Chapter 8Maintenance and Motivation2Outlin

Chapter 8
Maintenance and Motivation
2
Outline
The brain’s reward circuitry
Hunger regulation
Thirst regulation
Motivating the brain to work
Grooming
Barbering (Extreme Grooming)
Reward circuitry
Time budgets help us understand what people spend their time
doing/find rewarding
How might you experimentally determine the reward center of
the brain?
4

Reward circuitry
(a) Rats press a bar to receive electrical stimulation to the
mesolimbic dopaminergic pathway. (b) If rats increase bar press
responses to obtain stimulation to a specific brain area; this
indicates that the stimulation is rewarding.
5
Reward circuitry
We can also measure behavioral responses to particular stimuli
Similarities observed between rodents and humans suggest that
facial responses to sweet and bitter tastes have been conserved
across mammalian species.
6
Reward circuitry
Critical regions
mesolimbic dopaminergic pathway
septal nuclei
snucleus accumbens
Reward circuitry

Various brain areas and neurochemicals guide us to desired
outcomes based on how much we enjoy the activity (liking),
wish to engage in the activity (wanting), or have come to
associate specific stimuli with subsequent desired activities
(learning).
8
Reward circuitry
Liking vs. wanting vs. learning
Various brain areas and neurochemicals guide us to desired
outcomes based on how much we enjoy the activity (liking),
wish to engage in the activity (wanting), or have come to
associate specific stimuli with subsequent desired activities
(learning).
9
Reward circuitry
The environment can shape how our brain processes stimuli
How could we apply this research?
In this study, the rat’s habitat influenced the proportion of the
nucleus accumbens shell assigned to positive and negative
emotional responses.
10

Hunger Regulation
We eat to live, so the brain is good at motivating us to eat
How it accomplishes this feat is based in part on our
environment
Brain size and stomach size relate to habitat/food availability
Hunger Regulation
Orangutans, who eat only raw foods, require a large stomach for
storage. (b) Eating cooked foods enables humans to have
smaller stomachs, since we obtain necessary levels of nutrients
in smaller volumes of food
12
Hunger Regulation: Neurobiology
Hyperphagia
Lesions to VMH
Lesions to LH
Sensory-specific satiety
Key players: insulin, leptin, ghrelin

Mice expressing a recessive gene associated with leptin
deficiency have more body fat than mice that do not express the
recessive gene.
14
How can we determine which brain regions are involved in
regulating hunger?
As indicated by the presence of darkly stained Fos-positive
cells, there is less activation in the arcuate nucleus of (a) rats
that are fed to satiety and administered saline than in that of (b)
rats that are food deprived with a saline infusion. (c) However,
if the hungry animals receive an insulin infusion, less Fos
activity is observed.
15
Leptin and ghrelin interact with the arcuate nucleus to affect
hunger and energy regulation.
16
Can we be addicted to particular kinds of food?

Why is ‘junk food’ so good?
Is it adaptive to like junk food?
Sugar “withdrawal” in rats
Rats that had experienced greater access to sugar consumed
much more sugar after a period of sugar deprivation than did
control rats.
18
Extended access to food (buffet style) can raise reward
thresholds
Having people around also influences eating
Can you think of why?
Are there possible confounds?
(a) Eating with friends may be enjoyable, (b) but it leads us to
consume more calories.

20
Hunger regulation: Eating disorders
Anorexia nervosa
Bulimia nervosa
Anorexia nervosa
Bulimia nervosa
Still a lot of research to be done
22
Serotonergic receptors and anorexia. Research suggests that the
proportion of 5-hydroxyindoleacetic acid 1A and 2A receptors
in (a) healthy patients is distorted in (b) patients diagnosed with
anorexia
23

The insula plays a role in determining whether food is perceived
as positive or negative.
24
Hunger regulation
Some nutrients that we need for healthy brain function are
acquired by our diet
A lot of speculation about the benefits of supplementing these
nutrients
More research still to be done
Hunger regulation
Impact of high-fat maternal diet on offspring
Three groups of rats
HFD: High-fat pups raised by high-fat diet mothers
HFD-BD: High-fat pups raised by balanced-diet mothers
BD: Balanced-diet pups raised by balanced-diet mothers
Any predictions?
26
Hunger regulation

(a) The pups of rats placed on a high-fat diet during pregnancy
developed more orexin-producing neurons than did o spring
from mothers kept on a balanced diet during pregnanc y, even if
these offspring consumed a balanced diet after birth. (b) As
indicated by the arrows, more orexin cells were double stained
for bromodeoxyuridine in the brain tissue of offspring from the
mothers with the high-fat diet than from offspring of mothers
with the balanced diet.
27
Thirst regulation
Osmoregulatory thirst
Hypovolemic thirst
28
Thirst regulation: Osmoregulartory
Osmoreceptors
Anterior third ventricle
When a hypertonic solution was infused into the hypothalamic
area of goats, they started drinking water from the bucket.
very sensitive osmoreceptors have been identified in two areas
of the anterior third ventricle

29
Thirst regulation: Osmoregulartory
Human PET
Anterior and posterior cingulate activity
Insula also involved
When human subjects were thirsty, more activity along the
cingulate cortex was observed than after the subjects relieved
their thirst by drinking water.
30
Thirst regulation: Hypovolemic
Baroreceptors
Role of vasopressin
Angiotensin II
Motivation to work
Many projects require sustained work
Nonhumans have this problem too
32

Motivation to work: Anatomy
brain areas implicated in directing and sustaining work efforts
33
Motivation to work
Ratio strain
Why does caffeine help us work?
34
Motivation to work
Role of dopamine
Rats are more likely to exert more effort for highly desirable
food when their dopaminergic system is intact and functioning
normally.
35
Motivation to work: Plasticity
We learn the relationship between effort and outcome
Learned helplessness

Learned persistence
36
Grooming as a motivator
Many mammals spend lots of time grooming
Rats as much as 50% of their day
Grooming as a motivator: Neurobiology
Striatum lesions reduces grooming in rats
Parkinson’s patients and patients with depression also show
reduced grooming
Grooming in rat models of depression is restored via
antidepressants
38
Barbering
Extreme grooming, usually of a cage mate
No clear adaptive value (unseen in the wild)

Theories
Establish dominance
Cope with stress
Compensatory action response (increase stimulation in an
otherwise boring environment)
Barbering
40
Barbering
Relationship to humans?
Barbering patterns in mice resemble the bald patches resulting
from hair picking in humans diagnosed with a condition known
as trichotillomania
41
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NRNP/PRAC 6635 Comprehensive Psychiatric Evaluation

Template
Week (enter week #): (Enter assignment title)
Student Name
College of Nursing-PMHNP, Walden University
NRNP 6635: Psychopathology and Diagnostic Reasoning
Faculty Name
Assignment Due Date
Subjective:
CC (chief complaint):
HPI:
Past Psychiatric History:
· General Statement:
· Caregivers (if applicable):
· Hospitalizations:
· Medication trials:
· Psychotherapy or Previous Psychiatric Diagnosis:
Substance Current Use and History:

Family Psychiatric/Substance Use History:
Psychosocial History:
Medical History:
· Current Medications:
· Allergies:
· Reproductive Hx:
ROS:
· GENERAL:
· HEENT:
· SKIN:
· CARDIOVASCULAR:
· RESPIRATORY:
· GASTROINTESTINAL:
· GENITOURINARY:
· NEUROLOGICAL:
· MUSCULOSKELETAL:
· HEMATOLOGIC:
· LYMPHATICS:
· ENDOCRINOLOGIC:
Objective:
Physical exam: if applicable
Diagnostic results:
Assessment:
Mental Status Examination:
Differential Diagnoses:
Reflections:
References
© 2021 Walden University
Page 1 of 3
NRNP/PRAC 6635 Comprehensive Psychiatric Evaluation
Exemplar
INSTRUCTIONS ON HOW TO USE EXEMPLAR AND

TEMPLATE—READ CAREFULLY
If you are struggling with the format or remembering what to
include, follow the Comprehensive Psychiatric Evaluation
Template AND the Rubric as your guide. It is also helpful to
review the rubric in detail in order not to lose points
unnecessarily because you missed something required. Below
highlights by category are taken directly from the grading rubric
for the assignment in Weeks 4–10. After reviewing the full
details of the rubric, you can use it as a guide.
In the Subjective section, provide:
· Chief complaint
· History of present illness (HPI)
· Past psychiatric history
· Medication trials and current medications
· Psychotherapy or previous psychiatric diagnosis
· Pertinent substance use, family psychiatric/substance use,
social, and medical history
· Allergies
· ROS
· Read rating descriptions to see the grading standards!
In the Objective section, provide:
· Physical exam documentation of systems pertinent to the chief
complaint, HPI, and history
· Diagnostic results, including any labs, imaging, or other
assessments needed to develop the differential diagnoses.
In the Assessment section, provide:
· Results of the mental status examination, presented in
paragraph form.
· At least three differentials with supporting evidence. List them
from top priority to least priority. Compare the DSM-5
diagnostic criteria for each differential diagnosis and explain
what DSM-5 criteria rules out the differential diagnosis to find
an accurate diagnosis. Explain the critical-thinking process that

led you to the primary diagnosis you selected. Include pertinent
positives and pertinent negatives for the specific patient case.
Reflect on this case. Include: Discuss what you learned and
what you might do differently. Also include in your reflection a
discussion related to legal/ethical considerations (demonstrate
critical thinking beyond confidentiality and consent for
treatment!), health promotion and disease prevention taking into
consideration patient factors (such as age, ethnic group, etc.),
PMH, and other risk factors (e.g., socioeconomic, cultural
background, etc.).
(The comprehensive evaluation is typically the initial new
patient evaluation. You will practice writing this type of note in
this course. You will be ruling out other mental illnesses so
often you will write up what symptoms are present and what
symptoms are not present from illnesses to demonstrate you
have indeed assessed for all illnesses which could be impacting
your patient. For example, anxiety symptoms, depressive
symptoms, bipolar symptoms, psychosis symptoms, substance
use, etc.)
EXEMPLAR BEGINS HERE
CC (chief complaint): A brief statement identifying why the
patient is here. This statement is verbatim of the patient’s own
words about why presenting for assessment. For a patient with
dementia or other cognitive deficits, this statement can be
obtained from a family member.
HPI: Begin this section with patient’s initials, age, race, gender,
purpose of evaluation, current medication and referral reason.
For example:
N.M. is a 34-year-old Asian male presents for psychiatric
evaluation for anxiety. He is currently prescribed sertraline
which he finds ineffective. His PCP referred him for evaluation
and treatment.
Or
P.H., a 16-year-old Hispanic female, presents for psychiatric

evaluation for concentration difficulty. She is not currently
prescribed psychotropic medications. She is referred by her
therapist for medication evaluation and treatment.
Then, this section continues with the symptom analysis for your
note. Thorough documentation in this section is essential for
patient care, coding, and billing analysis.
Paint a picture of what is wrong with the patient. First what is
bringing the patient to your evaluation. Then, include a
PSYCHIATRIC REVIEW OF SYMPTOMS. The symptoms
onset, duration, frequency, severity, and impact. Your
description here will guide your differential diagnoses. You are
seeking symptoms that may align with many DSM-5 diagnoses,
narrowing to what aligns with diagnostic criteria for mental
health and substance use disorders.
Past Psychiatric History: This section documents the patient’s
past treatments. Use the mnemonic Go Cha MP.
General Statement: Typically, this is a statement of the patients
first treatment experience. For example: The patient entered
treatment at the age of 10 with counseling for depression during
her parents’ divorce. OR The patient entered treatment for detox
at age 26 after abusing alcohol since age 13.
Caregivers are listed if applicable.
Hospitalizations: How many hospitalizations? When and where
was last hospitalization? How many detox? How many
residential treatments? When and where was last
detox/residential treatment? Any history of suicidal or
homicidal behaviors? Any history of self-harm behaviors?
Medication trials: What are the previous psychotropic
medications the patient has tried and what was their reaction?
Effective, Not Effective, Adverse Reaction? Some examples:
Haloperidol (dystonic reaction), risperidone
(hyperprolactinemia), olanzapine (effective, insurance wouldn’t
pay for it)
Psychotherapy or Previous Psychiatric Diagnosis: This section
can be completed one of two ways depending on what you want
to capture to support the evaluation. First, does the patient

know what type? Did they find psychotherapy helpful or not?
Why? Second, what are the previous diagnosis for the client
noted from previous treatments and other providers. Thirdly,
you could document both.
Substance Use History: This section contains any history or
current use of caffeine, nicotine, illicit substance (including
marijuana), and alcohol. Include the daily amount of use and
last known use. Include type of use such as inhales, snorts, IV,
etc. Include any histories of withdrawal complications from
tremors, Delirium Tremens, or seizures.
Family Psychiatric/Substance Use History: This section contains
any family history of psychiatric illness, substance use
illnesses, and family suicides. You may choose to use a
genogram to depict this information. Be sure to include a
reader’s key to your genogram or write up in narrative form.
Social History: This section may be lengthy if completing an
evaluation for psychotherapy or shorter if completing an
evaluation for psychopharmacology. However, at a minimum,
please include:
Where patient was born, who raised the patient
Number of brothers/sisters (what order is the patient within
siblings)
Who the patient currently lives with in a home? Are they single,
married, divorced, widowed? How many children?
Educational Level
Hobbies:
Work History: currently working/profession, disabled,
unemployed, retired?
Legal history: past hx, any current issues?
Trauma history: Any childhood or adult history of trauma?
Violence Hx:Concern or issues about safety (personal, home,
community, sexual (current & historical)
Medical History: This section contains any illnesses, surgeries,
include any hx of seizures, head injuries.

Current Medications: Include dosage, frequency, length of time
used, and reason for use. Also include OTC or homeopathic
products.
Allergies:Include medication, food, and environmental allergies
separately. Provide a description of what the allergy is (e.g.,
angioedema, anaphylaxis). This will help determine a true
reaction vs. intolerance.
Reproductive Hx:Menstrual history (date of LMP), Pregnant
(yes or no), Nursing/lactating (yes or no), contraceptive use
(method used), types of intercourse: oral, anal, vaginal, other,
any sexual concerns
ROS: Cover all body systems that may help you include or rule
out a differential diagnosis. Please note: THIS IS DIFFERENT
from a physical examination!
You should list each system as follows: General:Head: EENT:
etc. You should list these in bullet format and document the
systems in order from head to toe.
Example of Complete ROS:
GENERAL: No weight loss, fever, chills, weakness, or fatigue.
HEENT: Eyes: No visual loss, blurred vision, double vision, or
yellow sclerae. Ears, Nose, Throat: No hearing loss, sneezing,
congestion, runny nose, or sore throat.
SKIN: No rash or itching.
CARDIOVASCULAR: No chest pain, chest pressure, or chest
discomfort. No palpitations or edema.
RESPIRATORY: No shortness of breath, cough, or sputum.
GASTROINTESTINAL: No anorexia, nausea, vomiting, or
diarrhea. No abdominal pain or blood.
GENITOURINARY: Burning on urination, urgency, hesitancy,
odor, odd color
NEUROLOGICAL: No headache, dizziness, syncope, paralysis,
ataxia, numbness, or tingling in the extremities. No change in
bowel or bladder control.
MUSCULOSKELETAL: No muscle, back pain, joint pain, or
stiffness.
HEMATOLOGIC: No anemia, bleeding, or bruising.

LYMPHATICS: No enlarged nodes. No history of splenectomy.
ENDOCRINOLOGIC: No reports of sweating, cold, or heat
intolerance. No polyuria or polydipsia.
Physical exam (If applicable and if you have opportunity to
perform—document if exam is completed by PCP): From head
to toe, include what you see, hear, and feel when doing your
physical exam. You only need to examine the systems that are
pertinent to the CC, HPI, and History. Do not use “WNL” or
“normal.” You must describe what you see. Always document in
head-to-toe format i.e., General: Head: EENT: etc.
Diagnostic results: Include any labs, X-rays, or other
diagnostics that are needed to develop the differential diagnoses
(support with evidenced and guidelines).
Assessment
Mental Status Examination: For the purposes of your courses,
this section must be presented in paragraph form and not use of
a checklist! This section you will describe the patient’s
appearance, attitude, behavior, mood and affect, speech, thought
processes, thought content, perceptions (hallucinations,
pseudohallucinations, illusions, etc.)., cognition, insight,
judgment, and SI/HI. See an example below. You will modify to
include the specifics for your patient on the above elements —
DO NOT just copy the example. You may use a preceptor’s way
of organizing the information if the MSE is in paragraph form.
He is an 8-year-old African American male who looks his stated
age. He is cooperative with examiner. He is neatly groomed and
clean, dressed appropriately. There is no evidence of any
abnormal motor activity. His speech is clear, coherent, normal
in volume and tone. His thought process is goal directed and
logical. There is no evidence of looseness of association or
flight of ideas. His mood is euthymic, and his affect appropriate
to his mood. He was smiling at times in an appropriate manner.
He denies any auditory or visual hallucinations. There is no
evidence of any delusional thinking. He denies any current
suicidal or homicidal ideation. Cognitively, he is alert and
oriented. His recent and remote memory is intact. His

concentration is good. His insight is good.
Differential Diagnoses:You must have at least three
differentials with supporting evidence. Explain what rules each
differential in or out and justify your primary diagnosis
selection. You will use supporting evidence from the literature
to support your rationale. Include pertinent positives and
pertinent negatives for the specific patient case.
Also included in this section is the reflection. Reflect on this
case and discuss whether or not you agree with your preceptor’s
assessment and diagnostic impression of the patient and why or
why not. What did you learn from this case? What would you do
differently?
Also include in your reflection a discussion related to
legal/ethical considerations (demonstrating critical thinking
beyond confidentiality and consent for treatment!), health
promotion and disease prevention taking into consideration
patient factors (such as age, ethnic group, etc.), PMH, and other
risk factors (e.g., socioeconomic, cultural background, etc.).
References (move to begin on next page)
You are required to include at least three evidence-based, peer-
reviewed journal articles or evidenced-based guidelines which
relate to this case to support your diagnostics and differentials
diagnoses. Be sure to use correct APA 7th edition formatting.
© 2021 Walden University
Page 1 of 3
Chapter 9
Sleep, Wakefulness, and Conscious Awareness

2
Outline
The Rhythms of Sleep and Wakefulness
The Neurobiology of Sleep
Why Sleep and Dream?
Sleep Patterns: Typical and Atypical Variations
Altered States of Consciousness: Beyond Sleep
Rhythms of sleep/wake
Circadian Rhythms
Stages of Sleep
Extreme Sleep: Hibernation
4
Circadian vs. ultradian
Why can’t we just rely on external environment for temporal
cues?
How often do we mess up our sleep schedule?

Why do so many species yawn?
Yawning across species. Scientists continue to debate the
evolutionary advantage of yawning and why it occurs in many
species, including (a) apes, (b) lions, (c) dogs, and
(d) humans.
6
Rhythms of sleep/wake: Melatonin
Figure 9.2
Neural circuits involved in circadian rhythms and peak
melatonin response. Melatonin appears to be a chemical trigger
signaling increased blood flow in distal areas of the body,
promoting heat loss and the onset of sleep.
7
Rhythms of sleep/wake: Sleep
Sleep occurs in stages
Characteristic EEG signals during each stage

8
Stages of sleep. Over the course of a night, sleeping individuals
cycle through several distinct stages: Stages 1 and 2, slow wave
sleep, and REM sleep, during which dreams occur. A
polysomnograph records the different brain wave patterns that
characterize these stages.
9
A full night’s rest. Slow wave sleep decreases and REM sleep
increases as the night progresses.
10
Rhythms of sleep/wake: Hibernation
Why would an animal hibernate?
Are there any obvious downsides to sleeping through the
winter?
Hibernation. Many animals, such as the (a) chipmunk, enter an

extended state of unconsciousness (b) in response to harsh
winter weather.
11
Neurobiology of sleep
Early Neuroanatomical Explorations
Sleep as lack of sensory input?
Tests via lesion method on nonhumans
Neuroanatomical / Neurochemical Circuits
Acetylcholine
SWS: GABA, galanin, adenosine
REM: PGO spikes
12
Neurobiology of sleep: ARAS
The ascending reticular activating system (ARAS). The ARAS
conveys sensory information to other parts of the brain and is
essential for maintaining wakefulness.
13
Neurobiology of sleep: Acetylcholine

The neurochemistry of wakefulness. tegmental nuclei (LDT)
contributes to the maintenance of wakefulness. Acetylcholine
from the pedunculopontine tegmental nuclei (PPT) and
laterodorsal
14
Total sleep could be dangerous for some animals
Why not just never sleep?
Dolphin sleep. EEG records of dolphins reveal that only one
hemisphere sleeps at a time.
15
Neurobiology of sleep: SWS
Hypothalamic projections from the ventrolateral preoptic area
(VLPO) to the tuberomammillary nucleus (TMN) function to
diminish wakefulness during slow wave sleep.
16
Which animal is experiencing REM sleep?
Why is loss of muscle tone advantageous during REM sleep?

Cat naps. The sleeping posture of animals reveals information
about the stage of sleep they are currently in. (a) The ability of
the cat to hold its head up indicates that it is in non-REM sleep.
(b) This cat has apparently lost muscle tone and entered REM
sleep.
17
Neurobiology of sleep: REM
Why dream?
Activation-synthesis model
18
Neurobiology of sleep: REM
Pontine nuclei and REM characteristics. Lesions of pontine
nuclei diminish specific aspects of REM sleep.
19
Why sleep and dream?
Homeostatic theory of sleep regulation
Adaptive theory of sleep
Cultural differences in sleep patterns

20
Why Sleep?
How would you test the role of sleep?
What ethical concerns should we be aware of?
Why Sleep?
Rats kept awake long enough got sick, stopped eating, died
Rodent model of sleep deprivation. Electroencephalograms
recorded from the experimental animals activate the movement
of the platform when the animal sleeps so that the disk
movement and threat of falling in the water wake the animal up.
The yoked animal also has its sleep patterns disrupted by the
platform movement, but, unlike the experimental animal, it can
engage in occasional sleep.
22
Why Sleep? Adaptive theory
Sleep patterns should reflect environmental demands
Different animals show very different sleep patterns
Environment change (e.g., captivity) can change sleep habits

Maybe we’ve been too hard on sloths
Why Sleep?
Variation exists in human sleep schedules
Number of sleep periods
Not all members of community sleep at same time
Not everyone sleeps same duration
24
Why Sleep?
Sleep may also play a role in learning and memory
Memory consolidation
Sleep replay
Synaptic homeostasis hypothesis
Theta rhythms and offline processing
Why Sleep? Sleep Replay
Sleep and learning. (a) When a rat sleeps after navigating
through a maze, the same neural patterns that the rat displayed
while in the maze are reactivated. (b) In humans, presentation
of stimuli during a learning task and subsequently when a
subject is in slow wave sleep can reactivate neural patterns

similar to those active during learning, facilitating
consolidation of the information.
26
Why Sleep? Theta rhythms
θ rhythms during REM and waking behaviors. Similar θ rhythms
observed during both REM and survival-related behaviors in
various mammals suggest that REM brain activity may facilitate
these behaviors expressed during waking hours.
27
Why Sleep? Immune function
Vaccine effectiveness in the sleep deprived?
Sleep efficiency vs. sleep amount
Neurons responsive to immune chemicals are located in
sleep/wake regions
brainstem, hippocampus, hypothalamus
Immune chemicals increase during SWS
28
Sleep Patterns: Typical vs. Atypical
How do we define what “normal” sleep is?
Take the average, take the mode?

What if most people are not getting “enough” sleep?
Sleep durations in the United Kingdom and the United States.
Sleep durations are evenly distributed in (a) the United
Kingdom and (b) the United States, with an average nightly
sleep of approximately seven hours in both groups.
29
Sleep Disorders
Insomnia
GABA implicated
Narcolepsy
Hypocretin/orexin system implicated
Sleep apnea
Obstructed airways, associated with obesity
30
Sleep disorders: Insomnia
No single treatment for Insomnia
Cognitive-Behavioral Therapy for Insomnia
31

Sleep disorders: Narcolepsy
The hypocretin system. Hypocretin/orexin cells are located in
the hypothalamus. They project to areas throughout the brain,
influencing wakefulness and other functions related to energy
expenditure and emotional processes.
32
Sleep disorders: Sleep apnea
Sleep apnea and brain volume. Postmortem analyses of
individuals with obstructive sleep apnea revealed smaller
cortical areas (shown in red) compared with healthy control
brains.
33
Altered states of consciousness
Neural networks and conscious awareness
Disorders of consciousness
Hard to study consciousness, hard to define disorders
Death and the end of consciousness
34

Conscious Awareness Network
Dissociation in brain regions for internal/external attention
Internal and external awareness. Specific brain areas are
activated during internal and external conscious awareness.
These functional magnetic resonance imaging scans show more
activation in the cingulate cortex and parahippocampal cortex
(blue) in strong internal awareness and more activation in the
dorsolateral prefrontal cortex and inferior parietal lobe (red)
during strong external awareness.
35
Disordered Consciousness
Conditions to keep straight
Locked-in syndrome
Vegetative state
Minimally conscious
Coma
Brain death
36
Disordered Consciousness
Minimally conscious patients show brain activity in response to
questions
Minimal behavioral response

Brain responsiveness of minimally conscious patient. When
asked to imagine hitting a ball on a tennis court (A/B) and
navigating through a city or their home (C/D), a minimally
conscious patient and a healthy individual showed similar brain
response patterns.
37
Brain death vs. vegetative state
Brain death. There is virtually no observable resting brain
activity in positron emission tomography scans of individuals
diagnosed with brainstem, or brain, death.
38
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Chapter 13

Mental Illness
2
Outline
The challenge of classifying and treating mental illness
Schizophrenia
Depression
Anxiety disorders and other related disorders
Classifying and treating mental illness
Where do mental illnesses come from?
The stars, the humors, the brain?
How do disruptions in neurons propagate to severe
cognitive/behavioral dysfunction?
4
Once we agree that the brain is the source of the illness, how do
you fix it?
Electroconvulsive therapy (ECT)
Drugs?
Surgery?

Nobel Prize
winning treatment
Although the lobotomy treatment strategy led to the Nobel
Prize, it is now known that the procedure lacked empirical
support and, unfortunately, resulted in severe impairment in the
patients who received the “treatment.” Shown here are a set of
Watts–Freeman lobotomy instruments.
6
At 12 years of age, Howard Dully was lobotomized by Dr.
Walter Freeman at the request of his stepmother, who was
concerned about his behavioral problems, including not cleaning
his room or wanting to bathe.
7
Even today we can’t agree on how to classify mental illness
Current efforts: ICD-10, DSM-5
Problems

Changing disorder criteria
Elusive bio/behavioral markers
Similar biological bases present different symptoms
8
Schizophrenia
1% prevalence
Does this seem high or low?
Positive Symptoms
Negative Symptoms
Positive symptoms: delusions, hallucinations
Negative symptoms: diminished emotions/thought processes
9
Schizophrenia
Potential Causes
Neurochemical
Dopamine
Acetylcholine
Glutamate

10
Schizophrenia
Potential Causes
Neurochemical
Dopamine
Acetylcholine
Glutamate
11
Schizophrenia
How does chlorpromazine work?
Neuroleptic drugs such as chlorpromazine block dopamine D2
receptors.
12
Schizophrenia
anti-NMDA receptor autoimmune encephalitis
Role of glutamate in schizophrenia-like symptoms

(a) Susannah Cahalan exhibited characteristic symptoms of
schizophrenia after developing anti-NMDA receptor
autoimmune encephalitis. (b) When cerebrospinal fluid from
patients with this disorder is applied to rat brains, antibodies for
NMDA receptors occupy the hippocampus (shown in blue).
13
Schizophrenia: Anatomy
Smaller
Temporal lobes
Frontal lobes
Thalamus
More loss of gray matter during adolescence
Larger
Ventricles
In identical twins disconcordant for schizophrenia, the twin
with schizophrenia has larger ventricles.
14
In identical twins disconcordant for schizophrenia, the twin
with schizophrenia has larger ventricles.
15

When compared with healthy controls, individuals diagnosed
with schizophrenia have altered receptors in the chandelier cells
of the cortex. ese chandelier cells are thought to communicate
with the cortical pyramidal cells.
16
In the hippocampus, pyramidal cells are characterized as being
disorganized in comparison to the more organized alignment
observed in healthy controls, a structural effect that likely
affects neuronal processing in this brain structure.
17
Schizophrenia: Genetics
Because the highest concordance rate of schizophrenia is
observed in identical twins and the lowest concordance rate in
two individuals who are not related, a genetic component is
acknowledged and is being investigated by researchers.
18

Schizophrenia: Environment
When individuals lived in the more urban settings at any year
during the first 15 years of their lives, this variable was
associated with a higher risk of schizophrenia. Additional
analyses indicated that individuals living in urban settings for
the entire first 15 years had the highest rates of schizophrenia.
19
Schizophrenia: Environment
Should we move out of cities?
What is it about cities that might cause/trigger schizophrenia?
When individuals lived in the more urban settings at any year
during the first 15 years of their lives, this variable was
associated with a higher risk of schizophrenia. Additional
analyses indicated that individuals living in urban settings for
the entire first 15 years had the highest rates of schizophrenia.
20
Schizophrenia: Treatment
Pharmacological treatment
Cognitive remediation
Compensatory therapy

Pharmacological treatment
22
Cognitive remediation & Compensatory therapy
Early reports suggest effectiveness without the side effects
Following 10 and 15 weeks of cognitive training, this patient
experienced increased activation in the le inferior frontal gyrus
(slice 1) and le lateral orbital gyrus
(slice 2). Activation in these levels was closer to that of the
healthy subject than observed prior to training.
24
How can we study schizophrenia treatments in nonhumans?
Develop a model for a specific symptom/neurochemical deficit
Treat the deficit

(a) Although the lesioned areas were similar in both trained and
untrained groups, confirmed by (b) similar lesion size scores,
(c) the trained animals performed similar to the non-lesioned
controls in the cognitive task, with fewer entrances into a shock
zone than the non-trained animals over the course of two days
of trials.
26
Depression
17% lifetime prevalence
Neurochemical basis
Monoamine hypothesis
Dopamine hypothesis
Molecular hypothesis
Cortisol
BDNF
Depression: Monoamine hypothesis

Imipramine blocks the reuptake of the monoamines, thereby
keeping them in the synapse longer.
28
Depression: BDNF
Comparing dendritic branches in medial prefrontal cortex in
mice with low BDNF
In an investigation of the role of varying levels of BDNF on
brain areas implicated in depression, mice with significantly
reduced BDNF levels exhibited increased atrophy of the
dendritic branches in the medial prefrontal cortex.
29
Depression: Anatomy
Symptoms suggest anatomical targets
Lank of motivation for pleasurable activities
Nucleus accumbens
Effort-based reward theory
Lack of concentration/cognitive difficulty
PFC
Chronic stress
Hippocampal volume/function
30

Depression: Network Hypothesis
Rather than a single “chemical imbalance” depression may
result from a disorder of connectivity
Activity-dependent neuroplasticity
How do you measure network activity in humans?
This theoretical model proposes that depression results from
compromised neural networks, and the symptoms subside when
the networks are recovered through effective treatments.
31
Depression: Treatment
ECT / rTMS
Pharmacotherapy
Cognitive and behavioral therapies
Emerging treatments
32
ECT
still used for patients that do not respond to other approaches
Some short-term effectiveness
Side effects include memory loss
rTMS

Magnetic stimulation
Less intense, fewer side effects
Data is still coming in
Treatment with rTMS involves positioning a very powerful
electromagnet on the scalp that ultimately depolarizes
underlying neurons.
34
Pharmacotherapy
MAOIs
Tricyclics
SSRIs
Need better double-blind studies
Prevalence of side effects may un-blind control vs. experimental
group
Cognitive
Focus on eliminating the destructive beliefs of the patient
Longer lasting effects

Combined drug/cognitive approaches are common
Behavioral
Focus on how the patient interacts with the external
environment.
Patients learn contingency between behavior and positive
outcomes (effort-based reward model)
36
Efficacy rates of various depression therapies. At two time
points, 8 weeks and 16 weeks, there is little difference between
antidepressant and cognitive therapies.
37
Deep brain stimulation
Common Targets: subcallosal cingulate gyrus, lateral habenula
Edi Guyton, after suffering from long-term depression, had
electrodes implanted into the subcallosal cingulate to treat the
depression symptoms
38

Neural plasticity may underlie all treatment effects
Several common treatment strategies impact neural plasticity
that restores the neural networks for competent rather than
impaired function
39
Bipolar Disorder
Lows of depression
Manic periods where those with this disorder often engage in
dangerous/risky behaviors.
Treatment most often lithium
Likely affects serotonin
70-80% effective
40
Anxiety Disorders
Anxiety is a feature of life, but out of control anxiety can cause
severe disruptions
State vs. trait anxiety

Anxiety Disorders: Causes
Often triggered by a stressful event
Amygdala and GABA system have been implicated
Chronic stress may damage stress response system
Measureable genetic component
Don’t forget about individual differences
42
Genetic predispositions, environmental factors, and anxiety
disorders. Exposure to the same life stressors can result in
different anxiety response outcomes in individuals with varying
genetic predispositions and environmental histories.
43
Environmental contexts, such as leaving a car in the parking lot,
can prompt sufficient uncertainty and anxiety to trigger
obsessions characteristic of OCD. For example, as fear and
worry are experienced, this may ultimately lead to a response

resulting in reduced anxiety (e.g., going back to the parking lot
to make sure the car is locked).
44
Anxiety Disorders: Treatments
SSRIs
not fast acting
Surgery
bilateral lesions to the lower medial OFC and the anterior
cingulate bundle area
Behavioral approaches, e.g., exposure therapy for phobias
A two-hour exposure therapy session resulted in persistent
decreases in self-reported phobia symptoms, self-reported fear
beliefs, the ability to approach a live tarantula, and the fear
associated with that fear.
46
How do we get (un)learning to generalize to new contexts?
Are there any phobias for which exposure therapy might be
impractical?
What about exposure in a virtual environment/video game
context?

After multiple context exposure (MCE) therapy in which
participants are exposed to spiders in various colored room
contexts or the single context exposure therapy, (b) the
participants in the MCE group were able to move a live spider
in a box closer to them in the behavioral approach test.
48
Anxiety Disorders
Anxieties can have adaptive value
Difficult to change behavior, when alternatives exist
e.g., Avoiding shaking hands
How do we decide when a compulsive behavior should be
modified?
To avoid germ transmission and calm his anxiety, the comedian
Howie Mandel greets others by tapping fists rather than shaking
hands.
49

|
Chapter 12
Learning, Memory, and Decision Making
2
Outline
Neurobiological foundations of learning and memory
Modifying memories
Attention as a gateway to learning and memory
Decision making
Behavioral Approaches
Cellular Mechanisms
Structural Neuroplasticity
Integrating Clinical and Laboratory Research

(a) Pavlov used dogs to assess saliva production in response to
varying stimuli; (b) his classic work pairing conditioned and
unconditioned stimuli laid the groundwork for empirical
investigations for learning.
4
Behavioral Approaches
Pavlov: Classical conditioning
Watson: Trial and error learning
Skinner: Operant conditioning
5
Classical conditioning
US:UR
NS+US:UR
CS:CR

6
Law of Effect
How did Thorndike measure learning?
Problem solving and puzzle boxes. Thorndike observed cats’
responses in puzzle boxes as they searched for ways to escape
and approach the food. Once a response was observed to lead to
the positive consequence of obtaining the desired food, that
same response was repeated in future exposures to the puzzle
box.
7
Operant Conditioning vs. Classical conditioning
8
Skinner box

Skinner developed operant chambers in which rats pressed
levers to receive food pellets. The rats adjusted their responses
to changing reinforcement schedules signaled with cues such as
lights or sounds.
9
Role of contingency in behavior
Is there a danger in only measuring lever presses?
10
Cellular mechanisms
Hebbian learning: neurons the fire together, wire together
What happens chemically to allow a neuron to change its
response to a stimulus?
Sensitization and Habituation
Eric Kandel used the aplysia as a model animal to investigate

cellular responses in forms of associative learning such as
sensitization and habituation.
12
Some cells help us learn specific kinds of information
Place cells
Grid cells
Direction cells
Rats need to navigate from early on in development
13
Neurobiological foundations of learning and memor y
Place cells and grid cells in the hippocampus and surrounding
areas are important for the rat’s movement of body and head
around its environment.
14
Long-term potentiation as a candidate for memory
Neurobiological foundations of learning and memor y
Microelectrodes are used to record postsynaptic potentials of
the hippocampal neurons.

Postsynaptic glutamate receptors have been identified as key
components of the LTP process.
15
What happens structurally during learning?
Restructuring of dendrites
Growing new neurons
Problems with always growing new neurons?
Slow
Space limitations
Energy cost
16
Learning-induced spine restructuring. During behavioral
learning, the structures of the dendritic spines are modified in
ways that are thought to facilitate neural networks supporting
the newly acquired learned behavioral responses.
17

New cells have increased rates of survival early in the learning
process; however, once the task is mastered, the death rate of
newborn neurons increases.
18
We can learn about brain function by studying patients with
brain damage
HM
Bilateral MTL lesions
Anterograde amnesia
Procedural vs. declarative memory
20
(a) Brain imaging has confirmed bilateral hippocampal damage
in H.M., which impaired his declarative memory while leaving

his procedural memory less impaired. (b) The ventral surface of
H.M.’s brain. (c) Following H.M.’s death, the neuroanatomist
Jacopo Annese conducted the necessary histological analysis of
the brain tissue; equipment was created to freeze and slice the
whole brain into pieces that could then be studied under a
microscope.
21
Memory engram
Theory of equipotentiality
22
Neural networks and memories. Although research suggests that
memories are not represented or coded in a single cell, it is
unclear whether memories are stored in networks characterized
as sparse or more distributed across the brain.
23
To study memory in animals, we need procedures with well
defined parameters
Different tasks allow study of different kinds of memory

Delayed nonmatching-to-sample task. (a) When monkeys are
assessed in this task that requires them to hold the information
in memory before making the correct response, (b) those with
lesions of the hippocampus and amygdala exhibit learning
deficits.
24
Delayed (non)match to sample
Morris water maze
Radial arm maze
Eye-blink condition
Rodent obstacle courses
deficits.
25

deficits.
26
When spatial ability is assessed in the Morris water maze, (b)
animals with hippocampal damage perform poorly during
training and testing.
27
Spatial memory is assessed in the radial arm maze in which
animals are required to remember arms or alleys of the maze to
avoid revisiting previously visited arms—a response recorded as
an error.
28

The interpositus nucleus of the cerebellum is integrally
involved in the rabbit conditioned eye-blink response.
Following conditioning, both the conditioned stimulus (CS,
tone) and the unconditioned stimulus (US, air puff) trigger the
eye-blink response (either as an unconditioned response (UR) or
as a conditioned response [CR]).
29
Obstacle course training and neuroplasticity.
(a) When rats were exposed to physical training (AC) in
challenging obstacle courses, (b) increased synapses were
observed in the Purkinje cells when compared with those of
nontrained animals.
30
In humans, fMRI and PET can be used to find regions active
while subjects perform different memory tasks
Drawbacks to fMRI vs. single cell recording?
When participants were asked to (a) retrieve and organize
pictures representing scenes from a movie in the order presented
in the movie as opposed to inferring how the order of the
pictures should appear, (b) more hippocampal activation was
observed.

31
Systematizing memory
Structural organization
Functional organization
Process-based organization
32
Cortical–hippocampal memory system
Cortical–hippocampal memory system. In both rodents and
primates, the hippocampus receives and sends information to
the parahippocampal and neocortical association areas. The
parahippocampal region can be considered a hub or convergence
area for this memory input—distributing it to the appropriate
hippocampal and neocortical areas.
33
Processing-based memory system
Fast vs. slow encoding
Single-item vs. associative encoding
Flexible vs. rigid representation

34
This model distinguishes among three different types of memory
systems: fast and flexible associations, slow and rigid
associations, and fast processing of single-input units. Each
proposed system is associated with specific brain areas.
35
Hippocampus implicated in complex memory across species
Similar to mammals, avian memory processing likely involves
the avian version of the hippocampus
36
Modifying Memories
How reliable is memory under normal conditions?
What about stressful situations?
Key ideas

Reconsolidation
Post-retrieval lability
Confabulation
Modifying Memories
(a) In this paradigm, rats are exposed to cats prior to being
tested in a memory task. (b) Rats previously exposed to cats
made more errors in the radial-arm maze than nonexposed rats.
38
Modifying Memories
Knowing that stress impairs memory, how can we help people
who experience stress (all of us, at one point or another)?
What about severe acute stress, or chronic stress?
Modifying Memories
PTSD
Imaging data reveal that PTSD is characterized by
hyperactivation of the amygdala, insula, and cingulate cortex
and diminished activity in the ventromedial prefrontal cortex.

Both hyper- and hypoactivation have been observed in the
hippocampus
40
Modifying Memories
Effect of stress can be cumulative
When rats were exposed to two hours of immobilization stress,
(a) they exhibited more densely populated spines on neurons in
the amygdala after 10 days as well as (b) persistent avoidance
of the open arm in an elevated plus maze. these data reflect
strong memories of the immobilization stress, with the effects
building over time.
41
Modifying Memories
Are some people more susceptible to stress-impaired memory?
How would you test this idea?
42
Modifying Memories

Posttraumatic stress disorder (PTSD) effects on conditional
discrimination. (a) After establishing light signals that predict
or do not predict a threatening stimulus (air blast), (b)
participants were exposed to a novel aversive noise stimulus
alone and in the presence of the light cues that were associated
with the air blast. (c) Participants in the high-symptom PTSD
category were less likely to inhibit threat expectation in the
presence of the safety signals than the control and low PTSD
participants.
43
Attention as the gatekeeper
In order to remember, we must first attend
Inattentional blindness
44
Inattentional blindness. When study participants were asked to
observe a video and focus on the number of times the ball was
passed among the players, they failed to see the gorilla that
walked across the room.
45

Parts of attending
Alerting
Orienting
Executive attention
46
Attentional modes in the brain. During the three aspects of
attentional modes including alerting, orienting, and executive
function, specific brain areas are engaged to facilitate these
responses.
47
responses.
48

responses.
49
Because attention necessarily affects memory, what can we do
about attention disorders
How do we decide when to give brain-altering drugs to
children?
50
Decision making
Decisions require integrating current sensory information and
memory
How many kinds of memory are required to verbally understand
and correctly answer a simple arithmetic question?
To study decision making, we start with simple tasks
Decision making

(a) When monkeys are exposed to a random dot decision-making
task, as they make the decision to respond in a certain way, the
(b) lateral intraparietal (LIP) area and (c) the dorsolateral
prefrontal cortex (DLPFC) are activated.
52
Decision making
Appreciating uncertainty is a necessary part of (rational)
decision making
Even a decision at a traffic light could be fraught with
uncertainty
Decision making
In everyday tasks such as driving, various categories of
uncertainty are encountered including sensory, state, rule, and
prediction uncertainty.
54
Decision making
We can not always learn a single stimulus-response rule
In everyday environments, the rules change from time to time

Decision making
Orbitofrontal cortex and flexible behavior
When rats were trained in an odor discrimination task in which
one odor predicted a desired sweet fluid and another odor
predicted an aversive bitter fluid, animals with lesions were
slow to inhibit the previous response– outcome association and
adapt by changing their responses to avoid the bitter fluid.
56
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Chapter 8Maintenance and Motivation2Outlin

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