Chapter 13 The Biology of Learning and Memory

Question 1

Describe the relationships among the conditioned and unconditioned stimuli and the unconditioned and conditioned responses in classical conditioning. 13.1

Answer 1

conditioned stimulus- initially elicits no responses of note
unconditioned stimulus-which automatically elicits an unconditioned response.
after some pairings=> conditioned response.

Question 2

Who discovered classical conditioning? what were the conditioned and unconditioned stimuli in his experiments? What was the unconditioned, and eventually the conditioned response?

Answer 2

Ivan Pavlov-discovered Classical Conditioning
Dog-(CS) is sound followed by food (UCS) => dog salivating (UCR)
eventually sound produces dog to salivate (CR)

Question 3

What is the fundamental difference between classical and operant conditioning

Answer 3

AKA instumental conditioning: response leads to reinforcement or punishment
e.g. two paths one least to froot loops = reinforcer
punishment => shock-mice won’t choose this path.

Question 4

Why is bird-song learning difficult to classify?

Answer 4

• after bird hears song of his own species during his first few months- he imitates it the following year
• there was no classical conditioning as it was not paired with any other stimulus
• he also learned the song without any reinforcement / punishment

Question 5

What is an engram? What did Lashley discover in his search for the engram?

Answer 5

engram- this physical representation of what has been learned.

• a connection between two brain areas would be a possible example of an engram.
• he could not find anything concrete.

Question 6

What two assumptions did Lashley make, that later investigators rejected?

Answer 6

equipotentiality-all parts of the cortex contribute equally to complex behaviours such as learning and any part of the context can substitute for another.
Mass action: the cortex works as a whole and more cortex is better.

Question 7

What brain area was found by Richard F. Thompson to be important for classical conditioning of the eye-bling response in rabbits?

Answer 7

Richard F Thompson- sought for the engram in the cerebellum

-Lateral interpositus nucleus (LIP) as essential for learning of the cerebellum.

Question 8

What area was important for the expression of the motor response, but not for the initial conditioning?

Answer 8

-medial geniculate nucleus- the auditory portion of the thalamus.

Question 9

Which areas showed increased activity on PET scans during eye-blink conditioning in humans?

Answer 9

cerebellum, red nucleus, and several other areas.

Question 10

Define short term memory and long term memory.

Answer 10

short term memory-recollection of events that have just occurred.
long term memory-events that have occurred in the past.

Question 11

How did Donald Hebb explain consolidation.

Answer 11

enters short term storage until memory has a chance to consulate into longterm memory.

Question 12

In what two ways do exciting experiences enhance memory consolidation?

Answer 12

emotionally exciting events form quickly

increased secretion of epinephrine (adrenaline) and cortisol.

Question 13

What brain areas are stimulated by the amygdala after an emotional experience? What is the effect of long term or excessive stress?

Answer 13

Small mounts of cortisol activate the amygdala and the hippocampus, where they enhance storage and consolidation of memory.
amygdala in Turm stimulates the hippocampus and cerebral cortex which are both impt for memory and storage.

Question 14

What is working memory?

What are its three hypothesized components?

Answer 14

• refers to the way we store information while we are working with it
• prefrontal cortex stores information
• the prefrontal cortex as well as the parietal cortex increases their activity
• the cells store additional Ca2+, increasing their readiness for when the time comes as opposed to more action potentials.

Question 15

What brain area seems to be especially important for working memory? What is a common test of working memory?

Answer 15

• the prefrontal cortex is important for working memory

- delayed response task which requires responding to soothing that you hear a short while ago.

Question 16

Why was H.M.’s hippocampus removed bilaterally? How successful was this treatment at relieving epilepsy? What were the other effects of the surgery?

Answer 16

-reduced his seizures to no more than two per year however he suffered sever memory impairment.

Question 17

What is the difference between retrograde and anterograde amnesia? Which is more evident in H.M.?

Answer 17

anterograde amnesia-inability to form memories for events that happened after brain damage

Question 18

Distinguish between declarative and procedural memory. Which is impaired in H.M.?

Answer 18

Procedural memory-development of motor skills and habits is a special kind of implicit memory.
Declarative memory- aka explicit memory which is the deliberate recall of information that one recognizes as a memory.

Question 19

Distinguish between explicit memory and implicit memory. What is the one text of implicit memory?

Answer 19

Explicit memory aka declarative memory - deliberate recall of information one recognizes as a memory
Implicit memory and influence of experiences or behaviours even if you do not recognize that influence.

Question 20

What seems to be the major function of the hippocampus? Why can we conclude that memories are not stored in the hippocampus itself? Where are well-consolidated memories stored?

Answer 20

Hippocampus is critical for declarative memory especially episodic memory. (which is something that you can describe in words.
??

Question 21

For what three types of memory is the hippocampus hypothesized to be important?

Answer 21

1. declarative memory especially episodic memory
2. spatial memory-spatial locations-eg like a route between ones house and a destination
3. contextual memory-describe something that you learned today or tomorrow

Question 22

Describe the delayed matching-to-sample and delayed non matching to sample tasks

Answer 22

Delayed matching to sample- an animal sees an object (i.e. the sample) then after a delay gets a choice between two objects from which it must choose the match.
Delayed non matching to sample same except must choose alternate sample to the one shown.

Question 23

Under what conditions does hippocampal damage impair performance on matching or non matching to sample tasks.

Answer 23

Both are impaired with hippocampal damage.

Question 24

What type of memory is tested by the radial maze and the Morris search task? (water maze). What two kinds of errors can rats make in the radial maze? Which the of error do rats make after damage to the hippocampus?

Answer 24

Spatial memory
Radial arm mistakes entering a correct arm twice or never correct arm.
With damage to hippocampus gradually learn to not enter the never correct arms but often enter correct arm twice.

Question 25

Describe the Morris search task (water maze) what deficits on this task are seen in hippocampally damaged rats?

Answer 25

rat has to swim to find resting platform
Damage to hippocampus causes the rat to swim haphazardly and even appears to have forgotten that there was a platform.
A rat can slowly learn to find platform if it is constantly in the same place.

Question 26

Describe the relationship between birds dependence on finding previously hidden food and the size of their hippocampus.

Answer 26

the bird that relied on memory of where they hid food had the largest hippocampus.

Question 27

What is the immediate cause of Korsakoff’s syndrome? what are its symptoms? In what group of people does is usually occur?

Answer 27

AKA Wernick-Korsakoff’s syndrome.

• Brain damage caused by prolonged thiamine deficiency.
• Occurs mostly in chronic alcoholics who go for weeks at a time on a diet of nothing but alcoholic beverages
• the brain reds thiamine (vit B1 to metabolize glucose (it’s primary fuel)
• prolonged deficiency=> loss/ shrinkage of neurons throughout the brain
• main area affected is the dorsomedial thalamus main input to the prefrontal cortex.
• symptoms: apathy, confusion, memory loss, impaired episodic memory.

Question 28

Which brain areas show neuronal loss in Korsakoff’s syndrome?

Answer 28

dorsomedial thalamus=>prefrontal cortex-the most but neuronal loss is throughout the brain.

Question 29

Describe the symptoms of Korsakoff’s syndrome in terms of anterograde vs retrograde amnesia and explicit vs implicit memory. What is priming, and why type of memory ca show priming effects?

Answer 29

Loss of memory for anterograde events

and loss of memory for explicit memories so the confabulate stories- i.e. the patient fills in memory gaps with stories.

Question 30

What symptoms do Korsakoff’s patients have in common with patients with frontal-lobe damage? What additional symptoms do Korsakoff’s patients have?

Answer 30

Apathy, confusion and memory loss. (like the prefrontal lobe damage)
Major impairments of episodic memory and sparing of implicit memory.

Question 31

Describe the symptoms of Alzheimers disease

Answer 31

Better procedural that declarative memory.
They learn new skills then surprise themselves with their good performance cause they don’t remember doing it before
Memory and alertness vary greatly suggesting that many of their problems result from malfunctioning neurons rather than death of neurons.
Symptoms: more serious memory loss, confusion, depression, restlessness, hallucinations, delusions, sleeplessness, loss of appetite.

Question 32

Why are some cases of Alzheimer’s Disease thought to be related to a gene on chromosome 21? How does the chromosomal abnormality differ from that in Down syndrome?

Answer 32

People with Down’s syndrome ; if they survive to middle age almost invariably get Alzheimers disease. Down’s patients have 3 copies of chromosome 21.

Question 33

What is amyloid precursor protein? What are two forms of amyloid beta protein? Which form is implicated in the formation of amyloid deposits?

Answer 33

amyloid B plaques accumulate both inside and outside the neuron.

Question 34

What other protein is implicated in Alzheimer’s disease? What is its normal function?

Answer 34

Tau protein-intracellular support structure of axons increase amyloid B causes more phosphate groups to attach to tau proteins-altered tau can’t bind to its usual target within axons so it starts spreading into the cell body and dendrites.

Question 35

Which brain areas are atrophied in Alzheimer’s disease? What physical signs are present in areas of atrophy?

Answer 35

as plaques increase the cerebral cortex, hippocampus and other areas atrophy.

Question 36

What are two temporary means of alleviating Alzheimer’s disease? what dietary factors may guard against Alzhemier’s disease?

Answer 36

3-5 cups of coffee! to prevent Alzheimers.
Drug treatment-drugs that stimulate acetylcholine receptors or prolong acetycholine release.
Curcumin is and interesting possibility

Question 37

What have we learned about memory from amnesic patients?

Answer 37

people do not lose all aspects of memory.

a person with great difficulty establishing new memories may remember events from long ago.

Question 38

What did Wilder Penfield conclude form his brian stimulations experiments? what are some problems with his conclusion?

Answer 38

Brain surgery for severe epilepsy on conscious patients who had only scalp anesthesia–when he applied a brief weak electrical stimulus to part of the brain it sometimes evoked vivid descriptions.
Penfield suggested each neuron stored a particular memory BUT stimulation produced more of a dream then a memory

Question 39

Describe G.A. Horridge’s experiments with headless cockroaches. Why was this experimental approach abandoned?

Answer 39

Headless cockroaches could learn.
Headless cockroaches suspended over water –if they dipped their feet in water = shock.
Decapitated cockroaches learn very slowly- results not able to duplicate easily there for usefulness of results are limited.

Question 40

Describe the experiments in planaria and rats that seemed to show transfer of training from one individual to another via RNA or protein. Why were these experiments abandoned?

Answer 40

Planaria (flatworms) cannibalized other planaria–they remember what other worm had learned.
experiments were unreproducable however.

Question 41

What is a Hebbian synapse? How is it related to classical conditioning?

Answer 41

In a Hebbian synapse pairing the activity of a weaker (CS) axon with a stronger (UCS) axon produces an action potential and in the process strengthens the response of the cell to the CS axon.
On later trials it will produce a bigger depolarization of the post synaptic cell which we ca regard as a conditioned response..

Question 42

Wy should anyone be interested in the cellular mechanisms of habituation or sensitization in lowly Aplysia?

Answer 42

Habituation is a decrease in response to a stimulus that is presented repeatedly.
Habituation in aplisya depends on a change in the synapse between the sensor neuron and the motor neuron.

Question 43

How is sensitization produced experimentally in Aplysia?

Answer 43

Sensitization, an increase in response to mild stimuli as a result of exposure to more intense stimuli.
A strong stimulus almost anywhere on the aplysia’s skin intensifies a later withdrawal response to a touch.

Question 44

Describe the cellular events that explain sensitization in Aplysia. How does a decrease in potassium outflow increase transmitters release?

Answer 44

Researchers traced sensitization to changes at identified synapses. Strong stimulus on the skin exits a facilitating interneuron that releases serotonin (5-HT) onto presynaptic terminals of many sensory neurons. Serotonin blocks K channels in these membranes. The result is tat after later action potentials the membrane takes longer to repolarize because K is slow to flow out of the cell. Therefore the presynaptic neuron continues releasing its neurotransmitter for longer.

Question 45

How does long-term sensitization differ from the short-term variety?

Answer 45

Repeating the process causes sensory neurons to synthesize new proteins that produce long term sensitization

Question 46

How is long-term potentiation (LTP) produced? How long does it last? In what brain area was it first discovered?

Answer 46

Hippocampus.
Longterm Potentiation is one or more axons connected to a dendrite bombard it with a rapid series of stimuli. The burst of intense stimulation leaves some of the synapses potentiated (more responsive to a new input of the same type) for mins/days/weeks.

Question 47

What is meant by specificity? Cooperativity?Associativity?

Answer 47

3 properties of LTP that make it an attractive candidate for a cellular basis of learning and memory.
Specificity-if some of the synapses onto a cell have been highly active and others have not. only the active ones become strengthened.
Co-operativity–nearly simultaneous stimulation by two or more axons produce LTP much more strongly than does repeated stimulation from one axon.
Associativity-pairing a weak input with a strong input enhances later response to weak input.

Question 48

Specificity

Answer 48

if some of the synapses onto a cell have been highly active and others have not. Only the active ones become strengthened.

Question 49

Co-operativity

Answer 49

Nearly simultaneous stimulation by two or more axons produce LTP much more strongly than does repeated stimulation from one axon.

Question 50

Associativity

Answer 50

Pairing a weak input with a strong input enhances later response to weak input.

Question 51

What is long term depression (LTD)? Where has it been observed? How does it differ from LTP?

Answer 51

LTD is long term depression–a prolonged decrease in response at a synapse occurs for axons that have been less active than others.
Its a compensatory mechanism as one axon strengthens another weakens.

Question 52

Which transmitter stimulates both NMDA and AMPA receptors? Why must AMPA receptors be stimulated in addition to NMDA receptors, in order to produce LTP?

Answer 52

AMPA receptor–a toe of glutamate receptor is excited by the neuro transmitter glutamate, but it can also respond to a drug called alpha-amino-3-hydroxy-5-ethyl-4-isoxazole proprionic acid (AMPA)
NMDA receptor: is ordinarily only excited by glutamate but can respond to a drug called N-methy-D-aspartate.

Question 53

Describe the sequence of events that follows the successful activation of NMDA receptors

Answer 53

NDMA receptors: its response to the transmitter glutamate depends on the degree of polarization across the membrane
When glutamate attaches to an NMDA receptor while the membrane is at its resting potential, the ion channel is usually blocked by Mg ions.
NMDA channel opens only if the Mg leaves

Question 54

What is CaMKII

Answer 54

CaMKII is a alpha-calcium-calmodulin dependent protein kinase II.
It sets in motion a series of reactions leading to release of a protein called CREB cyclic adenosine monophosphate responsive element binding protein.
CREB goes to the nucleus of the cell and regulates expression of several genes.
Expression sometimes lasts for months/years
The effects of CaMKII and CREB are magnified by BDNF-brain derived neurotrophic factor.

Question 55

List 5 changes in the post synaptic neuron that contribute to LTP

Answer 55

-Na enters thru AMPA channels => dendrites become sternly depolarized => Mg molecules displaced
Glutamate opens NMDA channels
Na and Ca enters NMDA channel.
Note: Ca is key to maintaining LTP.

Question 56

Are NMDA receptors important for establishment or maintenance of LTP

Answer 56

NDMA receptors are important for establishment of LTP because in order for Ca to enter the NMDA channel must be opened up by the glutamate and are impt for the establishment of the LTP.
Once LTP is established NMDA receptors revert back to their original conditions.

Question 57

What is a retrograde neurotransmitter? what changes in the presynaptic terminal may contribute to LTP?

Answer 57

Extensive stimulation of a post synaptic cell causes it to release a retrograde transmitter that travels back tot he presynaptic cell to modify it. In many cases it is nitric oxide.

Question 58

How beneficial is ginkgo biloba to memory? What is its mechanism of action? In what rout of people is it beneficial to?

Answer 58

Mild benefit with pt’s with impaired blood flow to the brain. But studies show no benefit.