Human Physiology Notes – Week 4
Nerves and Muscles Part 2.
Saltatory Propagation of AP in Myelinated Neurons.
Because of high membrane insolation by the myelin sheet, changes in membrane charge can
reach out towards the next Ranvier node bringing the sodium channels to the threshold for
opening.
AP jumps from node to node.
Synapse.
Presynaptic cell in close contact with the target postsynaptic cell.
Small space between cells is called the synaptic cleft.
Transmission is either electrical or chemical.
Chemical synapses operate by release of neurotransmitter (NT).
Transmission is only in one direction pre -> post.
Calcium is the signal for NT release at the synapse.
Excitory Synapses.
Ligand-gated postsynaptic ion channel opens.
Increased permeability for Na+ and K+ ions.
Much more Na+ ions than K+ ions leave.
Depolarization brings post synaptic membrane potential closer to threshold for AP
generation.
Inhibitory Synapses.
Ligand-gated postsynaptic ion channels open.
Increased permeability for K+ and Cl- ions.
Cl- ions enter, and some K+ ions leave.
Hyperpolarization drives postsynaptic membrane potential away from the threshold for AP
generation.
Transmitter Lifecycle.
Acetylcholine (ACh) (nicotinic receptors).
Release leads to excitation in postsynaptic membranes.
ACh opens specific ligand gated channels and sodium influx (depolarization).
ACh is degraded and chlorine fragments taken up again into synapse for reuse in transmitter
synthesis.
Turning Chemical Signal On.
Release of transmitter into synaptic cleft in response to AP.
Transmitter binds to receptor channels.
Receptor channels open for specific ions.
Turning Chemical Signal Off.
Released transmitter continuously removed from the synaptic cleft.
Nerves and Muscles Part 2.
Saltatory Propagation of AP in Myelinated Neurons.
Because of high membrane insolation by the myelin sheet, changes in membrane charge can
reach out towards the next Ranvier node bringing the sodium channels to the threshold for
opening.
AP jumps from node to node.
Synapse.
Presynaptic cell in close contact with the target postsynaptic cell.
Small space between cells is called the synaptic cleft.
Transmission is either electrical or chemical.
Chemical synapses operate by release of neurotransmitter (NT).
Transmission is only in one direction pre -> post.
Calcium is the signal for NT release at the synapse.
Excitory Synapses.
Ligand-gated postsynaptic ion channel opens.
Increased permeability for Na+ and K+ ions.
Much more Na+ ions than K+ ions leave.
Depolarization brings post synaptic membrane potential closer to threshold for AP
generation.
Inhibitory Synapses.
Ligand-gated postsynaptic ion channels open.
Increased permeability for K+ and Cl- ions.
Cl- ions enter, and some K+ ions leave.
Hyperpolarization drives postsynaptic membrane potential away from the threshold for AP
generation.
Transmitter Lifecycle.
Acetylcholine (ACh) (nicotinic receptors).
Release leads to excitation in postsynaptic membranes.
ACh opens specific ligand gated channels and sodium influx (depolarization).
ACh is degraded and chlorine fragments taken up again into synapse for reuse in transmitter
synthesis.
Turning Chemical Signal On.
Release of transmitter into synaptic cleft in response to AP.
Transmitter binds to receptor channels.
Receptor channels open for specific ions.
Turning Chemical Signal Off.
Released transmitter continuously removed from the synaptic cleft.