structure of neuronal synapses

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10 Terms

1
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what is a synapse

point of connection between 2 neurones

2
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what is a neurotransmitter

endogenous chemical that transmits signals across synapse from one neurone to another ‘target neurone, muscle cell or effector cells

3
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what is a neuromodulator

endogenous chemical that is released from one neurone but if affects groups of neurones or effector cells that have appropriate receptor

4
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differences between neurotransmitters (NT) and neuromodulators (NM)

  • NM acts through second messengers vs NT act directly on postsynaptic cells

  • NM produces long lasting effects vs NT have fast immediate response

  • NT is released at synapses vs NM not always released at synapses

  • NT = rapid, localised communication at synapses vs NM more longer duration responses

5
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name if these are NT and/or NM:

  • acetylcholine

  • monoamines 

    • catecholamines (dopamine, noradrenaline)

    • indolamines (serotonin)

  • amino acids - glutamate, GABA, glycine

  • peptides - endorphins

  • lipid substances 

  • nucleosides - adenosine

  • acetylcholine = NT

  • monoamines = NT and NM

    • catecholamines (dopamine, noradrenaline)

    • indolamines (serotonin)

  • amino acids - glutamate, GABA, glycine = NT and NM

  • peptides - endorphins = NT and NM

  • lipid substances = NT

  • nucleosides - adenosine = NM

6
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summary of the different ways drugs can modify neurotransmitter system in brain

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7
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what is a presynaptic autoreceptor

Receptor on a neuron that binds the same neurotransmitter it releases → typically inhibits further release

8
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what is presynaptic heteroreceptor

receptor on a presynaptic neuron that binds a different neurotransmitter → can inhibit or facilitate release of the main neurotransmitter

9
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how can drugs affect presynaptic receptors

they can block or enhance autoreceptors or heteroreceptors to modify neurotransmitter release

10
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how can presynaptic heteroreceptors produce presynaptic inhibition

inhibit release of neurotransmitter e.g. glutamate release by GABA b receptors so this causes reduction in postsynaptic activity