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Exam 4 Review.docx

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Department
Psychology
Course
PSB 2000
Professor
Berkley
Semester
Fall

Description
Learning and Memory •What is an engram, and what were Lashley’s critical mistakes in looking for the engram? o •A physical representation of a memory o •Lashley: trained rats, then cut* or lesioned^ certain areas of cortex  *no significant effect on performance; ^the bigger the lesion, the greater the impairment (location didn’t matter) o –2 false assumptions: o •(1) memory is in cortex o •(2) all memories are physiologically the same •What are implicit memory and explicit memory? What brain regions are important for each? o o Explicit: deliberate recall of info that one remembers as a memory (ie, who was the main character in the last novel you read?) o Implicit: the influences of recent experiences on behavior, w/o necessarily realizing that one is using memory o •What are some differences b/t short-term memory (working memory) and long-term memory? What brain region is important for working memory? o STM o •Small capacity  –CYZUAUF o •Fades quickly unless rehearsed o •Once forgotten, it is gone o •Working memory is alternate way of thinking of STM:  –lasts hours to days w/o rehearsal: where car is parked, when/where lunch date is  –Time needed for consolidation varies, especially depending on familiarity of topic & emotional content o LTM o •Infinite capacity o •Lasts indefinitely o •Could be forgotten and then later remembered w/ appropriate cues.  –Phone # vs. names of grade school teachers •What were some of HM’s impairments; what could he still do? o HM: anterograde amnesia o –Lost declarative (explicit) memory & spatial memory o –Intact procedural memory (a type of implicit) and working memory •With regard to memory, what are some functions of the hippocampus? o •Active during formation of memories & during recall o •Consolidation (STM  LTM) o •Declarative/explicit memory o •Spatial memory o –Increased activity in hippocampus when doing spatial task (ex: imagining best route; fMRI) o –Damage  impairment of spatial tasks o –London taxi drivers: hippo active during spatial tasks; larger posterior hippo & positive correlation to time being a taxi driver o –Birds that live at high altitude and bury seeds = larger “hippocampus” o –Place neurons o •Individual differences o –Size o –BDNF: 2 genes; people w/ 1 of them show worse performance on memory tasks and decreased hippocampal activity •What other brain regions are important in learning and memory, and what type of learning do they subserve? o •Cerebellum: for learning a conditioned response o –Also for motor learning (skills) & cognitive stuff too. o •Parietal lobe: if damage, don’t spontaneously elaborate on memories o •Temporal lobe (ant./inf.): damage causes semantic dementia o –SD: loss of factual knowledge o –Probably b/c this region is a hub for retrieving info; not the location of storage. o •Prefrontal cortex: learning reward and punishment o –Also working memory of course o hippocampus •What is a Hebbian synapse? o •Hebbian synapse: a synapse that increases in effectiveness b/c of simulataneous activity in pre- and postsynaptic neurons o –“cells that fire together, wire together” o –In other words, when an axon successfully stimulates a cell it will be even more successful in the future…the synapse is strengthened. •What is LTP? What receptors are necessary? o •LTP: a burst of stimulation from axons, e.g., 100 excitations per second for 1-4 seconds onto dendrites, results in potentiated (strengthened) synapses for minutes, days or weeks o •Necessitates glutamate receptors: AMPA and NMDA receptors o •specificity: only active synapses become strengthened o •cooperativity: nearly simultaneous stimulation by two or more axons results in LTP (more strongly than repeated stimulation by 1 axon) o •associativity: pairing a weak input with a 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? o •Retrograde transmitter from dendrite to axon terminal, usually nitric oxide (NO) o –Decreased threshold for producing APs o –Increased release of neurotransmitter o –Expansion of axon (seen in prev. slide along w/ increase in spine number o –Release of NT from more sites along axon •What is evidence that there is a functional connection between LTP and actual learning? o •Neurons change early in training, a preliminary step before behavioral change o o •Research with mice o –abnormal NMDA receptors impair learning o –drugs that block LTP block retention of learned material o –drugs that facilitate LTP facilitate learning o –LTP increases certain proteins, & blocking those proteins weakens memories o • LTP increases GAP-43 & over production of GAP-43 enhances learning and problem solving o –following training, LTP seen in hippocampus quickly and in cerebral cortex 90-180 minutes later (this might have been in rats) o •In people: partial NMDA agonist (so ramp-up excitability of synapses) given w/ behavioral treatment for PTSD  learn faster Alzhimers •What are some cognitive and non-cognitive symptoms of dementia? What are the 4 A’s of demenita? o •The diseases of aging o •Different causes; similar presentations o •Impairment in memory & cognition, accompanied by decreased ability to relate/function at home/work/social settings o •Noncognitive symptoms: delusions, suspicions, hallucinations, agitation, depression o –Up to 2/3 of AD patients develop delusions & hallucinations o –Depression & dementia are often comorbid…have to distinguish b/t the two o –Also have to distinguish b/t dementia and psychosis 4 A’s o •Amnesia o –Loss of memory (working memory goes first) o •Agnosia o –Loss of ability to recognize objects o •Apraxia o –Loss of knowledge about how to do things o •Aphasia o –Loss of speech •What are some symptoms of Alzheimer’s Disease (AD)? o •Deficits in explicit and implicit memory o –Better procedural than declarative memory o –First symptoms can be mild anterograde amnesia o •Gradual progression to more serious memory loss and o –Language problems (loss of vocabulary) o –Confusion o –Depression o –Restlessness o –Hallucinations o –Delusions o –Sleeplessness o –Loss of appetite o •“Sundowning” o •End stage is usually coma; death usually caused by an infection •What is the difference b/t early-onset and late-onset AD? Which one has a stronger genetic contribution? o •Early onset o –People <40 yr old o –Only about 1% (or up to 10%) of people w/ AD o –Gene on chromosome 21 (for APP…don’t want 3 copies of this) o –Gene for ApoE4 which breaks down beta-amyloid (this version isn’t very good at it) o –Mutations in presinilin (part of family of enzymes that chop APP into beta amyloid) can increase risk o –Other genes on other chromosomes linked to more of these cases o •Late onset: o –Over 60 yr old o –5% of people b/t 65-74 yr old o –50% of people over 85 yr old o –Some genes that increase risk, but only account for small percentage of cases o –Half of patients have no known relative with A.D. o –Yoruba people (Nigeria): lots of A.D. genes; very little A.D. o •Diet may be protective (low-calorie, low-fat, low-sodium) o Take-home message on genes: less contribution in late-onset vs early- onset. •What do the neurons and the brain of an AD patient look like? o •Brain atrophy o –Loss of neurons o –Loss of spines & synapses o –Loss of connections between neurons o •Proteins fold abnormally, clump, and interfere w/ neuronal activity •Plaques and tangles: Where are they (inside or outside of cells) and what forms them? o •Amyloid precursor protein o –Normally important in neuron growth, survival and post-injury repair (?) o –cleaved to A 40 o –in AD, cleaved to A 42 o –A 42cumulates (usually prior to behavioral symptoms)  widespread atrophy of cortex, hippocampus, etc  amyloid plaques (formed from degenerating axons & dendrites, in the places b/t neurons) o •Tau o –Normally part of intracellular support structure of neurons; involved in transporting things w/in the cell o –Abnormal form in AD (hyperphorphorylated; aggregates w/ other strands of tau) o –Produces tangles, from degenerating structures w/in neuronal cell bodies o •-amyloid (A-42) probably primary cause of AD (according to many experts, not all) o •-amyloid interferes w/ NMDA receptor o •Inject -amyloid  impairment in learning & memory o –Inject tau alone  no effect o •Suppress tau  decrease memory impairment (mouse model of AD) •What are some treatment options for Alzheimer’s Disease? o •Drugs to stimulate Acetylcholine receptors or prolong Ach release o –Ach system is first to go o –Aricept o –One area damaged (basal forebrain) is important in Ach system & for arousal o •NMDA receptor antagonists to block excitotoxicity o •Anti-inflammatory drugs (inflammation may be caused by plaques and lead to neuronal dysfunction) o •Drugs to stimulate cannabinoid receptors o –Limits overstimulation by glutamate o –Looks good in rat model of AD o •Antioxidants to block -amyloid o –Aged mice: curcumin (in yellow dye and tumeric) reduces amyloid and plaques o •Immunization o –to produce antibodies against -amyloid o –Researched in mice & humans (a few life-threatening side effect in humans though, so research stopped o •Worth mentioning: Memory books, respite for caregivers •Know causes, symptoms, and (when applicable) treatment options of Korsakoff’s Syndrome, Parkinson’s Disease, Huntington’s disease and CJD. o •Aka. Wernicke-Korsakoff Syndrome o •Brain damage caused by prolonged thiamine (vitamin B1) deficiency  –Usually in alcoholics: poor diet: lots of carbs; no vitamins  –Thiamine needed to metabolize glucose (fuel for the brain) o •Shrinkage of neurons, esp. in mammillary bodies & dorsomedial nucleus of thalamus, which sends axons to prefrontal cortex o •Damage of axons & myelin o •Can also involve other brain areas o Symptoms  •Like damage to prefrontal ctx  •Apathy  •Confusion  •Retrograde & anterograde amnesia  •Better implicit than explicit memory  •Difficulty reasoning thru memories (ex. what event happened first?)  •Confabulation: person takes a guess to fill in blanks of memory  –Learning becomes difficult b/c confabulate answers and then remember the confabulation instead of the correct answer  •Eye abnormalities (nystagmus, oculomotor paralysis, paralysis of conjugate gaze)  •Ataxia of stance and gait o Parkinson’s Disease o •Loss of dopaminergic cells in substantia nigra that project to striatum  less excitation of cortex o •Rigidity, muscle tremors, slow movement, difficulty initiating movement (or cognitive activity) o •Dementia can be similar to AD, but movement problems are first and predominant sign in PD  –Depression  –Deficits in memory and reason o •Mix of causes  –Genetics? Yes for early-onset  –Toxins? MPTP  MPP, which is toxic to SN neurons o •Exposure to MPTP or similar chemical in pesticides and herbicides  –Drugs: cigarettes & coffee decrease vulnerability; marijuana increases vulnerability  –Virus? PD symptoms in people w/ and who had encephalitis  –Head trauma? o Treatment  •L-DOPA  –Doesn’t help in late stages  –Doesn’t prevent continued loss of neurons  –Side effects  •Other drugs:  –Antioxidants to decrease further damage  –Dopamine receptor agonists  –Cannabinoid agonists  –Neurotrophins to promote neuronal survival and growth  –Anti-apoptotics  •Stimulation of GPi and nucleus subthalamicus (parts of the basal ganglia)  –Good for decreasing tremor  •Stem cell transplants  –Substantia nigra neurons or dopamine producing neurons in general  –Not great results… o Huntington’s Disease o •Loss of cells in caudate & putamen o •Arm jerks & facial twitches, later tremors and writhing o •Cognitive changes and psychiatric symptoms, which often develop prior to movement disorders  –Depression & anxiety  –sleep disorders  –memory impairment  –Hallucinations & delusions  –Poor judgement  –Alcoholism & drug abuse  –Sexual disorders o •Genetic (autosomal dominant)  –95% penetrance  –Chromosome 4  –Trinucleotide repeate (C-A-G)  –Normal gene makes protein huntingtin  –More repeats  get it earlier  –Earlier it begins  quicker it progresses  –Abnormal huntingtin harms neurons by:increasing NT release, decrease BDNF release, impairs mitochondria o CJD o •Creutzfeldt-Jakob Disease  –Familial (Inherited) or sporadic (spontaneous)  –New variant CJD (nvCJD): these are known as transmissible spongiform encephalopathies o •BSE or Mad cow disease o •nvCJD resulting from contaminated instruments or transplants •For PD, HD and Korsakoff’s, what brain regions are involved? o HD: striatum o PD: Cortex o Korsakoff: Thalamus •What are prions? o •Prions (protein-based infectious agent);  –Misfolded proteins that promote refolding of native proteins into diseased states o •There is a normal prion protein which is a membrane- bound protein that is implicated in LTP and long-term memory. This is what becomes abnormal and affects other prion proteins.  –Infectious (acquired), spontaneous (sporadic) or inherited (familial)  –Pruisner won Nobel Prize in 1997 o •Symptoms:  –rapidly progressing dementia, confusion, blurred vision, hallucinations, incoordination, changes in gait, muscle twitching and stiffness, seizures, personality changes, nervousness, speech impairment, sleepiness o •Rapid progression  –usually not capable of self-care after 6 months; death in 8- 24 months o •“Deadly Feasts” by Richard Rhodes Language o •What kind of “language” do other species have? What do we learn from studying how other species communicate or from their potential for language? o •Chimps: attempted to teach chimps ASL or other visual systems.  –Chimps didn’t use symbols in new original combinations  –Used symbols to request, not describe  –Produced requests more then they understood o •Bonobos: very human-like; what Kanzi learned:  –250 human words; language of 2-2 ½ yr old  –Understand more than they can produce  –Use symbols to name/describe  –Request items they don’t see  –Use symbols to describe past events  –Original, creative requests  –Why so much better than chimps?  •More language potential?  •Started younger?  •Method of training (observation/imitation) o •Elephants imitate the sounds they hear, including vocalizations of other elephants o •Dolphins learn to respond to gestures and sounds o •Alex, the African gray parrot  –Learned to give spoken answers to spoken questions (What color is the key? What object is gray? How many blue keys are there?) o •What do we learn from this?  –How to teach language to people who do not easily learn it  –Our concept of language is ambiguous… o •What are the hypothesis on how humans evolved language? o Hyp: 1) Byproduct of overall brain development  •But some people w/ normal sized brain don’t have normal language; language requires specialization, not just expansion  –Family w/ normal intelligence and normal activity in language centers but poor language skills (dominant gene)  •Another problem: Williams syndrome:  –Deletion of many genes on chromosome 7; decreased gray matter  –mental retardation, but skillful use of language o Hyp 2) an extra brain module, aka, a new specialization  •Language acquisition device  –Built-in mechanism (instinct) for acquiring language that is uniquely human  –Can be explained by evolution  –Steven Pinker’s The Language Instinct (also Noam Chomsky)  •Ease w/ which children learn language  –Even if no one teaches them, they invent their own  –Applies to deaf and hearing children  •Certain brain areas necessary for language, but language isn’t their only job  •Probably not a totally separate “brain module” o hyp 3)  •Selective pressure for social interactions among people, including those b/t parents and children, favored the evolution of language, and overall intelligence develo
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