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1

Myasthenia Gravis: symptoms

dysfunction of synaptic transmission. Causes fluctuating muscle weakness, problems chewing (dysphagia) and talking (dysarthria) and respiratory weakness

2

Synapse

the place where neurons come into close proximity with other neurons
pre synaptic- before the synapse
post synaptic- after the synapse

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Axodendritic synapse

the terminal buttons synapses with a dendrite of the post synaptic neuron

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Axosomatic synapse

the terminal button synapses with the cell body (soma) of the post synaptic neuron

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Axoaxonic

the terminal button synapses with the axon of the post synaptic neuron

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presynaptic membrane

the membrane of the presynaptic terminal button

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post synaptic membrane

the membrane of the postsynaptic neuron

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dendritic spine

a ridge on the dendrite of the post synaptic neuron, with which a terminal button from a pre synaptic neuron forms a synapse

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synaptic cleft

the tiny gap between the presynaptic and postsynaptic membrane (approximately 20 nanometers wide)

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synaptic vesicles

tiny balloons filled with neurotransmitter molecules; found in the release zone of the terminal button

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microtubules

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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release zone

part of the interior of the presynaptic membrane to which synaptic vesicles fuse in order to release their neurotransmitter into the synaptic cleft

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Release of a neurotransmitter 1

1. vesicles contain neurotransmitter (NT) molecules
2. an action potential in the pre synaptic cell triggers vesicles to move toward the cell membrane
3. vesicles are guided towards the membrane by proteins

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Release of a neurotransmitter 2

Guiding proteins act like ropes that help fuse the vesicle and pre synaptic membrane together

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Release of a neurotransmitter 3

1. an influx of calcium ions into the pre synaptic terminal button induces fusion of the two membranes
2. neurotransmitter molecules are then released into the synaptic cleft

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Excitatory post synaptic potential (EPSP)

Excitatory post synaptic potentials (EPSPs) depolarise the post synaptic cell membrane
EPSPs increase the likelihood that an action potential will be triggered in the post synaptic neuron

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Inhibitory post synaptic potential (IPSP)

Inhibitory post synaptic potentials (IPSPs) hyperpolarise the postsynaptic cell membrane
IPSPs decrease the likelihood that an action potential will be triggered

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neural integration

the interaction between the effects of EPSPs and IPSPs
IPSPs tend to cancel out the effects of EPSPs

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Reuptake

the neurotransmitter is removed from the synaptic cleft via special transporter molecules in the terminal buttons. These molecules use energy to draw the neurotransmitter back into the cytoplasm of the pre synaptic neuron

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Enzymatic deactivation

an enzyme in the synaptic cleft destroys the remaining neurotransmitter molecules. Such deactivation seems to occur only for one type of neurotransmitter, called acetylcholine (ACh). The enzyme that destroys ACh in the synapse is called acetylcholinesterase (AChE); it does the job of breaking ACh into its constituents, acetate and choline

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Seven steps of neurotransmitter action at the synapse

1. neurotransmitter (NT) molecules are synthesised from their precursors by enzymes
2. NT molecules are stored in vesicles
3. NT molecules that leak from vesicles are destroyed by enzymes
4. action potentials cause vesicles to fuse with the presynaptic cell membrane, releasing their NT into the synaptic cleft
5. released NT binds with autoreceptors in presynaptic membrane, limiting further release of the NT
6. released NT binds with the 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 by enzymes- reuptake or enzymatic deactivation

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Amino acids

Glutamate: the most common excitatory neurotransmitter in the CNS
GABA (gamma aminobutyric acid): the most common inhibitory neurotransmitter

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Monamines

Dopamine and Norepinephrine (catecholamines)
Serotonin (Indolamine)

present in groups of neurons that are located mostly in the brainstem

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Acetylcholine

Acetylcholine: the neurotransmitter that operates at synapses with muscles, as well as other parts of the CNS

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Agonist

increases the activity of the synapse

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Antagonist

decreases the activity of the synapse

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Agonists do the following...

1. increase the number of neurotransmitter (NT) molecules that are synthasised
2. increase the number of NT molecules stored in the vesicles
3. destroy the enzymes that attack NT molecules
4. increase the number of vesicles that fuse with the pre synaptic cell membrane
5. decrease the activity of autoreceptors
6. binding directly with the post synaptic membrane, causing ion channels to open
7. decreasing the amount of NT that is reuptaken or destroyed by enzymes

28

Anatgonists can do any of the following

1. decrease the number of neurotransmitter (NT) molecules that are synthasised
2. decrease the number of NT molecules stored in the vesicles
3. cause NT to leak from vesicles where they are attacked by degrading enzymes
4. decrease the number of vesicles that fuse with the pre synaptic cell membrane
5. increase the activity of autoreceptors
6. block the inotropic receptor, preventing the ion channels from opening
7. increasing the amount of NT that is reuptaken or destroyed by enzymes in the synapse

29

Myasthenia Gravis

Autoimmune disorder where the person's own immune system destroys ACh receptors which are located on synapses with the muscles
Treated with anticholinesterase (AChE) inhibitors- these increase and prolong the effects of ACh on the post synaptic membrane
Also treated with immunosuppressive drugs or by removal of the thymus gland