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Learning Memory and Amnesia

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Learning Memory and Amnesia PowerPoint Presentation

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Published on : Mar 14, 2014
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Slide 1 - Memory, Learning and Amnesia
Slide 2 - Memory, Learning and Amnesia Memory = site and/or process where knowledge and experiences are stored. Learning = the process of committing new knowledge and experiences into (semi-) permanent storage. Classical conditioning Operant conditioning Other neural mechanisms Amnesia = the inability to form or recall memories.
Slide 3 - Memory, Learning and Amnesia Types of memory and amnesia Brain areas involved in memory Sensory and working short-term memory Procedural memories Declarative memories Neural mechanisms of learning
Slide 4 - History of Memory Studies The study of memory 1885 Ebbinghaus publishes first studies on memory. 1889 Korsakoff describes severe anterograde amnesia. 1915 Karl Lashley begins a long-term study of memory. 1950 Lashley states “… the engram is represented throughout the region.” 1953 Dr. William Scoville removes the bilateral medial temporal lobes of H. M. to stop epileptic seizures and inadvertently discovers the role of the hippocampus.
Slide 5 - Areas of Memory Lashley was wrong. Memories are not evenly distributed over the cortex. Memories are not all stored in the same place. Different types of memory are found in different areas, but all rely on synaptic connections. There is no “grandma” neuron. All parts of the nervous system can learn and remember. Multimodal information is remembered better.
Slide 6 - Types of Memory - Data Declarative or explicit (conscious) Facts & events Easily formed, and easily forgotten Nondeclarative or implicit (unconscious) a.k.a. procedural memory Skills, habits and conditioning Skeletal muscle practiced movements. Emotional responses Requires repetition, but rarely forgotten
Slide 7 - Types of Memory - Data
Slide 8 - Types of Memory - Time Short-term Only good for seconds to hours Easily disruptable Long-term Lasts for days, months or years Permanent
Slide 9 - Short-term Memory Average capacity is 7 +/- 2 chunks, generally proportional to intelligence. Kept in right orbital cortex (frontal lobe). Data only remains there for a few seconds without rehearsal. Modulated by attention. Easily disrupted. Unrelated to long-term memory.
Slide 10 - Short-term Memory Short-term sensory memory The senses have independent short-term storage. Kept in the cortical area of the sense. Temporal lobe for audio data, etc. The lateral intraparietal cortex (LIP) seems to hold short-term visual memories in monkeys. If there is sufficient attention, the sensory information can be moved to short-term working memory areas. If not, the information will be lost.
Slide 11 - Types of Memory Short-term Memory Long-term Memory Consolidation Declarative Implicit Sensory Information Sensory Register Attention
Slide 12 - Loss of Memory Amnesia = The loss of (declarative) memory Retrograde Can’t recall previously available information. Sometimes very old memories are still available. Anterograde amnesia Can’t learn new information. Can affect short-term, long-term, or both. Usually accompanied by retrograde amnesia. Specific deficits Prosopagnosia, anomia, etc.
Slide 13 - Procedural Memory Areas The striatum seems to be strongly involved in procedural memories and conditioning. Huntington’s and Parkinson’s patients have difficulties learning procedural tasks because of damage to the striatum. The cerebellum is the primary site of coordinated movement learning.
Slide 14 - Declarative Memory Areas Amnesia, lobectomy and stimulation studies point to the temporal lobe as the primary site for declarative memories, or at least their recall. Stimulation of the temporal cortex produces more complex memories and hallucinations than any other brain area. Anomia and prosopagnosia tied to temporal lobe.
Slide 15 - Declarative Memory Areas – H.M. Case study: H. M. (1953, M, 27 y.o.) Dr. Scoville removed both medial temporal lobes to alleviate untreatable epileptic seizures. Seizures were greatly reduced, BUT… H. M. had severe post-op anterograde amnesia which never improved, but little retrograde or motor amnesia or short-term memory problems. From previous understanding (distributed memory), this could not occur. Research changed from place to process.
Slide 16 - Declarative Memory Areas Medial temporal lobe Removed in H.M. Hippocampus is directly below the amygdala (highlighted in pink).
Slide 17 - Implicit Memory Areas H.M.’s working memory is intact. H.M. can still learn habits and trained tasks. This shows that lack of the hippocampus impairs consolidation required for conscious recall, but not for implicit memories. Priming Exposure to a stimulus makes it easier to recognize that stimulus again (it is remembered). H. M. shows very limited signs of recognizing prior stimuli without cognitively realizing it.
Slide 18 - Declarative Memory Areas 8 other psychotic patients were examined Only those who had a hippocampusectomy had anterograde amnesia. They deduced the hippocampus is necessary for new memory formation, but not recall. It is not necessary for short-term memory. Modern procedures call for only one hippocampus to be removed, and it is now tested for functionality before the operation.
Slide 19 - Declarative Memory Areas Alzheimer’s disease A progressive disease causing loss of cells and deterioration in the association cortex. Marked by anterograde amnesia and later also by retrograde amnesia. Damage begins in medial temporal cortex and spreads to other areas. This is evidence that anterograde amnesia is related to the medial temporal cortex.
Slide 20 - Declarative Memory Areas Korsakoff’s Syndrome Symptoms Severe anterograde amnesia Confabulation Make up stories based on fragments of recent occurrences Caused by thiamine (vitamin B1) deficiency Alcoholism Malnutrition Damages the mammillary bodies, which relay information from the hippocampus to the thalamus via the fornix.
Slide 21 - Declarative Memory Areas Patient R. B. Permanent anterograde amnesia caused by anoxic ischemia of the hippocampus. On autopsy, it was found that the CA1 region of the hippocampus was gone. The CA1 region is especially rich in NMDA receptors (involved in learning). If only CA1 damaged: anterograde amnesia only. Anoxia causes NMDA receptors to allow excessive Ca++ influx, damaging cells.
Slide 22 - Declarative Memory Areas Further evidence of NMDA-Hippocampus connection: Mice with NMDA receptor knock out learn very slowly, if at all. Mice with excess NMDA receptor genes learn quicker than normal.
Slide 23 - Declarative Memory Areas Neuromodulation in the hippocampus 5-HT inhibits memory formation. NE, E, D, cocaine enhance memory formation. Cholinergic theta rhythms (5-8 Hz) from medial septum seem to be necessary. In rats, theta activity is correlated with exploratory behaviors. Info sampled into dentate gyrus and CA3 on theta. Info moved to CA1 when theta waves subside.
Slide 24 - Declarative Memory Areas Anatomical structures: Thalamus, sensory relay Amygdala, emotional memory Hippocampus, spatial memory Rat radial maze performance: evidence of place neurons Rhinal cortex, object & recognition memory Fornix and mammilary bodies Prefrontal cortex Surrounding limbic structures
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Slide 26 - Neural Mechanisms
Slide 27 - Classical Conditioning A form of learning where an otherwise unimportant stimulus acquires the properties of an important stimulus. Forms an association between two stimuli, one which would normally cause a behavior and one which would not. Implicit memory
Slide 28 - Classical Conditioning Ex. Rabbit eye blink A puff of air directed at a rabbit’s eye causes the rabbit to blink, an unconditioned response. A 1000 Hz tone is played independently and causes no eye blink response. A tone is played and shortly followed by an air puff and this sequence is repeated. The rabbit quickly learns to blink as soon as the tone is sounded, a conditioned response.
Slide 29 - Hebb’s Rule 1949 Donald Hebb proposes that a synaptic connection will be strengthened if a synapse repeatedly becomes active at the same time or just after the postsynaptic nerve fires (he could not verify his own theory).
Slide 30 - Operant Conditioning Similar to classical conditioning, except that it involves an association between a learned behavior and a response (instead of an automatic behavior and another stimulus). Permits an organism to adjust its behavior according to the consequences. Reinforcing stimuli increase the likelihood of the response, punishing stimuli decrease it.
Slide 31 - Operant Conditioning Dr. Skinner and his famous box
Slide 32 - Operant Conditioning Ex. Skinner Box - Training A hungry rat is placed in a box with a lever. It has no particular reason to press the lever. By random interaction, the rat learns that it will get a food reward for pressing the lever. This will increase the likelihood that the rat will press the lever to get more food (reinforcing stimulus).
Slide 33 - Operant Conditioning Ex. Skinner Box - Extinction Once trained, the rat is then also shocked (a punishing stimulus) when the lever is pressed, decreasing the likelihood of further lever presses. The lever pressing behavior is extinguished. Recent research suggests 2 mechanisms: Immediate: The new synaptic connection destroyed. Delayed: A separate learned inhibitory pathway forms. Consolidation seems to be required.
Slide 34 - Neural Mechanisms The basis of all learning is plasticity, the ability of the nervous system to change its neural connections by: Forming or destroying neural connections. Forming or destroying receptors. Activating or deactivating receptors.
Slide 35 - Learning Two major plasticity mechanisms Long-term potentiation (LTP) Creates associations by synaptic enhancement Long-term depression (LTD) Loosens associations by synaptic degradation
Slide 36 - Anatomy Review Hippocampus (a.k.a. Ammon’s Horn = cornu ammonis) is heavily involved in new memory formation. Neurons enter through the entorhinal cortex, relay through the granule cells of the dentate gyrus, and project to pyramidal cells of CA3 (30,000+ spines per dendrite). Output is from CA1.
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Slide 39 - Long-term Potentiation Glutamate is the predominant interneuronal neurotransmitter in the CNS. Two major glutamate receptor types: AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionate) Na+ ion channels NMDA (n-methyl-D-aspartate) Voltage and glutamate controlled Ca++ ion channel The channel is normally blocked by a Mg++ ion, which is expelled when the cell becomes depolarized.
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Slide 41 - Long-term Potentiation “Silent synapse” theory - new dendritic spines only contain NMDA receptors (no AMPA receptors). If the new synapse receives stimulation at the same time as the nerve fires, AMPA receptors will be created, unsilencing the synapse.
Slide 42 - Long-term Potentiation The NMDA receptors are assumed to be responsible for LTP. AP5 (2-amino-5-nopentanoate) blocks NMDA channels and temporarily inhibits learning, but not recall. Ca++ acts as a 2nd messenger, regulating the creation of new AMPA receptors. EGTA, which binds to Ca++ and makes it insoluble, also blocks learning.
Slide 43 - Long-term Potentiation Ca++ influx Activates type II calcium-calmodulin kinase (CaM-KII). Converts arginine to nitrous oxide (NO). Which signals presynaptic neuron to release Glu. CaM-KII self-phosphorylates, allowing continued action after Ca++ influx. CaM-KII controls synthesis of receptors, protein kinases and cytoskeleton, and phosphorylates the AMPA receptors.
Slide 44 - LTP Summary Initially only NMDA channels. Simultaneous presynaptic glutamate and postsynaptic depolarization let Ca++ enter NMDA channels. AMPA receptors are synthesized and strengthen the synaptic connection.
Slide 45 - LTP CaM-KII effects: Self-phos-phorylation Creation of new AMPA receptors Arginine to nitrous oxide conversion
Slide 46 - Long-term Potentiation NO release by the postsynaptic cell has retrograde causes further presynaptic glutamate release.
Slide 47 - Long-term Potentiation Recent evidence also shows that the presynaptic terminal button projects a finger-like extension into the postsynaptic dendritic spine. The projection divides the spine and causes a split into two buttons and two spines.
Slide 48 - Long-term Potentiation
Slide 49 - Long-term Potentiation Protein synthesis in LTP Proteins (i.e. AMPA receptors) don’t last long, but memories do. Something else must make memories permanent. Protein synthesis inhibitors have been found to interfere with the formation of long-term memories.
Slide 50 - Long-term Potentiation Protein synthesis experiments Experiments with Drosophila identified two proteins involved with long term learning, cAMP Response Element Binding proteins CREB-1 and CREB-2. CREB2 repressed memory formation. CREB1 gave super-memory. CREB formation is governed by protein kinases that results from varying Ca++ influx.
Slide 51 - Long-term Potentiation CREB-2 does not permit synthesis CREB-1 readily replaces CREB-2, but does not permit synthesis either. Phosphorylated CREB-1 does permit synthesis.
Slide 52 - Long-term Depression CPP, an NMDA antagonist blocks LTP but not LTD. This suggests at least two subtypes of NMDA receptors. AMPA receptors are dephosphorylated, decreasing their sensitivity to glutamate. AMPA receptors also decrease in number.
Slide 53 - Long-term Potentiation
Slide 54 - Hebb’s Rule After 50 years and many new tools (cellular recording, drugs, electron microscopy) we now have solid evidence for at least one mechanism of learning predicted by Hebb. Other mechanisms also exist, but they are not yet well understood.