Multitude of ion channels in regulation of transmitter release

Abstract

The presynaptic nerve terminal is of key importance in communication in the nervous system. Its primary role is to release transmitter quanta on the arrival of an appropriate stimulus. The structural basis of these transmitter quanta are the synaptic vesicles that fuse with the surface membrane of the nerve terminal, to release their content of neurotransmitter molecules and other vesicular components. We subdivide the control of quantal release into two major classes: the processes that take place before the fusion of the synaptic vesicle with the surface membrane (the pre-fusion control) and the processes that occur after the fusion of the vesicle (the post-fusion control). The pre-fusion control is the main determinant of transmitter release. It is achieved by a wide variety of cellular components, among them the ion channels. There are reports of several hundred different ion channel molecules at the surface membrane of the nerve terminal, that for convenience can be grouped into eight major categories. They are the voltage-dependent calcium channels, the potassium channels, the calcium-gated potassium channels, the sodium channels, the chloride channels, the non-selective channels, the ligand gated channels and the stretch-activated channels. There are several categories of intracellular channels in the mitochondria, endoplasmic reticulum and the synaptic vesicles. We speculate that the vesicle channels may be of an importance in the post-fusion control of transmitter release.

Isoflurane inhibits synaptic vesicle exocytosis through reduced Ca 2+ influx, not Ca 2+ -exocytosis coupling

“…Hippocampal glutamate and GABA containing SVs differ in their release properties during AP trains as well as in their adaptive response to strong depolarization (29)(30)(31). Different profiles of presynaptic ion channel expression underlie exocytosis in glutamatergic and GABAergic synapses (32)(33)(34). Our findings that greater isoflurane sensitivity of glutamatergic compared with GABAergic SV exocytosis is determined by larger effects on Ca 2+ influx are consistent with transmitter phenotype-specific differences in expression of the presynaptic ion channels that determine [Ca 2+ ] i , including distinct subtypes of Na v , Ca v , and K v channels (35).…”

Rapid change of quantal size in PC-12 cells detected by neural networks

“…Mechanical activity might alter secretion by initiating the activity of mechano-activated ion channels (K + , Ca 2+ , cation), which have been described in various preparations (Ingber, 1997;Patel et al, 2001), and which are involved in regulation of the secretory activity (Rahamimoff et al, 1999). Through such an action, the mechanical activity would directly affect both the amplitude and the shape of Ca 2+ transient (by altering the Ca 2+ entry through Ca 2+ or cationic channels), but also indirectly (by changing K + entry).…”

Biochemical and Physiological Processes in Brain Function and Drug Actions

“…These structures-constructed in the soma and transported along the axons, with their full complement of neurotransmitter-concentrate near the nerve terminal. The vesicular membranes contain many specific protein structures involved in the multiple functions of the storage vesicles (Kelly 1999;Krantz et al 1999;Rahamimoff et al 1999). Vesicular functions include neurotransmitter synthesis, neurotransmitter transport across the vesicular membrane, neurotransmitter binding inside the vesicle, docking proteins for attaching to the neuronal plasma membrane, calcium binding proteins for membrane fusion and neurotransmitter release, and special coating proteins for vesicular endocytosis and recycling processes.…”

“…A major mechanism for calcium entry results from the activation of voltage-gated ion channels located in the plasma membrane (Rahamimoff et al 1999;Zhang and Ramaswami 1999). Of course, the activation of the voltage-gated ion channels depends on many factors, such as the activity of numerous other membrane ion channels (Rahamimoff et al 1999) and a variety of presynaptic ligand-gated ion channels (MacDermott et al 1999) as well as autoreceptors (MacDermott et al 1999).…”

“…A major mechanism for calcium entry results from the activation of voltage-gated ion channels located in the plasma membrane (Rahamimoff et al 1999;Zhang and Ramaswami 1999). Of course, the activation of the voltage-gated ion channels depends on many factors, such as the activity of numerous other membrane ion channels (Rahamimoff et al 1999) and a variety of presynaptic ligand-gated ion channels (MacDermott et al 1999) as well as autoreceptors (MacDermott et al 1999). Given the absolute requirement for Ca ++ in the neurotransmitter release process, it is not surprising that proteins that comprise the voltage-gated calcium channel are intimately bound to specific proteins associated with storage vesicle docking and fusion processes (Catterall 1999).…”