Memory is the ability of the brain to store and recall information over time. There are four main types of memory: sensory memory (up to 0.5 seconds), short-term memory (minutes to hours), long-term memory (hours to years), and permanent memory. Information enters the brain and is either selected and stored in memory traces through processes like long-term potentiation, or neglected and forgotten. The hippocampus plays a key role in consolidating memories from short-term to long-term storage. Disorders like amnesia and Alzheimer's disease can impair memory formation and recall.
this ppt shares what synapses are and how information of one neuron is transmitted to other through the synapses. it also includes the properties and plasticity of synaptic transmission
this ppt shares what synapses are and how information of one neuron is transmitted to other through the synapses. it also includes the properties and plasticity of synaptic transmission
MEMORY
By JOYSRI ROY
M.SC APPLIED PSYCHOLOGY
SEMESTER 1
CALCUTTA UNIVERSITY
Definition
Our ability to encode, store, retain and subsequently recall information and past experiences in the human brain.It is the sum total of what we remember, and gives us the capability to learn and adapt from previous experiences as well as to build relationships.
In more Physiological and neurological term, memory is, at its simplest , a set of encoded neural connections in the brain.
MEMORY PROCESS
1)Encoding
2)Storage
3)Retrieval
NEURO-BIOLOGY OF ENCODING
Process of laying down a memory begin with attention, which is regulated by thalamus and fontal lobe, in which a memorable event causes neurons to fire more frequently making the experience more intense and increasing the likelihood that the event is encoded as a memory. Emotion increases attention in the amygdala. The perceived sensation are decoded in the various sensory areas of the cortex. Then combined in the hippocampus into one single experience. Hippocampus analyzing these inputs and ultimately deciding if they will be committed to long- term memory.
TYPES OF MEMORY
1)Sensory memory
2)Short term memory
3) Long term memory
MODELS OF MEMORY
1) ALLEN D. BADDELEY’S MODEL
2)ATKINSON AND SHIFFRIN’S MODEL (1968)
3)LEVELS OF PROCESSING ( CRAIK AND LOCKHART)
ZEIGARNIK EFFECT
Bluma Zeigarnik , a Russian Psychologist, compared memory for tasks that were successfully completed and those which were not. She interpreted the work and did not allow them to finish it. Interrupted tasks were remembered more frequently than those which were completed.
Dutta and Kanungo gave a new interpretations to this effect.
The intensity of emotiom arousal by the completed tasks or the interrupted task is the critical factor. Any aivity that gives to strong emotion, be it pleasant or unpleasant , is remembered better than ordinary everyday actions
METHODS OF STUDYING MEMORY
1)FREE RECALL
2)RECOGNITION
3)PRIMIMG
FORGETTING
1)TRACE DECAY THEORY
2)DISPLACEMENT FROM STM
3)LACK OF CONSOLIDATION
4)RETRIEVAL FAILURE
5)INTERFERENCE THEORY
6)AMNESIA
TYPES OF MNEMONIC DEVICES
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Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
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2. MemoryMemory
Def
It is the ability of the brain to store information and recall it
at later time
Capacity of the brain:
It is limited (total capacity of brain is 3x 108
bits)
So, informations entering brain are either;
A.Selected and stored (1%) → most important
B.Other (99%) → are neglected and forgotten
3. MemoryMemory
Information Unit:
It is bit
A bit is the simplest form of sensory experience i.e. figure,
sound, touch , or smell
All sensory systems send information to brain at 50 bit/sec
E.g. during reading 40 bits/sec, during mental calculation 12
bits/ sec, and during counting 3 bits /sec
Average rate of flow of information is 20 bits/sec
For learning a language about 40- 50 millions bits should be
stored in memory
To store 1 bit, 10 neurons are required
4. MemoryMemory
Types of memory:
There are four different types of memory:
[I] SENSORY MEMORY (Immediate memory).
[II] PRIMARY MEMORY (Short-term memory)
[III] SECONDARY MEMORY (Long-term memory)
[IV] TERTIARY MEMORY (permanent memory)
5. 11..Sensory MemorySensory Memory
• Duration: very short (about 0.5 seconds)
• Capacity: very small (15-20 bits)
• Entry into storage: automatic during perception
• Access to storage: very rapid
1. Vision: iconic memory
2. Hearing: echoic memory
• Mechanism:
• 1. Stimulation of reverberating circuits → repeated
activation of neurons
• 2. Synaptic sensitization if sensory experience coupled
with painful stimuli
6. 11..Sensory MemorySensory Memory
• Mechanism:
• 3. Posttetanic potentiation: multiple stimuli at
presynaptic terminal →↑ Ca content in presynaptic
terminal →↑ release of neurotransmitters
• Mechanism of forgetting:
• 1. Fading (spontaneous and gradual decline in the amount
of information)
• 2. Extinction (spont. disappearance of information from
memory)
7. 2. Short-term Memory2. Short-term Memory
Duration: (min to hours)
Capacity
– Small bits of informations
– Miller’s magical number: 7±2 chunks of information
Entry into storage: verbalization (describing the
items in words)
Recall or access to storage: rapid
Mechanism:
Made by formation of temporary memory traces
8. 2. Short-term Memory2. Short-term Memory
Memory trace:
Is a newly developed pathway or signal transmission
resulting from facilitation of new synapses → creation of
new circuits in the brain
This occurs by
1. Long term potentiation of synapses
2. Changes in physical properties of postsynaptic
membrane → ↑ sensitivity to chemical transmitters
Mechanism of forgetting:
New information replaces old
9. 3. Long-term Memory3. Long-term Memory
Duration: (hours to years )
Capacity
– Very large
– Information stored according to its significance
Entry into storage: 1. Stimulation of the reward or
punishment systems.
2.Repeated practice or rehearsal of the experience.
Recall or access to storage: slow
Mechanism:
Made by formation of memory engrams (long-
lasting memory traces) formed by structural
changes in presynaptic terminals
10. 3. Long-term Memory3. Long-term Memory
Mechanism:
memory engrams made up by;
1. increase in number of vesicles
2. increase in number of presynaptic terminals
3. increase in release sites of chemical transmitters
4. generation of new receptor sites
5. long term potentiation
Engrams remain for long time up to several years
Formation of new engrams requires protein
synthesis
11. 3. Long-term Memory3. Long-term Memory
Mechanism of forgetting:
Proactive inhibition : If the old information repels the
new one
Retroactive inhibition: If the new information
replaces the old one
12.
13. 4. Permanent Memory4. Permanent Memory
Duration: (permanent)
Capacity
– Very large
Entry into storage: very frequent practice
Recall or access to storage: very rapid (recall not
affected by brain injury (like name, write, and read)
Mechanism:
Advanced stage of long-term(permanent engrams)
Mechanism of forgetting :
No forgetting
14.
15. Phases of memoryPhases of memory
Consolidation-converting the encoded information into a
form that can be permanently stored. The hippocampal and
surrounding areas apparently accomplish this.
Encoding-information for each memory is assembled from
the different sensory systems and translated into whatever
form necessary to be remembered. This is presumably the
domain of the association cortices and perhaps other areas.
Storage-the actual deposition of the memories into the
final resting places–this is though to be in association
cortex.
Retrieval-memories are of little use if they cannot be read
out for later use. Less is known about this process.
16. Consolidation of memoryConsolidation of memory
It means the process of conversion
of STM to LTM
It takes from 5 min to 2 hrs
It is interrupted by
1. Deep anaesthesia
2. Brain concussion
3. Electroconvulsive therapy
17. Brain Regions involved in Consolidation ofBrain Regions involved in Consolidation of
memorymemory
• Hippocampus
• Anterior & lateral
temporal lobe,
• Medial temporal lobe
• Amygdala
18. Hippocampus and Consolidation of memoryHippocampus and Consolidation of memory
• The hippocampal region is critical for the consolidation of
information in long-term memory
Evidence
• Three major excitatory neural components of the hippocampus
Perforant pathway
• forms excitatory connections between the parahippocampal cortex
and the granule cells of the dentate gyrus
Mossy fibers
• connect the granule cells of the dentate gyrus to the CA3 pyramidal
cells
Schaffer collaterals
• connect the CA3 pyramidal cells to the CA1 pyramidal cells
19.
20. Encoding of memoryEncoding of memory
It means classification and placing memory items in their
proper memory stores in brain
Brain areas concerned with encoding of long term memory;
1. Hippocampus (major central role) all bits of information
go to it first
2. Amygdala (emotional memory)
3. Basal forebrain (Nucleus basalis or Meynerts nucleus)
4. Noecortex
5. Mammillary body of hypothalamus
6. Orbitofrontal cortex
21. Encoding of memoryEncoding of memory
Hippocampus
store
Mamillary
body
Orbitofrontal
cortex
Basal forebrain
Meynerts Nucleus
Amygdala
store
(Temporal lobe)
Neocortex
store
All bits
Select important informations
(reward or punishment)
Cholinergic projections
Cholinergic projections
Cholinergic projections
22. Disorders of MemoryDisorders of Memory
1) Amnesia → loss or impairment of memory
It may be;
a) Retrograde amnesia
•It means inability to recall memories from the past
(retrograde: going backwards), that is from the long- term
memory stores.
•It usually follows a traumatic event that interferes with the
normal activity of the brain, such as a strong brain
concussion and vascular strokes
23. Disorders of MemoryDisorders of Memory
b)Anterograde amnesia
• It is the inability to store new information in the long-term
memory for later recall.
• It usually results from lesions of the medial portions of the
temporal lobe, a region that include the hippocampus,
amygdala, and the adjacent areas of the temporal
c) psychogenic or hysterical amnesia
• Rare
• Sudden loss of memory of all information
• Exposure to severe psychological stress
24. Disorders of MemoryDisorders of Memory
2) Senile dementia and Alzheimer disease
It occurs in old age (senile dementia) and middle age
(Alzheimer), but it can occur at any age
•It is characterized by impairment of memory, lack of
concentration, inattentiveness
•Incidence: 10-15 % after age of 65 years
•Mechanism:
•Loss of cholinergic terminals that diffuse from nucleus
basalis to neocortex, amygdala and hippocampus
Consolidation : توحيد او دمج المعلومات
Consolidation of memory means the transfer of information from the Sensory and primary short-term memories to the secondary long-term memory.
This process takes from 5 minutes for minimal consolidation to two hours for maximal consolidation.
Brain concussion : ارتجاج الدماغ
Electroconvulsive therapy (ECT), formerly known as electroshock therapy, and often referred to as shock treatment, is a psychiatric treatment in which seizures are electrically induced in patients to provide relief from mental disorders
Accordingly, if a sensory impression is made, then followed within 5 minutes by brain concussion or ECT or anesthesia, the experience gets extinct. This explains why patients who had brain concussion in accidents cannot remember what happened at the time of the accident. If the concussion occurs 2 hours after" the sensory experience, the information remains unaffected. If it occurs within two hours, the memory is affected proportionately.
Rehearses : تكرار
Consolidation occurs to the information which attracts the attention of the mind. The brain automatically rehearses this information. A wide awake person consolidates memories far better than a person with mental fatigue. This is because the wide awake brain is more attracted by the new information and is capable of making rapid and more frequent rehearsals that would consolidate memory more effectively. Normal quiet sleep consolidates the memory of information received before the onset of sleep.
Consolidation is distinguished into two specific processes, synaptic consolidation, which is synonymous with late-phase long-term potentiation and occurs within the first few hours after learning, and systems consolidation, where hippocampus-dependent memories become independent of the hippocampus over a period of weeks to years. Recently, a third process has become the focus of research, reconsolidation, in which previously-consolidated memories can be made labile again through reactivation of the memory trace
FACIAL RECOGNITION AREA
The impression effaces is stored in the "facial recognition area" in the neocortex of the undersurface of the temporal and occipital lobes .In right-handed persons and some of the left handed ones, the facial recognition area is much better developed in the right (representational) hemisphere than in the left (categorical) hemisphere. Bilateral lesion in this area leads to "prosopagnosia" which is' inability to recognize people by their faces. In this case, the patient can recognize persons by their voices. A prosopagnostic patient develops emotional and autonomic reactions on seeing a familiar face, but he wouldn't identify the person until he hears him speaking.
NAMING OF OBJECTS AREA
This is the function of an area in the most lateral portion of both the anterior occipital and posterior temporal lobes. In this area, the names of different objects are stored. Like the facial recognition area, it is better developed on the right side than in the left side. Damage of this area leads to inability to name objects, although the patient is able to know what the object is, its value or its use. Only the name is lost from memory. This is probably the brain area which gave Adam the advantage over angels. According to the holy Qur'an, after the creation of Adam, angels failed to name objects when Allah asked them to do, Adam by the command of Allah, preceded and told the names of objects.
Hippocampus : The hippocampus (named after its resemblance to the seahorse يشبه فرس البحر , is a major component of the brains of humans and other vertebrates. Humans and other mammals have two hippocampi, one in each side of the brain. The hippocampus belongs to the limbic system and plays important roles in the consolidation of information from short-term memory to long-term memory, and in spatial memory that enables navigation. The hippocampus is located under the cerebral cortex (allocortical) and in primates in the medial temporal lobe. It contains two main interlocking parts: the hippocampus proper (also called Ammon's horn)[4] and the dentate gyrus . In Alzheimer's disease (and other forms of dementia), the hippocampus is one of the first regions of the brain to suffer damage; short-term memory loss and disorientation are included among the early symptoms. Damage to the hippocampus can also result from oxygen starvation (hypoxia), encephalitis, or medial temporal lobe epilepsy. People with extensive, bilateral hippocampal damage may experience anterograde amnesia (the inability to form and retain new memories).
ANTEROGRADE AMNESIA
It is the inability to form new memories. The memories consolidated before the onset of amnesia are retained. The sensory and primary memories are functional but cannot be consolidated. Anterograde amnesia occurs with bilateral lesions in the hippocampus or other structures involved in the encoding of memory.
The anticholinesterase drug serine (physostigmine) produces some improvement but it does not stop the progress of the disease.