Lecture 21- Communication Between Nerve Cells Flashcards

1
Q

What is synaptic plasticity?

A

-Is a form of neuromodulation

-Defined as the activity-dependent modification of the strength (or efficacy) of synaptic transmission

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2
Q

Is synaptic plasticity as a form of neuromodulation short or long lasting?

A

Short or long-lasting

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3
Q

What processes does synaptic plasticity underly?

A

Underpins learning and memory

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4
Q

What are the two ways which we can study learning and memory? What are they each ideal for?

A

-in vitro= molecular and cellular events

-in vivo= behaviour

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5
Q

What are some examples of in vitro techniques?

A
  • Cells in culture
  • Acute brain slices
    e.g. hippocampal slices (only last a few hours)
    Organotypic brain slices (last a lot longer than hippocampal)
  • others
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6
Q

What are some examples of in vivo techniques?

A
  • Simple invertebrate models
  • Vertebrate rodent models
  • Others
  • Cellular events too
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7
Q

What are some advantages and disadvantages of in vitro techniques?

A

-Advantage= easy to apply drugs and see effect

-Disadvantage= true circuitry isn’t actually actually being reflected

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8
Q

What are two examples of Invertebrate models?

A
  • Drosophila melanogaster
  • Aplysia californica
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9
Q

What are the advantages associated with the Drosophila melanogaster invertebrate model?

A

Small genome and rapid life cycle
* Drosophila is good for genetics
* Small nervous system
* ~135,000 neurons
* Easy to identify and circuits

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10
Q

What are the advantages associated with the Aplysia californica invertebrate model?

A
  • Small nervous system
  • ~1,000 neurons
  • Large neurons
  • Easy to impale and record from
  • Easy to identify individual neurons and
    circuits
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11
Q

What is the Aplysia californica method for learning and memory?

A

Siphon-gill-withdrawal reflex:
* Tactile stimulus to siphon causes gill withdrawal
* This reflex undergoes habituation or sensitization (a simple form of learning)
when a noxious stimulus is applied.

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12
Q

What are the two types of Nonassociative learning than result in behavioural responses? Draw what neural activity looks like in these processes on a graph…

A

Habituation: learning to ignore a stimulus that lacks
meaning

vs.
Sensitization: Stimuli results in increased sensitivity

Graphs shown in slides (12)

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13
Q

What pattern of receptors/ what is happening at the neural level in the siphon-gill-withdrawal reflex?

A

-Touch activates sensory
neurons in the siphon skin

-Relayed to motor neuron
(L7) in abdominal ganglion

-Stimulates gill muscles and
thus gill withdrawal

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14
Q

What neural changes happen when habituation occurs?

A

-weakened neurotransmission

-decreased neurotransmitter release from sensory neuron

-fewer vesicles released per action potential

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15
Q

How is Sensitization demonstrated in the Aplysia?

A

When the siphon of Aplysia is gently touched, the animal withdraws its gill for
a brief period.
* But, if the “touch” is preceded by an electrical shock to its tail, the same gentle
touch to the siphon will elicit a longer period of withdrawal.
* If the Aplysia is given multiple shocks its subsequent response to a gentle
touch on the siphon is much larger and is retained longer.

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16
Q

What does Sensitization to a noxious stimulus delivered to the Aphysia’s tail require neurally?

A
  • a sensory neuron that picks up the stimulus from the tail connecting to
  • interneurons that terminate on the sensory neuron in the siphon-gill pathway.
17
Q

What does Sensitization require?

A

Sensitization depends on increased synaptic activity, this process is called facilitation

18
Q

What is presynaptic facilitation? (within the context of the gill withdrawal response)

A
  • Stimuli results in increased sensitivity of the gill withdrawal response
  • Noxious stimuli activate interneuron
  • This enhances neurotransmitter release
    from the sensory neuron presynaptic terminal
    and
  • alters gene expression
19
Q

What happens at the neuron/ molecule level in presynaptic facilitation as a result of a single tail shock to the Aphysia?

A
  • L29 releases 5HT (serotonin)
  • 5-HT (5-hydroxytryptamine receptors), serotonin
  • activates 5HT receptors on presynaptic
    nerve terminal
  • stimulates formation of cAMP
  • activates protein kinase A (PKA)
    !Release of neurotransmitter
20
Q

What does PKA do in the context of presynaptic facilitation?

A

PKA increases phosphorylation of K+ channels:
-Phosphorylated K+ channels close
-K+ does not exit terminal as rapidly
-Prolonging the Action potential (limits repolarisation)
-Ca2+-channels increase their opening

21
Q

What happens in presynaptic facilitation with regards to synaptic vesicles?

A

Increased mobilisation of synaptic vesicles
-via PKC

22
Q

What does PKA do to calcium channels? and what is the result of this for the Aphysia?

A

PKA increases phosphorylation of Ca2+ channels
-voltage-sensitive Ca2+-channels open
-greater Ca2+ influx increases release of neurotransmitter
-stronger signal to motor neuron
-enhanced gill-withdrawal

23
Q

What happens during presynaptic facillitation where the Aphysia receives multiple tail shocks as opposed to just one?

A
  • L29 releases 5HT (serotonin)
  • 5-HT (5-hydroxytryptamine receptors), serotonin
  • activates 5HT receptors on presynaptic
    nerve terminal
  • Higher levels of cAMP
  • Activates protein kinase A (PKA) which
    now moves to the nucleus

-Altered gene expression
-new proteins stimulate synapse growth

24
Q

In vertebrate models what is long term potentiation?

A

-Long-lasting activity dependent increase in
synaptic responses

-Brought about by brief patterned high frequency stimulation to excitatory
pathways of hippocampus

25
Q

When long term potentiation is induced in a rodent hippocampus what occurs?

A

-The hippocampus is a site of memory processing in rodents (know because they show impaired performance on learning and memory tasks following a hippocampal lesion)
-Trisynaptic loop occurs

26
Q

What is the Trisynaptic circuit of the hippocampus?

A
  1. Entorhinal cortex → dentate gyrus (perforant path) synapses
  2. Dentate gyrus → CA3 (mossy fiber) synapses
  3. CA3 → CA1 (Schaffer collateral) synapses
27
Q

What are some features of long term potentiation?

A

Elicited in brain regions associated with memory
* Synaptically-located
* Specific to active synapses
* Associative (ie. interactions between active inputs can influence its induction)
* Persistent

28
Q

What mechanically/ neurological underpins long term potentiation?

A

Underpinned by increased glutamate receptor responsiveness

29
Q

What are the two types Ionotropic Glutamate Receptors? What are the features of both types?

A

AMPA receptor subtypes
α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor:
* Ligand-gated
* Mediate fast depolarisation
* Na+ channel

NMDA receptor subtypes
N-Methyl-D-aspartate receptor:
* Ligand and ion-gated
* Slightly slower response
* Not as slow as metabotropic receptors
* Ca2+ channel and Na+ channel

30
Q

What is the structure of AMPA receptors in terms of how they sit across membranes?

A

-Have an extracellular domain, an intracellular domain and also lots of regulatory molecules attached
-They vary in composition according to their function
-There is complex network scaffolding across the membrane

31
Q

Are receptors like islands?

A

No, they are more like trees with lots of routes and branches

32
Q

In vivo does long term potentiation last a long or short time?

A

-Long, it last a really long time

33
Q

What does long lasting change require and what does it result in?

A

-altered gene expression
-Happens via CREB phosphorylation
-Results in the growth of dendritic spines

34
Q

What is a summary of LTP?

A

-Ca2+ influx into dendritic spine activates protein kinases
-Such as Ca2+-calmodulin-dependent protein kinase II
-phosphorylates the AMPA receptor to increase conduction
-AMPA receptors are trafficked to the membrane
- Protein kinase A (PKA), CaMKII
=long term changes to gene expression