schneideri poison extract might be resulted in enhanced neurotransmitter release
elicited by a mechanism involving inhibitory effect on [Na.sup.+]-[K.sub.+]-ATPase pump (Rostelato-Ferreira et al., 2014).
The coupling between synaptic vesicles and ca2+ channels determines fast neurotransmitter release
. Neuron 2007;53:563-75.
These were (1) SNAP-23, the closest homolog of SNAP-25, which may be the substitution for SNAP-25 to mediate synaptic vesicle fusion ; (2) mammalian uncoordinated-18 (Munc-18), which has been found to have dual binding ability to syntaxin-1 and Vamp2, classified as the fourth crucial member of SNARE-pin assembly and may be another alternative for mediating neurotransmitter release
[27, 28]; and (3) as the synaptic vesicle [Ca.sup.2+] sensor, synaptotagmin-1 could be phosphorylated with calcium influx and trigger the synaptic release subsequently.
from a single vesicle activates a small postsynaptic voltage change and comprises the elementary unit of synaptic communication, and vesicle fusion is triggered by calcium entry through presynaptic VGCCs or may occur spontaneously in the absence of an action potential activity.
In the first section, we develop a model to explain a mechanism of neurotransmitter release
from the presynaptic cell caused by the external activities.
Cdk5/p35 also was indicated inhibits neurotransmitter release
through the phosphorylation of P/Q-type voltage-dependent Ca2+ channel and down-regulation of the channel activity (Tomizawa et al., 2002).
Subcellular localization suggested a possible role for synapsin III in the regulation of neurotransmitter release
and synaptogenesis (14,15).
It is thought that G[alpha]o modulates calcium channels and inhibits presynaptic neurotransmitter release
. G[alpha]i2, in contrast, is believed to primarily regulate potassium currents which occur both pre- and post-synaptically.
Recent research demonstrated that the hydroxylated metabolite 6-OH-BDE-47 increases neurotransmitter release
by releasing calcium ions ([Ca.sup.2+]) from intracellular stores at much lower concentrations than its environmentally relevant parent congener BDE-47.
PKC plays major roles in the regulation of neuronal excitability, neuroplasticity, and neurotransmitter release
. The long-established antimanic agents, lithium and valproate, both inhibit PKC function even though they are structurally very dissimilar.
Molecular mechanisms of neurotransmitter release
. (CD-ROM included)
When activated, these receptors inhibit neurotransmitter release
via mechanisms that involve inhibition of voltage-gated calcium channels whose function is necessary for proper release.