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neuroanatomy > synaptic transmission and plasticity > Flashcards

synaptic transmission and plasticity Flashcards

1
Q

Classes of neurotransmitters

A
  • small molecule (short term effect) e.g. amino acids, acteylcholine
  • Peptide (longer term effects) e.g. opioids, vasopression
  • can co-exist in the same terminal (co-transmitters)
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2
Q

Types of synaptic vesicles

A
  • small clear vesicles (Glu, GABA, Gly, Ach, ATP)

- dense-core vesicles (serotonin, histamine, neuropeptides, catecholamines)

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3
Q

What are SNARE proteins the targets of

A

Botulinum and tetanus toxins (proteases)

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4
Q

what is the effect of BoTX

A

affects peripheral and visceral neuromuscular synapses - weakness

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5
Q

what is the effect of Tetanus toxin

A

Binds to Ach receptors, gets internalised and taken up by motor neurons, transported into inhibitory spinal interneurons, causes tetanic contractions

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6
Q

Why is removal/recycling of neurotransmitters important

A

excess glutamate can cause excitotoxicity which can lead to neuronal cell death

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7
Q

what are the specific inactivating enzymes

A
  • AChE
  • MAO (monoamine oxidase)
  • COMT (catechol-O-methyltransferease
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8
Q

how are astrocytes important for the removal of excess neurotransmitters

A
  • tripartite synapse

- recycling of ions and neurotransmitters

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9
Q

What are some strategies for up-regulation of neurotransmission?

A
  • supplement the neurotransmitter or precursor (L-DOPA in parkinson’s - increase dopamine)
  • inhibit clearance by transporters (antidepressants that act on SERT e.g. SSRI’s - fluoxetine)
  • inhibit breakdown of neurotransmitter (AchE inhibitors in Alzheimer’s disease - galantamine, donepezil, rivastigmine )
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10
Q

What are some strategies for down-regulation of neurotransmission?

A
  • pre-synaptic this is not really possible as there is a conserved nature of machinery (may be possible with botox application)
  • Postsynaptic - block specific receptors (e.g. antipsychotics target D2 dopamine receptors)
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11
Q

What are the two classes of receptors

A

Ionotropic - allow different kinds of ions to travel in and out of the cell, ligand-gated transmembrane ion channels

metabotropic - linked to G-protien, G-protein activates a secondary messenger, which activates other particles

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12
Q

How is an IPSP/EPSP generated

A

IPSP - GABA (inhibitory neurotransmitter) causes chloride influx which causes an IPSP

EPSP - Glutamate (excitatory neurotransmitter) causes sodium influx which causes an EPSP

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13
Q

Define synaptic plasticity

A

increases or decreases in synaptic strength in response to patterns of synaptic activity

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14
Q

short-term plasticity

A
  • typically ms-s scale
  • temporary
  • generally related to amount of neurotransmitter release presynaptically
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15
Q

What is long-term plasticity (LTP and LTD) thought to be the basis of

A

learning and memory

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16
Q

In what disease is the hippocampus about a third of the thickness that it is supposed to be

A

In Alzheimer’s

17
Q

what is the trisynaptic circuit of the hippocampus

A
  1. From entorhinal cortex to the dentate gyrus via the perforant path
  2. From granule cells in the dentate gyrus to CA3 via the moss fibres
  3. From pyramidal cells in CA3 to pyramidal cells in CA1 via the schaffer collaterals
18
Q

Where are most LTP studies done and how

A
  • In the hippocampus
  • stimulate Schaufer collaterals
  • record from neurons in the CA1 field either from the entire field or individual neurons
19
Q

what are the mechanisms underlying LTP

A
  • induction is NMDA receptor independent
  • prolonged period of depolarisation following a period of high-requency stimulation and alleviation of magnesium block
  • induction is calcium dependent (influx)
20
Q

What happens during LTP

A
  • large, fast influx of calcium
  • kinase activation
  • insertion of additional AMPA receptors
  • retrograde signalling (presynaptic changes)
  • remodelling of dendritic spines
21
Q

How is LTD induced

A
  • prolonged low-frequency burst of stimulation
  • removal of AMPA receptors
  • small and slow increases of calcium
  • activation of phosphatases
22
Q

LTD in the cerebellum

A
  • paired stimulation of the climbing fibres and parallel fibres causes LTD
  • increases the output from the cerebellum as purkinje cells are inhibitory
  • Glutamate release from parallel fibres activates mGluR
  • climbing fibre activation depolarises purkinje cells and opens VGCC
  • synergistic activation of PKC
  • may be important for motor learning
23
Q

Spike-timing dependent plasticity

A
  • LTP/LTD associative
  • post after pre = depolarisation subsiding, less calcium influx (LTD)
  • pre then post = strong depolarisation, relieve magnesium block, large calcium influx (LTP)
24
Q

Disease relevant - synaptic plasticity

A

Atrophy of hippocampus in Alzheimer’s

epilepsy - kindling (seizure’s induced repeatedly)

Drug addiction - constant exposure of ventral tegmental area at the nucleus accumbens synapses can lead to LTD and hence the need for greater and greater doses to reach the same high

neuroanatomy (21 decks)

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