11/12 - Cognition learning and memory

Question 1

What did Charles Sherrington propose about synaptic alterations and the basis for learning?

Answer 1

That synaptic alterations were the basis for learning:

• Presynaptic, postsynaptic or both
• Increased NT release or effectiveness of receptors
• Structural changes for long term memory storage
• New synapses forming or synapse elimination
• Synaptic reorganization with training/experience

Question 2

List four synaptic changes that might store memories

Answer 2

• More/less NT changing the post synaptic potential
• Interneuron modulation
• Formation of new synapses
• Rearrangement of synaptic input

Question 3

List three changes observed with animal environment enrichment.

Answer 3

• Heavier, thicker cortex
• Enhanced cholinergic activity
• More dendritic branches (esp. basal dendrites near cell body)

Question 4

What is Hebb’s law?

Answer 4

When an axon of cell A is near enough to excite cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency as one of the cells firing B, is increased.

Neurons that fire together, wire together.

Question 5

How did aplysia demonstrate plasticity?

Answer 5

This invertebrate sea slug has a large and conspicuous nervous systems. Habituation could be observed in sensory neurons that fail to excite motor neurons as they did before habituation, due to less NT being released upon motorneurons. Over time, long term habituation is observed by a reduced number of synapses between sensory cell and the motor neuron.

Sensitization showed serotonin released from a facilitating neuron blocks potassium channels in a presynaptic neuron and prolongs release of a NT from a neuron, resulting in further prolonged sensitization.

Advantages of aplysia is that it has fewer nerve cells and you can create a detailed circuit map for particular behaviours, and there is little variation between individuals.

Question 6

What is a PEPSP?

Answer 6

Population excitatory postsynaptic potential

Observed with LTP and a possible mechanism for storing memories.

Question 7

What is facilitation in terms of synaptic plasticity?

Answer 7

The amplitude of the postsynaptic response increasing when the postsynaptic cell is activated several times in quick succession.

Question 8

What is tetanus?

Answer 8

A brief increase of electrical stimulation that triggers thousands of axon potentials.

Question 9

What is long term potentiation (LTP)?

Answer 9

A stable and enduring increase in the effectiveness of synapses.

First described by Bliss and Lomo at glutamatergic synapses in the hippocampal formation.

Question 10

When does LTP occur?

Answer 10

When one or more axons bombard a dendrite with stimulation. This leaves the synapse ‘potentiated’ for a period of time and the neuron is more responsive.

Question 11

List three properties of LTP that suggest it as a cellular basis of learning and memory

Answer 11

• Specificity: Only synapses on a cell that have been highly active become strengthened

Cooperativity: Simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by a single axon

Associativity: Pairing a weak input with a strong input enhances later responses to a weak input.

Question 12

What three areas of the hippocampal formation is synaptic plasticity observed?

Answer 12

Where LTP occurs:

• Hippocampus (CA1, CA2 and CA3)
• Dentate gyrus
• Subiculum (hippocampal gyrus)

Question 13

What is LTD?

Answer 13

Long term depression

A prolonged decrease in response at a synapse that occurs when axons have been active at a low frequency.

Question 14

How go glutamate receptors contribute to LTP?

Answer 14

Entry of calcium through NMDA channel triggers plastic changes:

• Protein kinases activated
• CaMKII (calcium-calmodulin kinase II) causes more AMPA receptors to be produces and inserted in postsynaptic membrane
• CaMKII moves existing nearby AMPA receptors into the active synapse
• CaMKII increased conductance of Na and K ions in membrane bound AMPA receptors

= More AMPA receptors are built and dendritic branching is increased

This is particularly seen in CA1

Question 15

How to retrograde messengers facilitate LTP?

Answer 15

CO and nitric oxide (NO) can travel across synapses and alter presynaptic neuron

• Decrease in action potential ‘threshold’ to increase release of NT
• Expansion of axons for NT release from additional sites

Additionally, these changes increase the later responsiveness of the dendrite to incoming glutamate

Question 16

Describe genetic changes associated with induction of LTP

Answer 16

Kinases activate CREB (cAMP responsive elements-binding) protein.

CREB binds to cAMP responsive elements in DNA promoter regions and changes transcription rate of genes that then produce proteins that effect synaptic function and contribute to LTP (eg. AMPA and NMDA receptors).

Question 17

Describe the transcription-dependent late phase of LTP and a drug that can inhibit it.

Give evidence of this in a rat study.

Answer 17

• Actinomycin D inhibits transcription by binding DNA at the transcription initiation complex and preventing elongation of RNA chain by RNA polymerase
• Actinomycin D inhibited the maintenance of LTP in rat hippocampal neurons ex vivo and in vivo

Question 18

Give three points as evidence that LTP may be a part of learning and memory formation

Answer 18

• Correlational observations (time course of LTP is similar to that of memory formation)
• Somatic intervention experiments: Pharmacological inhibition of LTP impairs learning
• Behavioural intervention experiments: training an animal in a memory task can induce LTP

Question 19

What does Trichostatin-A and sodium butyrate do to learning and what are they?

Answer 19

These are histone deacetylase inhibitors (HDACIs). Promote euchromatin.

They enhance induction of LTP ex vivo. This outlines the important of gene transcription for the induction of LTP.

HDACIs enhance formation of long term memory in vivo

Question 20

What does inhibition of DNMT activity in the hippocampus do?

Answer 20

Blocks formation of long term memory in vivo (observed with long term contextual fear memory)

Gene silencing appears to be needed for memory consolidation, in addition to gene transcription.

Question 21

What are iconic memories?

Answer 21

The briefest memories, these store sensory impressions that only last a few seconds

Question 22

What are the three components of short term memory?

Answer 22

• Phonological loop (auditory information)
• Visuospatial sketch pad (holds visual impressions)
• Episodic buffer (contains more integrated sensory info)

Question 23

Short term memory and long term memory rely on different processes to store information. How do they differ?

Answer 23

One artifact of STM is the primacy effect (beginning of list) and recency effect (end of list)

Long term memories have undergone consolidation

Short term memories have only undergone encoding of sensory information

Question 24

Which areas of the brain are most important for consolidation of short term memories to long term memories?

Answer 24

• PFC

- Parahippocampal cortex

Question 25

What is an engram

Answer 25

A memory trace. This is the physical change in the brain (eg. synapses/neural circuits) associated with a long term memory.

Question 26

True or false? The hippocampus stores long term memory.

Answer 26

False

LTM storage occurs in the cortex, near where the memory was first processed and held in short term memory. Retrieval is a process of reconstruction from all parts of the brain.

However, the hippocampus is involved in consolidation.

Question 27

How are PTSD memories enhanced?

Answer 27

During stressful experiences, stress hormones reinforce the formation of a memory.

Blocking chemicals that act on the basolateral amygdala may alter the effect of emotion on memories

Question 28

Which three neurotransmitters can enhance memory formation in animal models?

Answer 28

• GABA
• ACh
• Opiods

Question 29

What is reconsolidation?

Answer 29

The return of a memory trace to stable long term storage after it’s temporarily volatile during recall.

Reconsolidation can distort memories

Question 30

List two causes of old age memory problems

Answer 30

Some causes of memory problems in old age:

• Impairments of coding and retrieval— less cortical activation in some tasks (fMRI scans).
• Loss of neurons and/or neural connections; some parts of the brain lose a larger proportion of volume (MRI scans).

Question 31

Describe nootropics

Answer 31

Nootropics are a class of drugs that enhance cognitive function

• Cholinesterase inhibitors
• AMPAkines (enhance hippocampal LTP)
• protein kinase—PKMζ needed for long term maintenance of hippocampal LTP and cortical memory traces (engrams)

Question 32

What is the Yerkes-Dodson law?

Answer 32

Certain stimulants will enhance cognition in the general population, but only when used at a therapeutic dose. High dose will result in cognitive deficits (think inverted U of attention)

Question 33

What are the four Piaget periods of cognitive development?

Answer 33

• Sensorimotor (birth -2)
• Preoperational (2-6)
• Concrete operational (6-11)
• Formal operational (12 and up)

Question 34

What is the law of mass action in terms of cortical lesions and memory?

Answer 34

The severity of the memory impairment for maze performance correlated with the size of the cortical area removed and NOT WITH ITS SPECIFIC LOCATION!

Question 35

Which lobe did HM demonstrate was extremely important for the initiation/encoding of new memories?

Answer 35

The medial temporal lobe

Question 36

What is the brain structure critical for conditioning?

Answer 36

Cerebellum

Question 37

Describe the delayed non-matching-to-sample task

Answer 37

• Sample object presented with food underneath
• After time, presented with original and another object
• Monkey learns food under other object (not sample)

Lesions (similar to HM’s) impair this learning. Amygdala and hippocampus. A or H by themselves didn’t produce the same impairment, need both to be impaired to produce the anterograde amnesia observed.