this (Author's
last name, year). There are very few exceptions to this. Do not
write all of the author’s names for in-text
citations. If there is only one author, then write the name of the
principle author. If there are two authors,
then you must write both names and if there are multiple
authors write et al. after the name of the principle
author (Yes in italics- it's in Latin). Example: (Alberte et al.,
2012)
• Anything that you or other biology students reading your
report would not know off the top of your head,
needs to have a citation at the end of the sentence. This includes
anything looked up and used. This is

especially important in the introduction.
• Your textbook can be cited as the source of basic biological
information related to the topic of the report.
• Many sentences in the introduction and discussion will have
citations at the end, so make sure the content
flows smoothly from beginning to end. Try not to have every
sentence with a citation. Use connecting
sentences and your own ideas or summaries of the experiments
where possible. Remember to put the in-
text citation before the final punctuation of the sentence.
Rules for constructing a bibliography
1. Use APA, 6th Edition Citation guide for BOTH in-text
citations and your bibliography
2. References should be listed in alphabetical order
3. If a particular reference takes more than one line, then all
lines (except the first) should be indented
4. Include ALL authors, never write “et al.,” when writing the
full literature cited page
5. Remember to write “and” before the name of the last author,
if the article or book has multiple authors.
6. References should not be numbered nor bulleted.
7. Everything counts including but not limited to the placement
of period, italics, parentheses, etc.
8. If there are no in-text citations and no works cited section the
report will be considered plagiarized.

Part II: Guidelines for BSC1010 Lab Reports
A) General Rules:
• If you are not present in lab you cannot turn-in a lab report for
that lab.
• You need to be an active participant in all labs which contain
experiments for the lab report. You will clean
up your bench area before you leave the lab.
• You will be present (or have a make-up) for the lab. Refer to
the syllabus for the make-up policy.
• You will turn in your lab report in its entirety. Turning in one
or more components or sections of the lab
report after the due date and time will make the entire lab report
late.
• This lab report must be your own work (no plagiarism).
Content used from references needs to be cited. All
text and graphs should be original and not the same as your
partners. You cannot resubmit work
previously done in another class (per the plagiarism policy)
• You will need to turn in only an electronic copy. Turnitin will
be used to check for plagiarism. 10 points
per day will be deducted from your lab report until your
instructor has your report through Turnitin.
• It is your responsibility to turn your lab report on time
electronically to your instructor, per their
instructions. A late lab report will lose 10 points every day it is

late. It is your responsibility to know how to
properly submit your report AND to check to make sure it is
submitted. Even if it is a “careless little
mistake” it is a “careless little mistake” which cost you points
on your report. Be absolutely sure you
submitted your report.
• The due dates have been posted since the first week of the
term and are well known.
Hints for Scientific Writing: Note: Problems arise in writing
scientific papers because of specific aims of scientific
writing: to be clear, concise, unambiguous, and accurate. Due to
the space restrictions in journals and time
limitations of your instructor, every word must help to convey
the required information. The report as a whole
should be objective and self-explanatory. The following seven
recommendations should help you with your writing
for this scientific report.
1. Avoid wordiness. Eliminate redundancies.
2. Write in the past tense. You can use the present tense for
conjectures in the discussion section.
3. Do not use footnotes.
4. Be sure that there is text in the Results section. Also, make
sure that each graph and/or table is referred to
and that reference is not made to nonexistent tables or graphs.

5. Check that each section contains the proper information; for
example, do not put results in the Methods
section.
6. Check that each Literature Cited item is in the text and that
each citation in the text appears in the
Literature Cited section. This includes proper in-text citations.
7. Never write "My hypothesis is...", "The purpose of this
experiment is..", "My predictions are..."
Sections 0 1 2 Points:
Title Page No cover page Incomplete cover page
Cover page with proper
format, complete information,
and informative title
0 3 7
Abstract No abstract
Doesn't reflect on the entirety
of the report including all
major sections; too short, or
too long

Good- appropriate summary
provided with appropriate
length
5 10 15 20
Introduction
Poor- Missing information, or
too vague; too short; no
research
Adequate- Satisfactory
introduction with major topics;
information unclear; poorly
researched
Good- Proficient introduction
that states major topic and
hypotheses; information clear;
decently researched
Excellent- Well developed
introduction and clearly
introduces the topic; good
length; good unlabeled
hypotheses; well researched
0 3 6
Methods No Procedures
Incorrect procedures; missing
steps; improper format
Correct procedures with proper
format

3 5 7 10
Results
Results given either only in
tables/figures or only in text
Satisfactory description of
results; included insufficient
supporting tables/figures
Results stated vaguely with
some observations; included
tables/figures
Results stated with clear
description of observations;
tables/figures included with
captions and references in text
5 10 15 25
Discussion
Poor- Limited information of
topic; lack of discussion of
results; complete lack of
understanding of experiment
Adequate- Some aspects of
paper researched; limited
discussion of results; too short;
does not address hypotheses,
nor sources of errors; some
understanding; addresses few
questions

Good- Well researched, but
limited detail; addresses either
sources of error, OR
hypotheses; decent length;
good understanding of the
experiment
Excellent- Well developed
discussion of results;
exceptionally researched;
hypotheses and sources of
error evaluated; real-world
application included; good
conclusion; all possible
questions were addressed
1 3 5 8
Organization
Lacks clear and logical
development; does not follow
any format; no/poor transitions
Somewhat clear and logical;
follows some format; weak
transitions; improper section
formatting
Clear and logical; follows good
format; good transitions;
problems with section
formatting
Exceptionally clear and
logical; follows excellent

format; excellent transitions
1 5 10
Language/ Grammar
Inconsistent/inapropriate
grammar, spelling, and
paragraphing throughout
Some errors in grammar,
spelling, and paragraphing
Paper is clear and concise;
proper grammar, spelling, and
paragraphing
1 3 6
In-text Citations
Inconsistent use of in-text
citations with improper format
Somewhat inconsistent use of
in-text citations with proper
format
Cosistent use of in-text
citations with proper format
1 3 6
Bibliography
Lack of proper format, sources
missing or incomplete
Some errors in format; most

sources shown
Use of proper format; all
sources shown
Comments:
0
Deductions:
/100 Total
Score
PID:
BSC 1010L- General Biology I Lab Lab Report Rubric
Name:

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