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Exam 4 Study Guide.docx

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PSB 2000

Brain and Behavior Exam 4 Study Guide: Learning & Memory: Study Questions 1) What is an engram, and what were Lashley’s critical mistakes in looking for the engram? • A physical representation of a memory 2) 1a) what were Lashley’s critical mistakes in looking for the engram? • 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) • 2 false assumptions: • (1) memory is in cortex • (2) all memories are physiologically the same 3) What are implicit memory and explicit memory? What brain regions are important for each? • • Explicit: deliberate recall of info that one remembers as a memory (ie, who was the main character in the last novel you read?) • Implicit: the influences of recent experiences on behavior, w/o necessarily realizing that one is using memory. So thinking about skills, habits, emotional associations, and conditioned reflexes! Explicit: Hippocampus, nearby cortical areas, medial diencephalon Implicit: 1) Skills/habits= striatum, motor areas of cortex, cerebellum 2) Emotional associations: Amygdala 3) Conditioned reflexes: cerebellum Brain and Behavior 4) What are some differences b/t short-term memory (working memory) and long-term memory? What brain region is important for working memory? • STM: • Small capacity • –CYZUAUF • Fades quickly unless rehearsed • Once forgotten, it is gone • 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 • LTM: • Infinite capacity • Lasts indefinitely • Could be forgotten and then later remembered w/ appropriate cues. • –Phone # vs. names of grade school teachers 5) What were some of HM’s impairments; what could he still do? • HM: anterograde amnesia • –Lost declarative (explicit) memory & spatial memory • –Intact procedural memory (a type of implicit) and working memory 6) With regard to memory, what are some functions of the hippocampus? • Active during formation of memories & during recall • Consolidation (STM  LTM) • Declarative/explicit memory • Spatial memory • –Increased activity in hippocampus when doing spatial task (ex: imagining best route; FMRI) • –Damage  impairment of spatial tasks • –London taxi drivers: hippo active during spatial tasks; larger posterior hippo & positive correlation to time being a taxi driver • –Birds that liveat high altitude and bury seeds = larger “hippocampus” • –Place neurons 7) Individual differences • –Size • –BDNF: 2 genes; people w/ 1 of them show worse performance on memory tasks and decreased hippocampal activity • 8) What other brain regions are important in learning and memory, and what type of learning do they subserve? • Cerebellum: for learning a conditioned response Brain and Behavior • –Also for motor learning (skills) & cognitive stuff too. • Parietal lobe: if damage, don’t spontaneously elaborate on memories • Temporal lobe (ant./inf.): damage causes semantic dementia • –SD: loss of factual knowledge • –Probably b/c this region is a hub for retrieving info; not the location of storage. • Prefrontal cortex: learning reward and punishment • –Also working memory of course • Hippocampus 9) What is a Hebbian synapse? • Hebbian synapse: a synapse that increases in effectiveness b/c of simultaneous activity in pre- and postsynaptic neurons • –“cells that fire together, wire together” • –In other words, when an axon successfully stimulates a cell it will be even more successful in the future…the synapse is strengthened. 10)What is LTP? What receptors are necessary? • 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 • Necessitates glutamate receptors: AMPA and NMDA receptors • specificity: only active synapses become strengthened • cooperativity: nearly simultaneous stimulation by two or more axons results in LTP (more strongly than repeated stimulation by 1 axon) • associativity: pairing a weak input with a strong input enhances later response to the weak input 11)What are some presynaptic changes that occur in LTP? What are some postsynaptic changes that happen in LTP? • Retrograde transmitter from dendrite to axon terminal, usually nitric oxide (NO) • –Decreased threshold for producing APs • –Increased release of neurotransmitter • –Expansion of axon (seen in prev. slide along w/ increase in spine number • –Release of NT from more sites along axon 12)What is evidence that there is a functional connection between LTP and actual learning? • Neurons change early in training, a preliminary step before behavioral change • Research with mice • –abnormal NMDA receptors impair learning • –drugs that block LTP block retention of learned material • –drugs that facilitate LTP facilitate learning • –LTP increases certain proteins, & blocking those proteins weakens memories Brain and Behavior • LTP increases GAP-43 & over production of GAP-43 enhances learning and problem solving • –following training, LTP seen in hippocampus quickly and in cerebral cortex 90- 180 minutes later (this might have been in rats) •In people: partial NMDA agonist (so ramp-up excitability of synapses) given w/ behavioral treatment for PTSD  learn faster Alzheimer’s Disease and other Dementias Study Questions: 1) 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- Loss of memory (working memory goes first) o Agnosia- loss of ability to recognize objects o Apraxia- loss of knowledge about how to do things o Aphasia- loss of speech 2) 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 3) 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 Brain and Behavior 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. 4) What do the neurons and the brain of an AD patient look like? a. Less brain matter (tissue) called Brain Atrophy i. because the neurons have degenerated (loss of them) ii. Dendrites start to degenerate, so you lose SPINES and synapses iii. And lose connections between neurons. b. Also proteins fold abnormally, clump, and interfere with neuronal activity. 5) Plaques and tangles: Where are they (inside or outside of cells) and what forms them? a. Plaques are made from APP- amyloid precursor protein i. There are enzyme complexes (beta cecretases that first cut APP in extracellular part and make it small, then another beta cecretase cuts is again EVEN smaller, and the Abeta 42 is PROBLAMATIC! IT clumps together and interferes with neurons and messes up nmda receptors ii. Plaque stuck together strands of abeta42 along with pieces of dead generating neurons iii. This is probably the first major thing to go wrong with altz. disease b. Tau is made from 6) What are some treatment options for Alzheimer’s Disease? a. There is no cure. The treatments can slow it down b. First drug- is Aricept- which prolongs ach release c. Ach increases arousal, and so does coffee! So people who drinks 3-5 cups a day is thought to help prevent AD, d. Curcumin- is still being researched and is thought to help e. Immunization- was thought to help but not so much luck f.  Memory books, make scrap books add in words bc people with dementia can still read and it should take them thru their childhood, friends, family thru present day and including respite for caregivers….worth mentioning because it Brain and Behavior is a disease of aging and the baby boomers are now about 65 years old- so there will be a lot more people with this 7) Know causes, symptoms, and (when applicable) treatment options of Korsakoff’s Syndrome, (Parkinson’s Disease, Huntington’s disease  movement diseases!) and CJD Korsakoff’s syndrome:  Causes: - Brain damage caused by prolonged thiamine (vitamin b1) Deficiency o Usually in alcoholics: poor diet: lots of carbs; no vitamins o Thiamine needed to metabolize glucose (fuel for the brain) - Shrinkage of neurons, esp. in mammillary bodies & dorsomedial nucleus of thalamus, which sends axons to prefrontal cortex - Damage of axons & myelin - Can also involve other brain rdeas - *Also note the enlarged 3 ventricle  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, meaning a clumsy standing and walking  Treatments: - Some treat with thiamine, not shown to cure thought - Thiamine can help stop the progression of it. Parkinson ’s disease - A movement disorder  Causes: - Loss of dopaminergic cells in substantia nigra (this is part of basal ganglia (one structure of basal ganglia, in MID BRAIN ) that project to striatum  less excitation of cortex - We see not enough cortical activity - So there is slow and rigid movement  and this is also reflected on their cognitive activity - Rigidity, muscle tremors, slow movement, difficulty initiating movement (or cognitive activity) - Dementia can be similar to AD, but movement problems are first and predominant sign in PD o Depression o Deficits in memory and reason Brain and Behavior - Overall Mix of causes: o Genetics? Yes for early-onset, not for late though! o Toxins? YES! MPTP  MPP, which is toxic to SN neurons  Mptp is converted with something in brain to make mpp  Exposure to MPTP or similar chemical in pesticides and herbicides o Drugs: cigarettes & coffee decrease vulnerability; marijuana increases vulnerability of getting Parkinson’s disease. - Virus? PD symptoms in people w/ and who had encephalitis o *Awakenings – a movie about the discovery of aldopa to treat Parkinsons Disease in a group of people who got this disease from being exposed to encephalitis - Head trauma? Possibly – whether singe trauma or multiple trauma’s could cause this disease or even Alzheimer’s disease.  Symptoms: - Severe degeneration of substantai nigra. - Dopamine neurons in SN in rat destroyed; looking at striatum (where those neurons projected to): More D2 receptors on right and fewer dopamine terminals on right  so we see an increase in dopamine receptors. If you lose dopamine terminal input- your body will respond by ramping up the receptors— so they are ready to respond.  Treatments: - L-DOPA o Doesn’t help in late stages o Doesn’t prevent continued loss of neurons o Side effects o The problem is you cant turn this into dopamine! o So this has limited efficacy. - *if you try to ramp dopamine up too much then you could possibly get schizophrenic…but if you decrease dopamine you could get parkinsons disease so doctors must be very careful to find the balance of dopamine! - Other drugs: o Antioxidants to decrease further damage o Dopamine receptor agonists o Cannabinoid agonists o Neurotrophins to promote neuronal survival and growth o Anti-apoptotics (APOPTOSIS- programmed cell death) - Stimulation of GPi and nucleus subthalamicus (parts of the basal ganglia) o Good for decreasing tremor - Stem cell transplants o Substantia nigra neurons or dopamine producing neurons in general o Not great results 8) For PD, HD and Korsakoff’s, what brain regions are involved? 9) What are prions? Brain and Behavior Language Study Questions: 1) What kind of “language” do other species have? What do we learn from studying how other species communicate or from their potential for language?  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  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? They have more language potential than chimps. Also this animal is more able to learn language.  More language potential? Yes  Started younger? Yes- you have to be around language from the time you are a baby and you will develop language. There is a critical window when your young that you develop language, and during these early years of language you need to just be exposed to it.  Method of training (observation/ imitation)  Elephants imitate the sounds they hear, including vocalizations of other elephants  Dolphins learn to respond to gestures and sounds  *This does not mean it is LANGUAGE THOUGH!  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?) he was able to listen to the qs and answer correctly- does this constitute language? Idk- will he get creative and tell stories. Just because he can do this is it
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