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MBB1 > The synapse: L3 > Flashcards

The synapse: L3 Flashcards

1
Q

Define Myasthenia Gravis

  1. described by
  2. first symptoms
  3. later symptoms
  4. severe cases
  • > normal
  • > what does it arise from?
A
  1. Thomas Willis
  2. weakness - proximal muscles (more than distal muscles)
  3. chewing problem (dysphagia) and talking (dysarthria)
  4. respiratory distress
  • > normal = conduction of nerve messages (AP), muscles functioning
  • > synapses muscles
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2
Q

the name of the junction between the cell body and the axon (bit in between wide cell face and long body)

A

axon hillock

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3
Q

How does the AP communicate with the next neuron after reaching the terminal button?

A
  • terminal buttons release neurotransmitters
  • they diffuse across the synaptic cleft between the presynaptic terminal button and the cell body of the postsynaptic membrane
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4
Q

Synapse structure (3 types)

  1. axodendritic
  2. axosomatic
  3. axoaxonic
A
  1. terminal button synapses with a dendrite of the postsynaptic neuron
  2. terminal button synapses with the cell body (soma) of the postsynaptic neuron
  3. terminal button synapses with the axon of the postsynaptic neuron
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5
Q

define:
1. dendritic spine
2. synaptic cleft
3. synaptic vesicles
4. microtubules

A
  1. ridge on the dendrite with which a terminal button forms a synapse
  2. gap between presynaptic and postsynaptic membrane (20 nanometres wide)
  3. tiny balloons filled with neurotransmitter molecules found ini the release zone (before synapse)
  4. long tubes that run down the axon and guide the transport of synaptic vesicles from the soma to the axon terminal
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6
Q

Release of a neurotransmitter 1. APs trigger vesicles to

  1. influx of?
  2. then what happens?
A
  1. move towards the presynaptic neuronal membrane (just before synaptic cleft)
    - guided towards the cell membrane by protein structures (P)
  2. Ca2+ (calcium) ions into the presynaptic neuron -> fusion of the membranes of the synaptic vesicle and the presynaptic cell
  3. neurotransmitter molecules released into synaptic cleft (occurs in milliseconds = rapidly)
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7
Q

Activation of receptors on postsynaptic neurons

  1. what happens when neurotransmitters reach the postsynaptic receptors?
  2. once opened what happens?
  3. Neurotransmitters open ion channels directly - describe
A
  1. attach to specific binding sites located in the membrane of the postsynaptic cell (key + lock)
  2. once opened, permit the flow of specific ions into and out of the postsynaptic neuron
  3. receptors are equipped with their own binding sites called ionotropic receptors. When a transmitter locks onto a binding site -> channel opens -> ions move in or out
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8
Q

Movement of ions during postsynaptic potentials

  1. excitatory -> increases likelihood of?
  2. inhibitory -> increases likelihood of?
A
  1. depolarise = triggering AP

2. hyperpolarise = not trigger AP

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9
Q
  1. What determines whether a postsynaptic potential is excitatory or inhibitory?
  2. 3 types of channels
A
  1. by the specific channel opened by the neurotransmitter

2. NA +, K+, CL- (chloride)

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10
Q
  1. NA+ (sodium) trigger what type of potential?

2. K+ (potassium) trigger?

A
  1. excitatory postsynaptic potential (EPSP)

2. Inhibitory postsynaptic potential (IPSP)

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11
Q

what determines whether the postsynaptic neuron will be excited or inhibited

A

the type of postsynaptic receptor

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12
Q

Neural integration - EPSP

A
  1. depolarise the postsynaptic cell membrane

2. Increases likelihood of AP

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13
Q
  1. Postsynaptic membrane potential before neurotransmitter release
  2. Postsynaptic membrane potential after release
A
  1. resting level -70

2. if neurotransmitter binds to sodium ion channels = depolarising EPSP

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14
Q

Neural integration - IPSP

A
  1. hyperpolarise the postsynaptic cell membrane

2. reduce likelihood of AP

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15
Q
  1. the interaction between the effects of EPSP and IPSP is known as
  2. the rate at which the neuron fires is determined by
A
  1. neural integration
  2. relative activity of excitatory and inhibitory synapses on its dendrites and cell body
    - >activity of excitatory synapses increases = increases rate of firing
    - > activity of inhibitory synapses increases = decreases rate of firing
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16
Q

Termination of postsynaptic potentials (2 types)

A
  1. reuptake = removed via transporter molecules in the terminal button. use energy to draw neurotransmitter back into the cytoplasm of the presynaptic neuron
  2. enzyme deactivation = destroys. occurs for neurotransmitter acetylcholine (ACh). the enzyme that destroys it is called acetylcholinesterase (AChE)
    - > breaks ACh into its constituents, acetate and choline
17
Q

What do termination of postsynaptic potentials ensure?

A
  1. postsynaptic receptors are exposed to neurotransmitters for a brief period of time
  2. allowing depolarisation & hyperpolarisation to occur in a v short space of time
18
Q
  • 7 steps of neurotransmitter (NT) action at the synapse
A
  1. NT synthesised from their precursors by enzymes
  2. NT stored in vesicles
  3. NT molecules that leak from vesicles are destroyed by enzymes
  4. AP cause vesicles to fuse with presynaptic cell membrane -> releasing NT into synaptic cleft
  5. NT bind with autoreceptors in presynaptic membrane, limiting further release of NT
  6. Released NT binds with receptors on postsynaptic membrane causing ion channels to open
  7. free NT molecules in the synaptic cleft are taken back up by transporter molecules in the presynaptic membrane or destroyed
19
Q

classes of neurotransmitters

  1. 4 classes of small
  2. 1 class of large
  3. Glutamate
  4. GABA
  5. Monamines (dopamine, norepinephrine, serotonin) are located
  6. Acetylcholine
A
  1. amino acids, monoamines, soluble gases and acetylcholine
  2. neuropeptides
  3. most common excitatory neurotransmitter in CNS
  4. most common inhibitory neuron transmitter
  5. brainstem
  6. operates at synapses with muscles
20
Q

Effects of drugs on synaptic functions

  1. agonist
  2. antagonist
A
  1. increases activity in synapse

2. decreases activity on synapse

21
Q

Agonists can (7)

A
  1. increase number of NT synthesised
  2. increase number of NT in vesicles
  3. destroy enzymes that attack NT
  4. increase number of vesicles that fuze with cell membrane
  5. decrease activity of autoreceptors
  6. bind directly with postsynaptic membrane causing ion channels to open
  7. decrease amount of NT that is reuptaken or destroyed
22
Q

Antagonist can (7)

A
  1. decrease NT synthesised
  2. decrease NT stored in vesicles
  3. cause NT to leak from vesicles -> attacked by degrading enzymes
  4. decrease number of vesicles that fuse will cell membrane
  5. increase activity of autoreceptors
  6. block the ionotropic receptor, preventing ion channels from opening
  7. increase NT reuptaken or destroyed
23
Q

Agnostic drug examples

A
  1. L-dopa (treats parkinsons)
  2. Black widow spider venom
  3. nicotine
  4. amphetamine, cocaine
24
Q

Antagonistic drug examples

A
  1. PCPA - inhibits synthesis of serotonin
  2. Reserpine - stops storage of monoamines in vesicles
  3. Botulinum toxin - blocks release of Ach
  4. Apomorphine - stimulates dopamine autoreceptors
  5. Curare - blocks postsynaptic ACh receptors
25
Q

Neurotransmitter projection pathways

A
  • different neurotransmitters are produced by particular clusters of neurons and distributed in the CNS
  • most clusters are in the brainstem and midbrain
26
Q

Myasthenia Gravis - disorder of ACh receptors

A
  • person’s immune system destroys ACh receptors - located on synapses with the muscle = weakness
  • by using the drug physostigmine (which deactivates AChE) the amount of ACh is increased and prolonged = increase strength of synaptic transmission at the muscles

MBB1 (7 decks)

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