Study Questions Learning and Memory What is an engram and what were Lashley s critical mistakes in looking for the engram Engram a physical representation of a memory Lashley trained rats and lesioned areas of cortex He had 2 mistakes false assumptions 1 memory is in discreet regions of cortex FALSE 2 all memories are physiologically the same FALSE Anatomical substrates of memories says there are DIFFERENT TYPES OF MEMORIES and DIFFERENT BRAIN AREAS IMPORTANT FOR THESE What are implicit memory and explicit memory What brain regions are important for each Implicit memory an influence of experience on behavior even if the influence is not recognized not deliberate recall Skills habits emotional associations conditioned reflexes Cortex Amygdala Cerebellum Explicit memory deliberate recall of information that one recognizes as a memory Remembering events episodic memory Knowing facts semantic memory Hippocampus What are some differences b t short term memory working memory and long term memory What brain region is important for working memory STM working memory SMALL CAPACITY once forgotten its gone time needed for consolidation remember where car is parked when where lunch date is Hippocampus important for CONSOLIDATION of declaritive explicit STM LTM LTM INFINITE CAPACITY lasts indefinitely could be forgotten but later remembered with cues ex phone numbers names of elementary school teachers What were some of HM s impairments what could he still do They removed HM s hippocampus to decrease seizures HM lost declaritive explicit memory spatial memory Suffered anterograde amnesia inability to form new memories Intellect language and personality remained the same HM s short term working memory remained intact however as soon as he gets distracted a memory is gone unable to transfer to LTM With regard to memory what are some functions of the hippocampus active during formation of memories during recall of memories consolidates declarative explicit memories from STM LTM spatial memory ex hippocampus is active in london taxi drivers What other brain regions are important in learning and memory and what type of learning do they subserve Basal ganglia gradual learning establishing habits for example learning via trial error pariteal lobe where were you Parts of prefrontal cortex important for learning about rewards and punishments What is a Hebbian synapse Hebbian synapse synapse that increases in effectiveness because of simultaneous activity in pre postsynaptic neurons synapse strengthened every time it successfully stimulates a cell What is LTP What receptors are necessary Long term Potentation LTP a burst of stimulation from axons 100 excitations per seconds this burst of intense stimulation can leave some synapses potentiated for minutes days or even weeks Glutamate receptors AMPA and NMDA necessary Understand cooperativity specificity and associativity in terms of LTP How does classical conditioning probably depend on the associative nature of LTP specificity only active synapses become strengthened cooperativity almost simultaneous stimulation by 2 axons results in LTP associativity pairing a weak input w strong input enhances later response to the weak input What are some presynaptic changes that occur in LTP What are some postsynaptic changes that happen in LTP Presynaptic changes in LTP Retrograde transmitter from dendrite to axon terminal usually nitric oxide dec threshold for producing action potentials inc release of neurotransmitters expansion of axon release of NT from more sites along axon Postsynaptic changes in LTP ionotropic glutamate receptors open channels AMPA receptors glutamate opens sodium channels NMDA receptors glutamate opens channel for both sodium and calcium What is evidence that ther e is a functional connection between LTP and actual learning mice rat research shows abnormal NMDA receptors impair learning drugs that block LTP block retention of learned material drugs that facilitate LTP facilitate learning LTP increases certain proteins and blocking these proteins weakens memory Study Questions Alzheimer s Disease Other Dimentias What are some cognitive and non cognitive symptoms of dementia What are the 4 A s of demenita Cognitive symptoms impairment in memory decrease ability to relate and function at home work and social settings Noncognitive symptoms delusions suspicions hallucinaions agitation depression 4 A s of dementia 1 Amnesia loss of memory 2 Agnosia loss of ability to recognize objects 3 Apraxia loss of knowledge about how to do things 4 Aphasia loss of speech What are some symptoms of Alzheimer s Disease AD Defecits in explicit and implicit memory better at procedural than declarative memory gradual progression to more serious memory loss language problems loss of vocabulary confusion depression restlessness hallucinations delusions sleeplessness loss of appetite sundowning What is the difference b t early onset and late onset AD Which one has a stronger genetic contribution Early onset is people earlier than 40 yrs old STRONG genetic component gene for APP on chromosone 21 Late onset is people over 60 yrs old genetics are small percentage of cases What do the neurons and the brain of an AD patient look like Loss of neurons spines synapses loss of connections between neurons Proteins fold abnormally clump and interfere w neuronal activity more clumpy less dendrites Plaques and tangles Where are they inside or outside of cells and what forms them Plaques Amyloid plaques made by beta amyloid aka A beta Tangles Made by an abnormal form of the intracellular protein Tau What are some treatment options for Alzheimer s Disease Drugs to stimulate Acetlycholine receptors or prolong Ach release stimulates arousal in Alzheimer patient s the Ach system is the first to go Research being done on curcumin an antioxidant that reduces amyloid deposits hyperphosporylation of tau Immunizations to produce antibodies against amyloid Know causes symptoms and when applicable treatment options of Korsakoff s Syndrome Wernicke Korsakoff syndrome Parkinson s Disease Huntington s disease and CJD WERNICKE KORSAKOFF SYNDROME Causes Thiamine deficincy usually in alcoholics poor diet lots of carbs no viramins Shrinkage of neurons damage to axon and myelin Symptoms Like damage to ctx apathy confusion retero antero amnesia better implicit than explicit memory difficulty reasoning thru memories what happened first confabulation person takes a guess to fill in blanks of memory
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