PHYS20008 Lecture Notes - Lecture 6: Skeletal Muscle, Cytoskeleton, Nicotinic Acetylcholine Receptor

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Lecture 6
- Electrical signal → Chemical signal (neurotransmitter)
-
- Synapse: AP travels down presynaptic neuron → voltage-gated calcium channel
(opens up and calcium moves freely, +134mV, move into cells) → synaptic vesicles
(vesicle walls are made up of phospholipid bilayer, loaded with high concentration of
neurotransmitters, walls have neurotransmitter pumps) fuses with membrane at the
end (docks and release neurotransmitters) → membrane open up to synaptic cleft →
receptors on post synaptic cell (ion channels, e.g. chemically-gated sodium channel
allows a bit of sodium to move into cell → depolarisation locally in membrane) → RMP
increases closes to threshold (excitatory signal, depolarises)
- Reuptake transporters: Presynaptic cell have transporters → scoop neurotransmitters
back into presynatic cell → repackage into vesicles to be released again
- Break down/metabolise: Glial cells (more than neurons) → metabolise and break
down neurotransmitters left in synapses
- Drug effects: activating/inhibiting the receptors directly, imitating the neurotransmitter,
blocking reuptake of the NT, causing spontaneous release of NT, blocking the
release of NT
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- Agonist: activate receptor
- Antagonist: inhibit/block receptor
- Excitatory neurotransmitters: lead to a small depolarisation in the target cell, bring it
closer to threshold;
- Inhibitory neurotransmitters: lead to a small hyperpolarisation in the target cell, bring
it further from threshold (closer to RMP)
- Doesn’t depend as much on neurotransmitters, more to receptors in post synaptic
cell
- Glutamate (most common excitatory neurotransmitter; 9 different types of receptors;
8 - excitatory, 1 - inhibitory, depends on receptor it’s interacting with)
- Neuron can release neurotransmitters and depending on type of cell it’s interacting
with can be excitatory or inhibitory
- Ionotropic: chemical/ligand-gated ion channels - the receptor itself is an ion channel
which opens and allows a specific ion to pass through when it comes in contact with
the neurotransmitter, simple, fast, effective, causes local effect
- Metabotropic: G protein-coupled receptors - when in contact with the
neurotransmitter, initiate a series of intracellular events (e.g. Upregulation of receptor
expression, opening nearby ion channels, etc.), more complex, longer term
maintenance mechanisms, not as fast
- Major Neurocrines
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Document Summary

Reuptake transporters: presynaptic cell have transporters scoop neurotransmitters back into presynatic cell repackage into vesicles to be released again. Break down/metabolise: glial cells (more than neurons) metabolise and break down neurotransmitters left in synapses. Drug effects: activating/inhibiting the receptors directly, imitating the neurotransmitter, blocking reuptake of the nt, causing spontaneous release of nt, blocking the release of nt. Excitatory neurotransmitters: lead to a small depolarisation in the target cell, bring it closer to threshold; Inhibitory neurotransmitters: lead to a small hyperpolarisation in the target cell, bring it further from threshold (closer to rmp) Doesn"t depend as much on neurotransmitters, more to receptors in post synaptic cell. Glutamate (most common excitatory neurotransmitter; 9 different types of receptors; 8 - excitatory, 1 - inhibitory, depends on receptor it"s interacting with) Neuron can release neurotransmitters and depending on type of cell it"s interacting with can be excitatory or inhibitory.

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