PHGY 313 Lecture Notes - Inhibitory Postsynaptic Potential, Resting Potential, Porosome
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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 similar to the sodium channels
o There is a large inward driving force on Ca2+
o The resulting elevation in [Ca2+]I is the signal that causes neurotransmitter to be released from synaptic
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 Ca2+ enters at the active zone, precisely where synaptic vesicles are ready
and waiting to release their contents
o The precise mechanism by which [Ca2+]I stimulates 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
In the presence of high [Ca2+]I, these 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 [Ca2+]i.
o Secretory Granules also release peptide neurotransmitters by exocytosis, in a calcium –dependent
fashion, but not at the active zones
Because the sites of granule exocytosis occur at a distance from the sites of Ca2+ entry, peptide
neurotransmitters are usually not released in response to every action potential invading the
Release of peptides generally requires high-frequency trains of action potentials, so that
the [Ca2+]I throughout 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-gated 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