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
• 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
• 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?
• Small capacity
• 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
• 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
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
• –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
• Prefrontal cortex: learning reward and punishment
• –Also working memory of course
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
• 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
• –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
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 –Loss of appetite
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
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
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
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
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
- 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
- Like damage to prefrontal ctx
- 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
- Some treat with thiamine, not shown to cure thought
- Thiamine can help stop the progression of it.
Parkinson ’s disease
- A movement disorder
- 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
- Rigidity, muscle tremors, slow movement, difficulty initiating movement (or
- Dementia can be similar to AD, but movement problems are first and
predominant sign in PD
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
- Head trauma? Possibly – whether singe trauma or multiple trauma’s could cause
this disease or even Alzheimer’s disease.
- 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.
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
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