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McGill University
PHGY 313
Sebastien Breau

 Neurotransmitter Release o Neurotransmitter release is triggered by the arrival of an action potential in the axon terminal o The depolarization of the terminal membrane causes voltage-gated calcium channels in the active zones to open.  These membrane channels are very simi2+r to the sodium channels o There is a large inward driving force on Ca o The resulting elevation in [Ca ]Iis the signal that causes neurotransmitter to be released from synaptic vesicles o The vesicle releases their contents by a process called exocytosis. o The membrane of the synaptic vesicle fuses to the presynaptic membrane at the active zone, allowing the contents of the vesicle to spill out into the synaptic cleft (See Fig. 5.11.). o Exocytosis is quick because Ca 2+enters at the active zone, precisely where synaptic vesicles are ready and waiting to release their contents 2+ o The precise mechanism by which [Ca ] stimIlates exocytosis is poor understood o The speed of neurotransmitter release suggests that the vesicles involved are those at ready “docked” at the active zones.  Docking is believed to involved interactions between proteins in the synaptic vesicle membrane and the active zone 2+  In the presence of high [Ca ], Ihese proteins alter their conformation so that the lipid bilayers of the vesicle and presynaptic membranes fuse, forming a pore that allows the neurotransmitter to escape into the cleft.  The mouth of this exocytotic fusion pore continues to expand until the membrane of the vesicle is fully incorporated into the presynaptic membrane  The vesicle membrane is later recovered by the process of endocytosis and the recycle vesicle is refilled with neurotransmitter o During periods of prolonged stimulation, vesicles are mobilized from a “reserve pool” that is bound to the cytoskeletons of the axon terminal  The release of these vesicles from the cytoskeleton, and their docking to the active zone, is also triggered by elevations of [Ca ].i o Secretory Granules also release peptide neurotransmitters by exocytosis, in a calcium –dependent fashion, but not at the active zones 2+  Because the sites of granule exocytosis occur at a distance from the sites of Ca entry, peptide neurotransmitters are usually not released in response to every action potential invading the terminal.  Release 2+ peptides generally requires high-frequency trains of action potentials, so that the [Ca ] Ihroughout the terminal can build to the level required to trigger release away from the active zones  Neurotransmitter Receptors and Effectors o Transmitter-Gated Ion Channels  Receptors known as transmitter-gated ion channels are membrane-spanning proteins consisting of four or five subunits that come together to form a pore between them.  In the absence of neurotransmitter, the pore is usually closed.  When neurotransmitter binds to specific sites on the extracellular region of the channel, it induces a conformational change which opens the pore.  Transmitter-gated channels generally do not show the same degree of ion selectivity as do voltage-gated channels (e.g. Ach-gated ion channels are permeable to both Na ions and K ions).  As a rule, if the open channels are permeable to Na , the net effect will be to depolarize the postsynaptic cell from the resting membrane potential.  Since it tends to bring the membrane potential towards threshold for generating action potentials, this effect is said to be excitatory.  Transient postsynaptic membrane depolarization caused by the presynaptic release of neurotransmitter is called an excitatory postsynaptic potential (EPSP) (Fig. 5.14.).  Synaptic activation of Ach-gated and glutamate-g-ted ion channels causes EPSP’s.  If the transmitted gated channels are permeable to Cl , the net effect will be to hyperpolarize the postsynaptic cell from the resting membrane potential  Since it brings the membrane potential away from threshold for generating action potentials, this effect is said to be inhibitory.  A transient hyperpolarization of the postsynaptic membrane potential caused by the presynaptic release of neurotransmitter is called an inhibitory postsynaptic potential (IPSP) (Fig. 5.15).  Synaptic activation of glycine-gated or GABA-gated ion channels causes an IPSP. o G-Protein-Coupled Rece
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