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Psyc 2330 Final > Lecture 9 > Flashcards

Lecture 9 Flashcards

(39 cards)

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1
Q

What is learning?

A

the process by which experiences change our NS

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2
Q

Changes associated with learning are referred to as?

A

memories

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3
Q

What are memories?

A

changes in the circuits that participate in perceiving, performing, thinking and planning

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4
Q

Explain the Hebb Synapse

A

The persistence or repetition of a reverberatory (something that keeps coming back) activity (or “trace”) tends to induce lasting cellular changes that add to its stability
- a connection between 2 neurons (anatomical connection) takes place only if bother neurons are firing at the same time

= Simultaneous activation

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5
Q

Explain the Hebb Rule

A

How and when will the brain change to represent a memory?
- if a synapse becomes repeatedly active at about the same time the post synaptic neutron fires, changes will take place in the structure or chemistry of the synapse that will strengthen it

E.g.
puff of air to the eye –> neuron of somatosensory system –> synapse P –> blink
1000 Hz tone –> neuron in auditory system –> synaps T –> blink

puff of air + tone –> eye blink; test: tone –> eye blink??
- during conditioning tone and blink neurons are active at the same time (not sequential; happening simultaneously)

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6
Q

What type of learning is involved with habituation and sensitization?

A

Repetition learning

- not associative

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7
Q

Is Hebb’s law specific to associative learning?

A

Yes

- associating two things at a time

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8
Q

What is non-associative learning?

A

repeat stimulation/lack of stimulation (not associating S-S or S-R)
- all about amount of usage

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9
Q

Explain topographical maps

A
  • change with the use of afferent (input) pathways
  • details vary between individuals
  • E.g. increased use of fingers –> enlarged image of fingers
  • intense disuse of a hand produces enlargement of cortical areas neighbouring the hand (e.g. face)
  • evidence that these maps change with experience

–> repeated stimulation of one synapse

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10
Q

What is synaptic enhancement?

A

Pre-synaptic action potentials leave an after-effect that alters the release of neurotransmitters in response to subsequent action potentials
- If the after-effect increases the amount of neurotransmitters released by successive action potentials = synaptic enhancement

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11
Q

What is synaptic depression?

A

Pre-synaptic action potentials leave an after-effect that alters the release of neurotransmitters in response to subsequent action potentials
- if the after-effect educes the release of neurotransmitters by subsequent action potentials = synaptic depression

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12
Q

Explain facilitation

A

1 pre-synaptic action potential in a burst of stimulation

- 1 second duration of enhancement

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13
Q

Explain augmentation

A

A few hundred action potentials in a burst of stimulation

- 10 second duration of enhancement

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14
Q

Explain potentiation

A

A few thousand action potentials in a burst of stimulation

- 5 minute duration of enhancement

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15
Q

Explain what tetanus is

A

Form of synaptic potentiation that was first described at a neuromuscular junction
- because of this, potentiation follows a sustained, high frequency burst of action potentials = post-titanic potentiation

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16
Q

What triggers short term synaptic enhancement?

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A

buildup of intracellular calcium inside the pre-synaptic terminal during action potential activity

17
Q

Complex biological functions of calcium

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A

In neurons - allow release of neurotransmitters (ion goes in and allows docking of synaptic vesicle, fusing –> release of neurotransmitters)

Repetition - calcium buildup –> more neurotransmitters released at stimulation

  • only pre-synaptic
  • short lasting
  • general change (not specific to particular neutron/neurotransmitter)
18
Q

Associative learning utilizes?

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A

longterm potentiation

- long term changes in synaptic strength

19
Q

What is longterm potentiation?

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A

neuronal activity can lead to long term after effects that alter the release of neurotransmitters, the anatomy and the sensitivity of post synaptic sermonical on a time scale of hours or days

20
Q

What are some characteristics of LTP?

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A
  1. lasts longer
    - hours, days; in the brain forever
  2. requires the activation of special receptors
  3. mediated by pre- and post-synaptic changes
  4. some changes are anatomical
  5. hetero-synaptic
    - changes specific to synapses are active at the same time
  6. associative
    - 2 events happening at the same time
21
Q

Schizophrenia patients have problems with which learning system?

22
Q

Effects of induced LTP

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A

Enhancement of response

- form of selectivity induced by simultaneous stiulation

23
Q

What is the role of glutamate?

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A

principal excitatory neurotransmitter of the brain and spinal cord (very abundant)

24
Q

What receptors are stimulated by glutamate?

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A

NMDA and AMPA receptors

25
What receptor is very important in LTP response?
NMDA
26
Explain how the NMDA receptor works
- allows movement of ions when open (ion channel) - glutamate released from AMPA receptor --> depolarization - binding site for glutamate on NMDA - when released from pre-synaptic --> nothing happens/no movement of ions (blocked by Mg ion) - can be blocked by PCP (induced by taking ketamine-like drugs)
27
In order for NMDA receptor to work:
- release glutamate - remove Mg --> simultaneous stimulation of the pre- and post-synaptic terminal (two stimulating events at the same time) = LTP engaged (DUAL SIMULTANEOUS STIMULATION)
28
What is dual simultaneous stimulation
two events at the same time - release of neurotransmitter (glutamate) - removal of Mg pre and post synaptic depolarization at the SAME time (coincidence detector)
29
What triggers LTP
Opening of NMDA receptor channels allowing calcium influx
30
When LTP is initiated?
acquisition of learning takes place
31
Affect of calcium and its association with initiating LTP
1. Ca goes in and turns pathway on Arg --> NO - functions as a neurotransmitter in NS - diffuses through the membrane; to the pre-synaptic terminal and can produce changes - mRNA, protein - pre-synaptic terminal (even in the absence of NMDA) --> more neurotransmitters can be produced (long term training) = enhanced release of glutamate next AP 2. calcium --> intracellular signalling --> AMPA receptor - can make AMPA more sensitive and in some cases influence gene expression (increase #) - amplify system receiving glutamate (post-synaptic changes) 3. About the size of synapse - active zone = release of pre-synaptic neurotransmitters (and this is where receptors are found) - LTP - size of active zone becomes bigger --> perforated synapse - perforation in the active zone and then a duplication (increase size of neurons that communicate with each other) = more surface for communication (anatomical changes) --> release more, more sensitive, more surface for communication
32
What would a drug do if it blocked NMDA receptors?
Block LTP --> block system that is engaged in associative learning --> prevent conditioning
33
Explain why we can't use NMDA antagonist + morphine to prevent morphine tolerance?
Doesn't make sense to use two addictive drugs to change the properties of one (marketing point of view)
34
What would be the effect of an NMDA antagonist after learning/LTP?
Wouldn't matter, learning is already done
35
According to the Hebb rule, the ? of the two neurons is essential for the formation of an association between them
simultaneous activation
36
The Hebb rule provides a physiological explanation of?
associative learning
37
Synaptic enhancement
- occurs at a single synapse - is observed after repeated stimulation - is a form of learning
38
Which of the following is false about synaptic enhancement? - it is dependent on calcium entrance in the pre-synaptic terminal - it can last for days - it results from repeated stimulation of a synapse - is a form of non-associative learning
it can last for days
39
Which of the following is not a characteristic of LTP? - dependent on the activity of NMDA - heterosynaptic - non-associative - it is mediated by pre and post synaptic changes
it is non-associative

Psyc 2330 Final (11 decks)

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