Behavioral Neuro Test 3 Flashcards
Pavlovian Learning
CS=Sound, US=blow of air, CR=blink
Hebbian Learning
if presynapse becomes active at same time as postsynaptic neuron(repeatedly), relationship will be strengthened between the two.
“neurons that fire together wire together”
Engram
biological substrate of memory
anything that has been biologically changed (strengthened synapse)
Karl Lashley
most of his work is wrong, but we can learn from it.
- believed size of deficit in rat brain corresponded to size of cortical lesion (used maze running to test this) – bigger lesion= worse off
- concluded that engram was diffuse (stored across the brain) and intact brain regions can compensate for damage (equipotential)
How was Karl Lashley’s work wrong
- equipotentially- believed that all parts of cortex contribute equally to complex behaviors and all any part of cortex can substitute (this is not true lol)
- needed to look at more than 1 task- doesn’t represent all learning types
- mass action- cortex works as a whole, more cortex= better. This was wrong.
- his task was too complex
- cerebral cortex isn’t the only place to look for engram
Modern day search for engram
Task used: eyeblinking
Location: engram found in cerebellum (lateral interpostitus nucleus)
Method: pavlovian conditioning. used muscimol to shut down areas of the brain.
CR: blinking with tone and no air.
Groups that had red nucleus inhibited, didn’t blink. When it was activated after a few days, they did blink right away, indicating that they had learned the association but couldn’t actually blink due to motor skills involved in red nucleus. On the last day, they inhibited the red nucleus again and found that they didn’t blink, supporting the finding that red nucleus was involed in the action of blinking
Groups that had cerebellum inactivated didn’t blink. When they activated the cerebellum, individuals slowly started blinking over trials, meaning they were just beginning to learn and the cerebellum was involved in learning. On the final day, they inhibited the cerebellum again and individuals did not blink, indicating that the cerebellum was not only where the learning took place, but it was also where it was stored, thus where the engram was located.
a->b->c->d->e->f
you need ALL parts of the process for learning to occur
eyeblink conditioning in humans- neural findings
PET Scans- developing eyeblink conditioning response is associated with increased activity in cerebellum and red nucleus
Cerellar damage= weaker conditioned eyeblings, and blinks are less accurately timed relative to onset of air puff
HM- who was he, why do we care
had epilespy. doctors found out medial temporal lobe was where the issue was, so they removed it. seizures went away but now had memory issues.
intact areas HM
reterograde memory
immediate memory
IQ
vision
logic/reasoning
language
motor control
impaired things HM
anterograde amnesia
retrieving recent memories pre operation ( a little retrograde amnesia)
retrograde amnesia
cannot remember events prior to damage. Temporally graded, function of consolidation, only episodic memories only are impaired
temporally graded meaning + another name for
recent memories impacted, older aren’t as much. called ribots law
episodic memories
memories unique to your experience
semantic memory
vocab or facts
Patient EP
also had MTL damage(but it was due to injury).
Patient EP vs patient HM (what was wrong with the brain)
HM: Bilateral MTL lobectomy to treat epilepsy
EP: viral encephalitis damaged the brain
Why do we care about HM and EP?
demonstrates that certain brain areas can be tied to particular memory functions. Memory isn’t diffusely or equivalently spread throughout the whole brain as Lashley thought.
Also demonstrates that there are different modes of storage for short term vs long term memory vs remote memory. this led to the concept of memory consolidation (ST to LT memory conversion)
Demonstrates there are multiple memory systems in the brain
HM had damage to declarative/explicit memory system, but he also had damage to the area around it. (the entire medial temporal lobe and amygdala)
medial temporal lobe consists of
hippocampus and parahippocampal gyrus (entorhinal perirhinal, parahippocampal(aka postrhinal in rats))
medial temporal cortex consists of what
parahippocampal gyrus (entorhinal, perirhinal, parahippocampal)
name for parahippocampal in rats
postrhinal
declarative/explicit memory
recall and recognition
Monkey Experiment for memory
Method: give monkey object and underneath it is food. Then cover animal’s view of the object(I.e. lowering a screen. When the screen is opened, give them the same object (no longer food under it) and a different object (w new food)
Results: does monkey know they ate the old food? Monkeys with MTL lesions had major decrease in object recognition.
The longer the delay period was, the worse memory was.
location of hippocampus (rodents vs monkey)
rodents: more dorsal
monkey: more ventral
rat experiment and memory: mumby box
similar to the monkey experiment, but there are doors in a box with objects.
results: only a decrease in performance when medial temporal cortex was lesioned (NO difference when hippocampus and amygdala were lesioned)
this shows that the hippocampus isn’t critical for object recognition.
what is the hippocampus needed for
spatial and contextual memory
tests for spatial memory
- morris water maze
- radial arm maze
- T maze or plus maze
- place cells
place cells
neurons that respond only when subject is in specific locations
repetition priming tests
dont need to have explicit memory of actually learning
* stem completion test
* incomplete pictures
* mirror tracing task
* skeletal conditioning
* emotional conditioning
stem completion test
have participants read a list of words and then have a ‘delay period’ (aka distract them)
Then give them the stem (beginning) of a word and have them finish the word
results: more likely to fill in the word that they say even if they didn’t remember ever doing the initial task)
incomplete picture task
same as stem completion but with incomplete pictures instead. For example, after many trials HM ‘guessed’ the object very quickly but he doesn’t remember doing the trial before.
mirror tracing task
targets implicit memory in motor skills. trace an object by looking at your reflection in a mirror. HM improved in this task over time even though he didn’t remember doing it
skeletal conditioning example
eyeblink pavlovian
emotional conditioning example
fear pavlovian
declarative memory areas
medial temporal lobe- hippocampus and MTC
repetition priming areas
semantic (meaning)=frontal lobe
modality(visual)=visual cortex
motor skill learning areas
basal ganglia (dorsal stratum=caudate+putamen)
skeletal conditioning for eyeblink area
cerebellum
emotional conditioning for fear area
amygdala
place vs response
place=spatial skills, response=muscle memory
Place and response study
used a plus maze and moved where the rat started. this shows place vs response learning.
Found that animals with inactivated caudate showed place learning and those with inactiviated hippocampus relied on response learning. place vs response was mediated by different neural systems- this was evidence that multiple memory systems function independently.
Place learning (hippocampus) is acquired faster than response learning (caudate).
Learning occurs concurrently. One does not get ‘erased’ from the brain, it is always in tact but one might just take over. Time can also influence which one is used.
LTP- what it stands for, where it is, what it is usually suggested to underly.
LTP is a cellular and molecular mechanism that enhances synaptic strength between neurons after repeated stimulation to presynaptic neurons. It is thought to be one of the key processes underlying learning and memory. This mechanism fulfills hebbian synapses.
Long Term Potentiation. It is usually studied in the hippocampus but there is also evidence of LTP in amygdala. It is kinda like the engram but is the underlying celluluar and molecular mechanisms and usually suggested to underly auditory fear conditioning (I.e. tone and shock).
LTP key properties
- can last for a long time. for several months to a year after multiple high frequency stimulations
- many forms can develop only If there is a co-occurrance of activity in presynaptic and postsynaptic cells.
Learning vs memory
Learning: how experience changes brain
Memory: how changes are storied and reactivated
Short term memory
Storage of new info for brief periods of time while person attends to it
Long term memory
Storage of new info once a person stops attending to it
Remote memory
Memory for experiences in the distant past. Even though HM’s long term memory was messed up, his remote and short term memory was not.
3 discoveries from HM
- MTL influences long term memory but not short or remote
- Couldn’t do explicit memory but COULD do implicit
- Challenged idea that memory is diffusely and equivalent distributed through brain
Lobectomy vs. lobotomy
Lobectomy- removes lobe of brain
Lobotomy- severs connections
What type of surgery did HM have?
lobectomy (medial temporal)
General definition of amnesia
Pathological loss of memory s
Global cerebral ischemia
Interruption of blood supply to entire brain. This often results in medial temporal lobe amnesia due to damage in CA1 of hippocampus and other surrounding areas.
Transient global amnesia
Sudden onset in the absence of any obvious causes. Causes severe anterograde amnesia and moderate retrograde amnesia for explicit episodic memories.
Amnesia is transient, so it only lasts about 4-6 hours.
What Betty had. It is likely that is occurs from ischemia-induced damage (loss of blood supply), specifically in the CA1 subarea of the hippocampus and other areas around it. Any abnormalities in CA1 show up a few hours after beginning and clear up around 10 days later.
Two subtypes of explicit memory
Semantic and episodic
Semantic memory
Explicit memories for facts or info
Episodic memory
Explicit memory for specific moments. HM had more difficulty with this rather than semantic
What type of memory do repetition tests assess?
Implicit memory
Lesion in monkey of hippocampus vs lesion in rat of hippocampus :
Monkey: aspiration via inferior surface of brain, medial temporal cortex damage
Rat: aspiration via dorsal surface of brain would cause parietal neocortex damage SOOOO, they have to inject intracerebral neurotoxins because otherwise there would be more extraneous damage
mumby box
Nonmatching-to-sample-test. Rat test. Similar to the monkey test but they are in a mumby box. They go on one side and have to move the object to find food. Then the door on the other side is opened and they have to move the different object. Both for monkey and rats, there is worse results when there is a MTC lesion beginning even as little at 15 seconds. It is time sensitive. More time passes, worse they do.
Bilateral removal of MTC
Severe and permanent issues in delayed nonmatching-to-sample-tests and object recognition in general
Animals with medial temporal cortex lesion perform worse compared to healthy animals
Bilateral removal of the hippocampus+amygdala
Only modest issues with object recognition. Since there are only moderate issues, this is what showed researchers that ischemia is only only CA1 but other areas too.
Animals with hippocampus + amygdala lesion: don’t see a different drop off in retention relative to healthy animals
grid cells (also where is it located)
(entorhinal cortex) Entorhinal neurons that each have repeating pattern of evenly spaced hexagon shaped place fields that tile the surface of an environment. Could be related to spatial recogntion,
Hexagonal Pattern:
Each grid cell fires when an animal is in specific locations that form a hexagonal lattice across the environment.
These patterns are invariant across different environments but can scale or rotate with environmental changes.
Multiple Scales:
Different grid cells have grids of varying sizes, forming modules that scale from fine to coarse.
This multi-scale representation enables spatial encoding over both small and large areas.
Periodic Activity:
The repeating nature of grid cell firing provides a robust metric for distance and direction traveled.
Context Independence:
Unlike place cells in the hippocampus, grid cell activity does not depend on specific landmarks or environmental features, though it can align with them.
Emotional conditioning: amygdala and experience
Emotional. Active during retention of experience. This could be why we remember emotion provoking events better than neutral.
Fear conditioning circuit
LTP
Form of synaptic plasticity. persistent strengthening of a synapse based on recent patterns of activity at synapse. Considered a major cellular mechanisms of learning and memory. it is long lasting
Requirements of LPT
Co-occurrence
Specificity
Cooperativity
Associativity
Co-occurrence
LTP is enhanced when pre- and postsynaptic activity occurs together in time, strengthening the synapse.
specificity
LTP is specific to the active synapses and does not spread to neighboring inactive synapses.only active ones become strengthened
cooperativity
LTP is more likely to occur when multiple presynaptic inputs are activated simultaneously, leading to stronger synaptic connections, rather than repeated stimulation by just one axon
associativity
pairing weak input w stronger input enhances later response to weak input
Prader-Willi Syndrome
genetic disorder. Results from gene deletion on chromosome 15 from the father(NOT mother). It is very rare.
Symptoms/associations: hypotanial (weak muscles), feeing issues in infants due to weak muscles, short stature, small hands and feet, hyperphagia(excessive eating to the point of death), obeisity if unsupervised.
Brain mechanisms are unknown but the hypothalamus likely plays a role.
Leptin- what is it, where is it made, where is it mainly located, what does it help with
peptide hormone made by adipose (fat) cells- hypothalamus(specifically arcuate nucleus).
Helps with: energy balance, inhibit food intake, metabolism, endocrine regulation, immune function
Negative feedback: sends signal to hypothalamus to stop eating when nourished
Leptin deficiency experiement
parabiosis: surgical joining of 2 organisms allowing for shared blood circulation
Mix ob/ob (leptin deficient) and wildtype. Results: wildmouse saw no changes, ob/ob had reduced food intake, reduced blood sugar, and reduced insulinemia. Why? It gave ob/ob leptin
mix db/db mouse (leptin receptor defieicient) and wildtype. Results: db say increased bodyweight and adipose tissue mass. wildtype saw decreased food intake, lower insulinemia, lower blood sugar and died of starvation. why? db/db mouse doesn’t have leptin receptors so all leptin went to other mouse and caused starvation.
congenital leptin deficiency
leptin deficiency since birth. This is extremely rare but in the case that it happens, leptin replacement therapy can be done
leptin replacement therapy
you can inject leptin into individual. only works for people with genetic congenital leptin deficiency.
Could there be a ‘set point’ for the body’s energy reserves that determines when to eat?
No. The prevalence of eating disorders suggests that there is not.
calories avg american eats
3800 (twice avg requirement)
how many adults in US are clinically obese
over 1/2
% of adolescents that sugger with anorexia or bullimia
3%
definition of obesity
BMI = weight (kg)/[height(m)]^2
does not take into account sex, age, muscle fat distribution, etc.
Newer index rather than BMI
BRI- body roundness index. This is the waist circumference with respect to height. Waist circumference is more predictive of health issues.
Ranges from 1-20 (1=narrow, 20=round)
purpose of eating
provide body with molecular building blocks and energy
digestion
breaking down food and absorbing nutrients. Carbs are unique because they are digested beginning in the mouth.
energy is delivered into the body in what 3 forms
lipids (fats)
amino acids(proteins)
glucose(carbs)
energy is stored as what 3 forms
fats, proteins, glycogen
most efficient form of energy storage
fats. 1g fat=2x energy of 1g glycogen. Why? fat doesn’t attract/hold as much water so it provides denser energy storage
energy metabolism
chemical changes that make energy available
cephalic phase
preparing for eating
absorptive phase
energy is absorbed
fasting phase
withdrawing energy from reserves. ends with the next cephalic phases
the 3 phases of metabolism are controlled by:
insulin and glucagon
insulin
high during cephalic and absorptive phases. It prepares the body to eat. Triggers glucose use as fuel by the body. Triggers conversion of energy to fat, glycogen and proteins. Also triggers energy storage in adipose cells, liver and muscles.
glucagon
high during the fasting phase. Triggers change of stored energy into usable fuel. Fat to free fatty acids and then ketones. Low levels of insulin during the fasting phase trigger the conversion of glycogen and protein to glucose.
Set Point Assumption
many believe hunger is response to an energy need (to keep at set point). But there is a lack of evidence.
typical assumption of hunger and eating
eating works like a thermostat. Negative feedback system- turns on when energy is needed and off when set point reached.
glucostatic theory
glucose is what is monitored to maintain energy
lipostatic theory
fat is what is monitored to maintain energy(and this is why we maintain constant weight)
What are the problems of glucostatic and lipostatic theories
- eating disorders
- reduction in glucose or body fat doesn’t reliably induce eating
- evolutionary- access to food is proactive, not reactive
-does not account for influence of external factors on eating and hunger
positive-incentive perspective on eating and hunger
drawn to eat because it makes you feel good- drawn by the anticipation of the pleasure of eating. We evolved to crave food. Many factors can determine positive incentive of eating. accounts for external factors too.
mealtime and food
Eating is like an ‘attack’ to homeostasis and as a response, insulin lowers glucose in the blood.
We tend to get hungry at mealtime. As mealtime approaches, the body enters the cephalic phase, leading to a decrease in blood glucose.
The expectation of a meal triggers a compensatory response, which we experience as hunger. Internal clock
hunger is actually the body’s preparation to get ready for this ‘attack’ due to the expectation that it is getting close to mealtime when we usually eat.
Pavlovian conditioning of hunger
Cue-potentiated eating/feeding.
Training:
food restricted rats.
Cue and tone: eat food
Test:
not food-restricted. Play tone for some moments and don’t play tone for other moments. measure how much food they eat when tone is played vs without tone.
Results:
Association forms with the tone and ‘suggests hunger’ to rats. They eat more when the tone is played vs not.
sweet and fatty foods
high energy
salty foods
sodium rish
bitter foods
often associated with toxins
learned preferences/aversions. Rats learn to prefer what foods
- a diet with vitamins
- flavors associated with mother’s milk (smell)
- food smell in other rat’s breath
hippocampal-dependent experiment rats
This task relies on the hippocampus, as it requires the observer rat to form and retrieve a memory of the demonstrator’s specific food choice during the social interaction.
- demonstrator rat- we give rat food.
- Exchange info- demonstrator rat interacts with experimental rat. Experimental rat smell’s demonstrator’s breath
- Preference test- give experimental rat 2 foods, one of which is the same that demonstrator rat ate. Rat often chooses demonstrator’s food. (this could maybe be a safety thing. if rat ate the food and is safe, then they can)
conditioned tast avoidance experiment
give rats sucrose (they make the yum face). Then give rats the sucrose again and inject them with lithium chloride (illness). When you give them sucrose again (usually by force), they will show yuck face
Cue-potentiated eating: neural circuitry
external stimuli (e.g., sight or smell of food) can override homeostatic signals, promoting eating even in the absence of hunger.
Medial prefrontal cortex to lateral hypothalamus
Basolateral amygdala (BLA) to lateral hypothalamus
Basalateral amygdala to AND from medial prefrontal cortex (mPFC)
satiety
stops a meal, “being full”
satiety signals
food in gut and glucose in the blood CAN induce satiety signals
sham eating (+ experiment)
satiety signals from gut and blood are not necessary for meal termination.
allow rat to taste a food but it doesn’t fulfill them. Cut esophagus so that it doesn’t go to stomach, instead falls out of cheek onto ground.
Rats doing this sham eating eat normal-sized meal if food is familiar. Why? because Satiety is a function of PAST EXPERIENCE. They were familiar with that food so they have an expectation that that food will provide enough energy at a certain amount.
If you redo the test multiple times with familiar food, they start to increase how much they eat because its not filling them up.
When it was unfamiliar food, there was no expectation and they ate more.
Sensory specific satiety
Can get more full to a specific taste or food. If you swap the flavor with someone who is full they tend to still eat more. (i.e. dessert menu after being full at restaurant).
Eat more with a “cafeteria diet”(wide variety of flavors)
tasting food immediately decreases the positive incentive value of same or similar tastes.
decreases the palatability of ALL foods about 30 minutes later(post-ingestion)
Signals from taste receptors produce an immediate decline in positive-incentive value of the specific food (sensory specific satiety)
Signals associated with postingestive consequences produce general decrease in positive-incentive value of all foods in general.
appetizer effect
small amounts of food may actually increase hunger. Could this be due to cephalic-phase response?
social influence and how much we eat
Even rats eat more when in a group. Could this be habituation? The taste of food is a stimulus. The first taste is often the BEST bite. But if you are distracted when the stimulus is being given (I.e. eating in a social group) and it slows down habituation, so you tend to eat more and it tastes better.
why does sensory-specific satiety exist?
adaptive- encourages a varied diet.
study the graphssssss
do it
long term depression
opposite of LTP. prolonged low level stimulation of presynaptic neurons. strength between two neurons is decreased
metaplasticity
LTP and LTD induction can be modulated by prior synaptic activity. how easily or strongly future changes in synaptic strength (plasticity) can occur.
Infantile amnesia (two studies)
we remember nothing from being infants.
Study 1: kids shown photos of preschool kids, some were their classmates. even if they couldn’t explicitly remember they were their classmates, they showed more skin conductance when viewing the photos with previous classmates.
Study 2: incomplete picture test. showed drawings to 3yr olds, 5yr olds and adults. they tested it 3 months later for the simplicity memories (I.e. what is it before it is complete). 5 year olds and adults explicitly remembered doing the task earlier more often than 3 year olds, but all of them implicitly did well (‘guessed’ the photo).
smart drugs (aka nootropics)
substances thought to improve memory.
About: most well-done studies are done on animals, not humans. so do they actually work on humans? there are a few with humans but are low quality/funding. there isn’t any concrete evidence of nootropics helping.
posttraumatic amnesia
case of RM. fell and got concussion and suffered from retrograde and anterograde amnesia episodic memories. couldn’t form new memories- he was trapped in the present moment. Eventually he regained his memory.
8 steps of digestion
- chewing breaks up food and mix w saliva
- saluva lubricate food and begin digestion
- swelling moves down esophagus to stomach
- stomach is storage reserve. hydrochloric acid breaks food down and pepsin begins breaking down protein molecules into amino acids
- stomach epties gradually through pyloric sphincter into duidenum(upper portion of intensitne where absorption takes place)
- ensymes in duodenum break down protein molecules into amino acids and starch, and complex sugar into simple sugar. they them pass through wall into blood and are carried to liver
- fats are broken down by bile. it cant pass through wall so it is carried by ducts in the wall to lymphatic system
- remaining water and electrolytes are absorbed from waste in large intestine and remaining is ejected.
Winters: What is meant by a double dissociation?
two related brain functions are shown to be independent of each other. This is demonstrated when damage to one brain area impairs one cognitive function but not the other, while damage to a different brain area impairs the second function but leaves the first one intact. This pattern provides strong evidence that the two functions rely on different neural systems.
What is the main finding/result of the Winters study?
(perirhinal cortex)PPRH is needed for object recognition. The PPRH group decreased in discrimination ratio at 15 minutes.
HPC (hippocampus) is needed for spatial recognition. HPC had more errors in probe compared to HPC and control.
What is the perirhinal cortex? What is the postrhinal cortex? (Winters)
Perirhinal- object recognition. Postrhinal- spatial memory.
(Winters)What test of object recognition memory did the authors use? How is this an improvement over other versions of rodent object recognition tasks?
Y arm maze- the goal was to prevent spatial and contextual cues as much as possible. This is better than other mazes because there were less spatial cues.
(Winters)What test of spatial memory did the authors use? What was the point of rotating the maze during the probe trials?
Radial arm maze- rotated it to see if rats were using place or response memory.
(Winters)What are the two opposing views of medial temporal lobe (MTL) memory function put forth in the introduction of this paper?
Does MTL all do the same thing or do different areas have different functions?
(Winters)Why did they use a discrimination ratio for their measure of time spent exploring the objects in the object recognition task?
standardize the measure of exploration behavior and control for individual variability. This ensures that the measure reflects the relative preference for novelty rather than absolute exploration time, which could vary due to non-memory-related factors like activity levels or attention.
(Myers)Why was an IG catheter used? What does this allow for?
Allows for quick infusion of water or glucose.
(Myers)What was the CS and what was the US in this paradigm?
CS was the liquid they drank and US was the IG infusion.
(Myers)What is meant by extinction in this paradigm?
They did not continue to use IG catheter infusions.
(Myers)What is meant by orosensory properties of food vs. postingestive consequences of food?
Orosensory properties of food are sensory things like tastes and postingestive are physiological effects of food like illness.
(myers)Describe/explain flavor-nutrient conditioning.
Flavor-nutrient conditioning refers to a type of associative learning where an individual develops a preference for a flavor after it has been paired with positive postingestive consequences
(myers)What is the main finding/result of this study?
After one single pairing, rats made an association.
above what number is obese BMI
25
fear conditioning circut - quickest
simple pavlovian conditioning. CS-> sensory thalamus-> lateral amygdala central->response
fear conditioning quicker path
CS->sensory thalamus->sensory cortex->association cortex->lateral amygdala->response
fear conditioning: slower path
CS->sensory thalamus->sensory cortex->association cortex->perirhinal cortex->lateral amygdala->response
fear conditioning. slowest path
CS->sensory corte->association cortex->perirhinal cortex->hippocampus (contextual)->lateral amygdala->response.
allocentric
object-to-object, place learning
Jennifer aniston cells
Jennifer Aniston neurons (or concept cells) refer to specific neurons in the human brain that respond to highly individualized concepts or famous individuals. In a groundbreaking study, these neurons were found to activate when participants were shown pictures of well-known people, including Jennifer Aniston. These neurons seem to encode abstract concepts, not just sensory representations, allowing for the recognition of complex stimuli like people, objects, or places based on personal significance or familiarity.
egocentric
self-to-object, response learning
Alzheimers
primarily affects episodic memory. involves both anterograde amnesia and retrograde amnesia
