Learning and memory

Question 1

What is learning and memory?

Answer 1

Lifelong adaptation of the brain to the environment.
Enables appropriate responses to new situations.
Learning is acquisition of new information or knowledge.
Memory is retention of the learned information.

Question 2

What is declarative memory?

Answer 2

Explicit
Available for conscious recollection.
Easy to learn but easy to forget.

Question 3

What is nondeclarative memory?

Answer 3

Implicit
Not available for recollection.
Requires repetition over long times.
Less likely to be forgotten.

Question 4

What are the components of declarative memory?

Answer 4

Long term memory - recalled after a long time period.
Short term memory - lasts for a short period of time (seconds to hours).
Vulnerable to disruption - trauma, electroconvuslive therapy (ECT).

Question 5

What is the theory of memory consolidation?

Answer 5

Memory consolidation can either be:
Short term memory formed after sensory information received, then considlated to long term memory.
Sensory information forms both short term memory and long term memory in parallel.

Question 6

What is amnesia?

Answer 6

Loss of memory and learning ability.
Consequence of concussion, tumour, stroke, alcoholism, encephalitis (brain inflammation).

Question 7

What are the types of amnesia?

Answer 7

Dissociated amnesia - no other deficits.
Retrograde and anterograde amnesia.
Transient global amnesia - forget everything, but memory is regained after a period of time.

Question 8

What is retrograde and anterograde amnesia?

Answer 8

Retrograde amnesia - forgets the events before the injury e.g. like a concussion.
Anterograde amnesia - memory and learning is only affected post injury, prior to the injury memory is intact.

Question 9

What did Lashley theorise about memory?

Answer 9

The severity of a deficit is related to the size of a lesion, but is not related to the location of lesion.
All cortical areas are involved equally in memory storage.

Question 10

What was wrong with Lashley’s theory about memory?

Answer 10

He experimented using rat brains, which are very small.
When dissecting parts of the cortex, the connections between the cortical areas were severed and the white matter tracts damaged, so there was no location specificity.

Question 11

What is the location of declarative memory?

Answer 11

Declarative memory relies on the function of the medial temporal lobe.
Receives input from cortical association areas via relaying to the Parahippocampal region and then provides feedback back to the cortical association areas.

Question 12

Where is the location of different types of memory?

Answer 12

Information from sensory modality is stored in the cortical region that serves that modality.
Visual memory is stored in the extrastriatal cortex.
Complex memories (rely on more than one sensory input) are stored in the lateral temporal lobes.

Question 13

What is the medial temporal lobe for memory processing?

Answer 13

Consolidation of declarative memory.
Temporary memory storage in the medial temporal lobe - consolidation in the cortex.

Question 14

What is memory in the hippocampus?

Answer 14

Spatial memory - place cells.
Working memory - related to ongoing behaviour.
Relational memory - ties together things happening at the time of memory storage. e.g. listening to music when revising.

Question 15

What are the consequences of a temporal lobectomy?

Answer 15

Loss of short term memory which affects declarative memory.
Loss of anterograde and retrograde memory.
Maintained procedural memory.
Maintain some long term memory (from childhood).

Question 16

Why would you do a temporal lobe lobectomy?

Answer 16

Some forms of epilepsy arise from the temporal lobe and are resistant to drug treatments.
The only remaining solution is to remove part of the temporal lobe.

Question 17

What is Hebb’s theory about brain wiring?

Answer 17

Anatomical connections between neurones are set by genetics, but the strength and effectiveness of synapses are not predetermined and can be altered by experience.
Some metabolic or growth process can take place in cells that are near enough to excite the other, and change the efficiency of the synaptic transmission of the cell.

Question 18

What is Hebb’s model of learning?

Answer 18

The memory trace - engram of an object is the assembly of cortical cells activated by the external stimulus.

Cell assembly is reciprocally interconnected - two way connections between cells - establishes short term memory.
Cells that fire together wire together, synaptic strength is increased - the basis of long term memory consolidation.

Question 19

What does Hebb’s model of learning mean?

Answer 19

Learning is modifications of synaptic transmission.
Synaptic modifications are triggered by neuronal activity.
There is alterations of existing synapses.
Long term potentiation and long term depression.

Question 20

How do synapses become stronger?

Answer 20

When strong activation of pre-synapses leads to firing of the postsynaptic neurone, this leads to potentiation of the post-synaptic response - higher level.
There needs to be coincidence in the firing of the pre and postynaptic neurone.
See picture.

Question 21

What is coincidence of firing?

Answer 21

When there is repeated stimulation from the presynaptic neurone, the postsynaptic neurone starts firing at the same time, and the amplitude of the action potentials increases - potentiated by the repeated rapid firing.
If the neurones are firing together, the synaptic connection between the presynaptic neurone and postsynaptic neurone is strengthened, and they wire together long term.

Question 22

What is required for long term potentiation?

Answer 22

Coincidence of pre- and post-synaptic firing allows Ca2+ influx through the NMDA receptor coincidence detector.
The NMDA receptor detects coincidence of the pre- and postsynaptic cells firing, due to the release of Ca2+ that occurs because the NMDA receptor is activated, by both ligands and voltage.

Question 23

What is the mechanism of Ca2+ influx on potentiation?

Answer 23

Glutamate is released from the presynaptic cell and activates AMPA receptors on the postsynaptic membrane to produce an action potential.
This depolarisation removes the Mg2+ block on NMDA receptors.
When the presynaptic cell releases more glutamate, it activates both the AMPA and NMDA receptors to produce an action potential and a big Ca2+ influx into the postsynaptic cell.

Question 24

What is the consequence of Ca2+ in the postsynaptic cell?

Answer 24

Ca2+ activates Ca2+ calmodulin kinases (CaMKII).
This phosphorylates other proteins, including AMPA receptors.
Phosphorylation of AMPAR increases the conductance of the receptors - increases signal intensity so there is a bigger action potential.
CaMKII also inserts cytosolic AMPA receptors into the membrane, so increases the number of AMPA receptors and increases signal intensity.

Question 25

What are the characteristics of LTP and LTD?

Answer 25

Long term potentiation is for consistent and strong coinciding firing. Caused by coincidental firing activating NMDA and Ca2+ influx and AMPAR phosphorylation. Long term depression is for occasionally coinciding firing. No coincidental firing so no NMDAR activated, and no Ca2+ influx, so low number of AMPAR and conductance.

Question 26

What is the concentration of calcium that causes potentiation?

Answer 26

Ca2+ influx that causes a postsynaptic concentration of more than 2uM changes AMPAR conductivity and number, so causes long term potentiation. Ca2+ concentration of less than 1uM, the phosphatase activity dominates, there is reduced number and conductance of AMPAR so causes long term depression. See picture.

Question 27

Which synapses will become stronger?

Answer 27

Cells that fire together have something in common - they respond to the same feature. Synaptic strength is adjusted, based on the degree of firing, coincidence, which reflects shared information between the cells.

Question 28

How did synaptic strength differ in eyes?

Answer 28

Experiment where one eye is open and the other closed. The open eye has lots of sensory input so the axons cause long term potentiation in the postsynaptic cell and strengthens the connection between the presynaptic and postsynaptic cell. The closed eye does not have much firing so there is no potentiation and the synapses are not adjusted to the flow of information.

Question 29

How does long term potentiation strengthen synapses?

Answer 29

Neuronal activity is able to increase neurotrophin synthesis, secretion and signalling in the pre and postsynaptic cell. Increase in postsynaptic responsiveness. Alters synaptic morphology - bigger and more fenestrated (new synapses). Increases presynaptic transmitter release. Increases membrane excitability. Which causes modification of synaptic transmission and connectivity.

Question 30

What are the pathways of learning and memory?

Answer 30

Short term memory is stored in the hippocampus, and this is also where learning occurs. The hippocampus links to the thalamus and hypothalamus, which stores long term memory for recollection.

Question 31

What is the variation of synaptic plasticity?

Answer 31

The limbic system - hippocampus, Parahippocampal, is responsible for integrative learning, so is very plastic. Association cortical regions plastic but to a lesser degree. Primary sensory and motor areas have descriptive and executive functions so are very rigid. This is because the cortex connections allows you to localise where sensory input is coming from, so cannot change.

Question 32

How could drugs be used to aid learning?

Answer 32

Learning is modification of synaptic transmission triggered by neuronal activity, by altering the existing synapses. So nootrophics, which aid neurotrophins, should theoretically be able to increase the ability of learning and memory.

Question 33

What are the effects of nootrophics?

Answer 33

Drugs that increase brain metabolism, cerebral circulation, or protection of the brain from physical and chemical damage over time. But these interventions only work, to a certain degree, in those affected with diseases that affect learning and memory. They do not have effect in healthy people to improve learning.