chapter 11

what type of learning did D. O. Hebb discover?

Hebbian learning

H.M

bilateral lobectomy to treat epileptic seizures, anterograde amnesia, mild retrograde amnesia (for pre-op, childhood is intact)

E.P

similar MTL damage to HM, but incurred through viral encephalitis (brain illness, kills chunks of hippocampus and surrouding cortex damaged)

what's Hebb's big phrase, and what does it mean?

neurons that fire together wire together, repeated reactivity strengthens synapses between neurons

Hebbian learning can roughly be equated to what other learning theory?

long term potentiation

what is the engram?

a physical representation of what has been learned -- the biological substrate of a memory

what is equipotentiality?

the idea that all parts of cortex contribute equally to complex behaviors. *NOT TRUE

what is mass action?

the cortex works as a whole, and more cortex is better, engram is diffuse *SOME TRUTH, but specialization does exist

what is the definition of learning?

how experience changes the brain

what is memory in relation to learning?

how these experiential changes are stored and reactivated

retrograde amnesia

trouble remembering events prior to onset/injury

anterograde amnesia

inability to form new memories after injury

what is the digit span +1 test, and what type of memory does it test?

remember a span of 5,6,7 etc numbers (add 1 and recite and continue), tests capacity of working memory

mirror-drawing test

IMPLICIT: motor skill learning, trace a star looking into a mirror at your hand drawing

incomplete-pictures test

IMPLICIT: series of incomplete pictures, each more filled in (1-5), how many errors in guessing what it is?

eye-blink pavlovian conditioning

IMPLICIT: skeletal conditoning -- RESPONSE

repetition priming test (most common and what does it test?)

tests implicit memory, shown list of words and later fill in the blanks of word letter

what is global cerebral ischemia?

basically just a stroke; interruption of blood supply to entire brain

what do those with global cerebral ischemia also often suffer from?

MT lobe amnesia

what is transient global ischemia?

ischemia spurred by a sudden onset and with the absense of a specific cause (short term, 4-6 hours); abnormalities in CA1 subfield (hippocampus)

what is the connection between korsakoff's syndrome and memory loss?

memory loss due to thymine deficiency induced by excessive drinking

what amnesia does korsakoff's syndrome result in?

medial diencephalic amnesia -- damage to mediodorsal nuclei. *similar to MT anmesia

how does amnesia progress for those with korsakoff's syndrome?

starts as anterograde amnesia for explicit episodic memories, and progresses to also develop retrograde amnesia

explain the amnesia of Alzheimer's disease, and what may be a contributing factor to its presence?

mild, but progressive, deterioration of memory, which eventually develops into dementia (terminal). Alz. pts have reduced levels of acetylcholine, which contributes to the degeneration of the basal forebrain and is a contributing factor

explain post-TBI amnesia

begins with a coma (can last from seconds-weeks), then a period of confusion (during which anterograde amnesia is present). usually also retrograde occurs in the events leading up to the TBI

what is the consolidation/dual-trace theory regarding memory?

new engrams are stored and strengthened. each time a memory is activated, it is updated and linked to additional memories (connections BETWEEN units) -- a memory is consolidated when it no longer relies on the hippocampus to reinstate it into cortex, more dependent on cortical structures

what are place cells?

cells that respond only when a subject is in specific locations *where it THINKS it is, not where it actually is. also may receive input from entorhinal grid cells

what is the entorhinal cortex important for?

major source of neural signals to the hippocampus

what are grid cells?

entorhinal neurons that have a pattern of hexagonal shaped place fields that tile the surface of an environment. they fire when individuals cross into another hexagon or their gaze crosses into another

what are Jennifer Aniston neurons? (aka concept cells)

neurons in hippocampus, very selective, respond to ideas/concepts or one's perception rather than particular specifics. only fired in response to J.A. pic

what do engram cells experience, and how were they identified?

undergo persistent changes as result of experience, retrieve memory of original experience, identified via optogenetics

what is the implication of inferotemporal cortex in memory?

storing memories of visual input, complex visual functions

what is the implication of the amygdala in memory?

emotional significance of experiences *critically these are stored in other areas

what is the implication of prefrontal cortex in memory?

episodic memory (temporal order of events), working memory (series of responses)

what is the implication of the cerebellum in memory?

storage of memory of learned sensorimotor skills

what is the implication of the striatum in memory?

storage of memory for consistent relationships between stimuli + responses (habit formation)

what are the two proposed cellular mechanisms of memory?

long term potentiation and long term depression

explain LTP

persistent strengthening of a synapse based on recent patterns of activity at that synapse

induction: learning, activates NMDA glutamate receptor --> association

maintenance + expression: storage and recall
--> changes in both pre and post synaptic neurons, can be specific due to dendritic spines
--> structural changes
--> transcription factors activated by neural activity

facilitation of synaptic transmission following high frequency electric stimulation to presynaptic neurons

what does LTP require?

co-occurence of pre and post synaptic neurons (both must fire APs simultanenously or VERY close together, fractions of ms)
*SPECIFICITY, COOPERATIVITY, and ASSOCIATIVITY

explain LTD

effective flip side of LTP, in response to continuous low-frequency stimulation of pre-synaptic neurons

what is metaplasticity?

the fact that LTP/LTF induction can be modulated by prior synaptic activity

what is the role of oligodendrocytes in learning?

following learning, oligo. modulate their myelination of axons in response to experience (can be lengthened/shortened, thinned/thickened, unmyelinated/myelinated, etc)

what is infantile amnesia?

the fact that we explicitly remember almost nothing of the events of our infancy, but there are preserved implicit memories

what are nootropics?

"smart drugs," claim to enhance memory -- not convincing.

place vs response learning, and what brain areas are they mediated by?

place = landmarks, go to same arm, mediated by hippocampus
response = muscle memory, remember to take a R and therefore go to wrong arm when entrance switched, mediated by caudate nucleus

what does delayed non-match to sample task demonstrate?

having explicit memory, see a sample object that has food under it and then undergo a delay period, later presented w/ two objects -- can they correctly differentiate the one they saw previously?

mumby box is the?

rodent version of delayed non match to sample task

what type of memory is hippocampus critical for?

spatial memory (but not explicit object recognition)

what brain area subserves declarative memory (EXPLICIT)?

MT lobe (hippocampus - spatial, MT cortex)

what brain area subserves repetition priming (IMPLICIT)?

frontal cortex (for word stems), visual cortex (for image priming)

what brain area subserves motor skill learning (IMPLICIT)?

basal ganglia (dorsal striatum = caudate and putamen). makes sense = voluntary motor response

what brain area subserves the skeletal conditioning (IMPLICIT) for conditioned eye blink?

cerebellum

what brain area subserves emotional conditioning (IMPLICIT)?

amygdala! especially fear

why is hm important?

1. particular brain regions could be tied to particular memory functions (multiple memory systems)

2. there are different modes of storage for short term/ long term/ remote memory

3. amnesiac patient may not have explicit memory but still show implicit proof of learning (improved performance of a task)

conditioned eye blink engram

lateral interpositus nucleus

medial temporal cortical areas damaged in h.m.

hippocampus, parahippocampal gyrus and amygdala

parahippocampal gyrus in primates

entorhinal cortex, perirhinal cortex, parahippocampal cortex

parahippocampal gyrus in rodents

entorhinal cortex, perirhinal cortex, and postrhinal cortex

lobotomy

when lobe/major part of area is removed from the brain

lobectomy

when a lobe/major part of one is separated from the rest of the brain by a large cut (NOT removed) (HM)

lesions in monkey HPC

aspiration via inferior surface of brain, medial temporal cortex damage

lesions in rat HPC

via dorsal surface of brain, causes parietal neocortex damage

hpc tests of spatial memory

morris water maze, radial arm maze, t-maze, plus maze

allocentric

object to object - location of object relative to location of other object

egocentric

self to object - location of object relative to body axes of the self

place learning

spatial environmental cues, early on, landmark-dependent, HPC

response learning

less effortful, autopilot, after many times, learned motor response, caudate

specificity

if some of the synapses onto a cell become active, and others not, only active synapses become strengthened

cooperativity

nearly simulatanous stimulation by 2+ axons produce LTP stronger than does repeated stimulation by one axon

associativity

pairing a weak input with a strong input will enhance later responses to the weak input

auditory fear conditioning

LTP is thought to underlie this, as amygdala recieves input from sensory thalamus, associative cortex, perirhinal cortex and hippocampus

prader-willi syndrome cause

gene mutation on chromosome 15 from the father (gene deletion)

prader-willi syndrome symptoms

excessive eating, inability to feel full, mild intellectual disability, emotional dysregualtion, short stature

prader-willi syndrome cause

hypothalamus? could be bc of bombesin or ghrelin

leptin - where

peptide hormone found in adipose (fat) cells. densest in the arcuate nucleus of the hypothalamus

leptin function

many physiological processes: energy balance, metabolism, endocrine regulation, immune function = INHIBIT FOOD INTAKE

leptin deficiency: ob/ob mouse

mutation on chromosome #6 so they cant produce leptin- super fat!

congenital disorder in humans

super rare and genetic bc of mutation in LEP gene (human analog of ob gene)

parabiosis

surgically joining 2 mice so that they share a bloodstream

ob/ob mouse and lean

ob/ob mouse lowered food intake and blood sugar while lean mouse had no change. this indicates that the ob/ob mouse was lacking something that was circulating in the wild type mouse’s bloodstream

db/db mouse and lean

leptin receptor deficient mouse gained weight while the lean mouse had decreased food intake/blood sugar/died by starvation. this means the db mouse could make leptin just didnt have its receptors to respond to it. lean mouse recieved too much leptin signaling which led to a leptin overdose

insulin brain levels reflect

VISCERAL fat (surrounding organs)

leptin levels reflect

subcutaneous fat (long term signal to regulate food intake)

BMI

weight (kg)/ (height (m))2

BRI

based on circumferences, such as height and waist size. it measures/estimates visceral fat. ranges from 1-20

8 steps in digestion

1. chewing

2. saliva lube

3. swallow

4. HCI in stomach breaks down food; pepsin breaks down protein molecules

5. empty contents through pylonic sphincter to duodenum to be absorbed

6. digestive enzymes break down protein

7. fats emulsified by bile

8. remaining stuff absorbed from waste in large intenstine and pooped out!

salivary amylase

ehzyme in saliva that aids in food breakdown

energy delivery

lipids (fats), amino acids (proteins) glucose (carbohydrates)

energy storage

stored as fats, proteins and glycogen. fat is most efficient storage (1g fat = 2x energy of glycogen — bc doesnt hold as much water so its denser)

cephalic

prepatory phase, triggered by smell/thought of food (INSULIN HIGH, GLUCAGON LOW)

absorptive

energy from food absorbed in blood stream to meet immediate energy needs, excess is stoteed (INSULIN HIGH, GLUCAGON LOW)

fasting

body is non relying on energy reserves to meet needs (withdrawing energy from resources, ends with next cephalic phase) (INSULIN LOW, GLUCAGON LEVELS HIGH)

insulin

high during cephalic and absorptive phase.