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Brain Processes > Learning in Aplysia > Flashcards

Learning in Aplysia Flashcards

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1
Q

Learning definition

A

relatively permanent change in behaviour as a result of experience

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2
Q

Memory definition

A

when current behaviour is under control of past experience

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3
Q

Non-associative learning

A

animals learn about properties of stimulus they encounter

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4
Q

Associative learning

A

Classical (pavlovian) learn about relationship of one stimulus to another. Instrumental learn about the relationship between a stimulus and an action

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5
Q

Early proposal for memory?

A

Reverberating circuits. But results like those of Squire, Slater and Chase 75 showed that ECT did not disrupt memory in the long term

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6
Q

Hebb

A

Postulate for learning. Summarised as cells that fire together wire together

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7
Q

Habituation (Non associative)

A

decrease in response to increasingly repeated non-noxious stimuli

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8
Q

Dishabituation (non-associative)

A

increase in response to a stimulus following its intense presentation

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9
Q

Sensitisation (non-associative)

A

enhanced response to a range of stimuli following an intense or noxious stimulus

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10
Q

Sherrington

A

studied habituation of flexion in animals. Suggested habituation was result of a decrease in function of synapses to motor neurons

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11
Q

Spencer and Thompson

A

Habituation in spinal reflexes of cat. Showed changes at synapse were responsible

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12
Q

Kandel

A

Extensive work on the aplysia earning him the nobel prize

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13
Q

Aplysia Californica

A

20,000 neurons but 200 consistent and major ones. Consistent wiring in all Aplysia

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14
Q

Withdrawal reflex

A

US touch mantle or siphon, UR gill withdrawal

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15
Q

Mechanism of habituation

A

Repeated tactile stimulation and UR decreases. Castellucci et al 1970 (fewer action potentials from gill withdrawal motor neurons with each touch). Castelluci and Kandel 1974 (However sensitivity to artificial neurotransmitter does not decrease and the sensory neurons are still firing a signal). Therefore sensory neurons must be releasing less transmitter

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16
Q

Why do sensory neurons release less transmitter?

A

Klein, Shapiro and Kandel 1980 - less calcium enters presynaptic terminal reducing exocytosis. Gingrich & Byrne, 1985 - depletion of neurotransmitter in sensory neuron

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17
Q

Mechanisms of sensitisation

A

Facilitatory interneurons driven by tail sensory neurons synapse on the axon terminals of siphon sensory neurons. Release of neurotransmitters at axon terminals of siphon sensory neurons modifies their response to siphon stimulation. Presynaptic facilitation

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18
Q

Role of interneurons and serotonin

A

Serotonin mimics sensitisation. Interneurons increase cAMP –> increases depolarisation of presynaptic neuron, allows more calcium into the terminal which increases exocytosis and alters the way calcium participates in mobilizing transmitter vesicles

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19
Q

Plasticity

A

Habituation and sensitisation are the result of a plastic change in the function of neurons but changes can also be long term. Evidence for structural changes of neurons at the synapses for long term effects

20
Q

Pavlovian conditioning

A

allows animals to learn the relationship between one stimulus and another. Allows us to deal with unobservable mental phenomena (ideas) by studying them through observable behavioural processes

21
Q

Associative learning in Aplysia

A

CS - light siphon touch, US - tail shock, UR - gill withdrawal and CR strong gill withdrawal

22
Q

Rescorla 1968

A

Rats presented with a tone and unconditioned stimulus. Only when the CS and US were contingently presented did they produce a CR. Therefore the CS-US paired are associative learners and CS-US unpaired are sensitisation group

23
Q

Differential conditioning

A

these experiments on the Aplysia prove that it is not sensitisation but conditioning. CS1 and CS2 paired seperately with one US. When tested with CS2 on a CS1 group the response (CR) is lower than the CS2 test would be

24
Q

In paired CS-US training the effect of the US on active CS-UR sensory synapses is much stronger (conditioning). Why?

A

timing crucial to processes promoting enhancement. in addition to effects of cAMP (see sensitization), a G-protein, adenylate cyclase is increased. one form of this protein binds to calcium (which is in greater abundance) and promotes more production of cAMP. similar processes detected in Drosophila and Hermissenda - mammalian systems seem to differ

25
Q

Mechanism of classical conditioning

A

US - tail shock excites interneuron. CS - Mantle sensory neuron and interneuron simultaneously active – large change in subsequent sensory neuron transmitter release

26
Q

Memory in Aplysia

A

Mostly presynaptic effects. No evidence of memory cells or reverberating circuits

27
Q

Bliss and Lomo 1970

A

long term potentiation. studied slices of hippocampus in vitro. Stimulated axons in the perforant path and measured activity in the dentate gyrus.

28
Q

Properties of LTP

A

Long term and only occurs when firing of presynaptic neuron is followed by firing of postsynaptic neuron. In Bliss and Lomo experiments a tetanic stimulation bought about a higher EPSP even after a week or month

29
Q

NMDA receptor

A

LTP most widely studied at these sites. Acts as a coincidence detector only firing when pre and post neurons are. Mg ion displaced when post synaptic neuron is patially depolarised. Allows glutamate to bind and so channel opens allowing calcium ions through. These ions initiate changes in the cell.

30
Q

Evidence for post synaptic changes in LTP

A

Muller, Joly and Lynch (1988) - showed that the change in synaptic efficacy was mediated by changes in AMPA receptors. AFTER induction of LTP potentiation effect was abolished by blocking AMPA but not NMDA receptors
Tocco et al. (1992) measured the number of AMPA and NMDA receptors using radio-labelled ligands and found that LTP changed AMPA, but not NMDA, receptor numbers
Blocking protein synthesis prevents LTP (Nguyen, Abel & Kandel, 1994)

31
Q

What will more AMPA receptors do?

A

More dendritic spines are being produced
More AMPA receptors are sitting on these spines, more space for them as well
Signal is therefore more likely to be detected

32
Q

Presynaptic changes in LTP

A

Calcium entering post synaptic cell activates secondary messengers (kinases) and NO is released. Acts as retrograde transporter effecting pre-synaptic cells. Possible by acting on soluble guanyl cyclase–>cyclic GMP–>more glutamate release

33
Q

Glanzman, 1995

A

Classical conditioning of Aplysia’s withdrawal reflex mediated by
Activity-dependent presynaptic facilitation (ADPF): at synapses between central sensory and motor neurons.
Postsynaptic mechanism: Hebbian potentiation of the sensorimotor synapses
Plasticity at sites other than central monosynaptic sensorimotor connections, including peripheral sites

34
Q

Walters and Byrne

A

differential conditioning results from different presynaptic effects

35
Q

Carew, Pinsker & Kandel, 1972

A

Habituation lasts 2 or 3 hours following a single 10-stimulus habitation session, but several such sessions can produce habituation that lasts for weeks

36
Q

Emptage & Carew, 1991

A

As a result of presynaptic facilitation – sensory fibres from the Aplysia tail synapse on facilitatory serotonergic inter-neurons, which in turn synaps on the buttons of siphon sensory neurons

37
Q

Byrne & Kandel, 1996

A

Applications of serotonin to Aplysia sensorimotor synapses produces sensitisation lasting minutes to days

38
Q

Cleary, Lee & Byrne, 1998

A

Long term sensitisation: multiple mechanisms, including lasting increases in motor neuron excitability

39
Q

Carew, Walters & Kandel, 1981

A

Increase in intensity of the reflex is much greater that if the two stimuli are presented in an unpaired fashion. proves associative nature of effect CC in aplysia

40
Q

Carew, Hawkins & Kandel, 1983

A

Performed the discriminated classical conditioning tasks

41
Q

Bailey & Chen (1983, 1988)

A

electron microscopy: long-term habituation & sensitisation leads to structural changes in synaptic terminals of siphon sensory neurons. Sensory neurons:
 Fewer active zones of NT release
 Smaller active zones of NT release
 More synaptic vesicles

42
Q

Pinel

A

Changes in postsynaptic neurons can be rapid through ion-channel linked receptors or slow and enduring though NT binding G-protein linked receptors and 2d messengers produced as a result

43
Q

Secondary messengers (Pinel)

A

second messenger increased in buttons of siphon-sensory neurons in response to the serotonin released by tail-shock-activated inter-neurons.
o Activates protein kinase A which closes many potassium channels in buttons which increases duration of each action potential which increases influx of calcium & release of NT in response to each touch of siphon.
 Byrne & Kandel (1996): this mechanism largely accounts for short-term synaptic facilitation; long-term depends on a second cascade of changes mediated by protein kinase C.

44
Q

Kelso, Ganong & Brown, 1986

A

LTP Develops only if the firing of the presynaptic neuron is followed by firing of postsynaptic neuron

45
Q

Evidence for LTP in learning and memory (Pinel)

A
  1. LTP can be elicited by low levels of stimulation (mimic normal neural activity)
  2. Effects are most prominent in structures that have been implicated in l&m (e.g. hippocampus).
  3. Behavioural changes can produce LTP-like changes in Hippocampus (Iriki et al., 1989)
  4. Drugs that influence l&m have parallel effects on LTP (Brown et al., 1988; Skelton et al., 1987)
  5. Induction of maximal LTP blocks learning of a Morris water maze until LTP has subsided (Castro et al., 1989)
  6. Mutant mice that displat little hippocampal LTP have difficulty learning the Morris water maze (Silva et al., 1992)
46
Q

Calcium in LTP

A
  • Calcium probably exerts its effects by activating protein kinases in the neural cytoplasm (Grant & Silva, 1994; Linden & Routtenberg, 1989).

Brain Processes (11 decks)

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