Acetylcholine quantal release

Misler S, Falke LC (1987) Dependence on multivalent cations of quantal release of transmitter induced by black widow spider venom. Am J Physiol 253 C469-76 Misler S, Hurlbut WP (1979) Action of black widow spider venom on quantized release of acetylcholine at the frog neuromuscular junction dependence upon external Mg2+. Proc Nad Acad Sci U S A 76 991-5... 

Sket, D., Dettham, W-D., Clinton, M.E., Sketelj, J., Cucek, D., Brzin, M. (1991a). Prevention of diisopropylphosphoro-fluoridate-induced myopathy hy hotulinum toxin type A blockage of quantal release of acetylcholine. Acta Neuro-pathol. 82 134 2. 

Levesque PC, Atchison WD. 1987. Interactions of mitochondrial inhibitors with methylmercury on spontaneous quantal release of acetylcholine. Toxicol Appl Pharmacol 87 315-324. 

Release. It is presently believed that a neurotransmitter is released during the exocytotic process from the presynaptic membrane in discrete quanta, or finite amounts these quanta are released spontaneously in nerves at rest at the rate of approximately one or two per second. Excited nerves increase the quantal release of transmitter by about fivefold. It has been estimated that at the neuromuscular junction each quantum contains about 10 molecules (0.166 X 10 mol) of the transmitter acetylcholine. It is also established that neurotransmitters such as acetylcholine can passively diffuse across the cell membrane by mechanisms unrelated to exocytosis. The number of moles of transmitter per quantal release for neurotransmitters in the central nervous system has not been accurately quantified. 

One of the clinical signs associated with MeHg intoxication is a myasthenia gravis-like muscle weakness in adults (Rustam et al. 1975), a syndrome which responded well to therapy with neostigmine, a reversible acetylcholinesterase inhibitor. In this syndrome, two effects of MeHg on synaptic transmission at the neuromuscular junction were demonstrated using intracellular microelectrode recording techniques (Atchison and Narahashi 1982 Atchison et al. 1984). First, nerve-evoked, synchronous quantal release of acetylcholine (ACh) is inhibited, as indicated by a decrease in end-plate potential (EPP) amplitude. Second, spontaneous quantal release... 

Chemical transmission between nerve cells involves multiple steps 167 Neurotransmitter release is a highly specialized form of the secretory process that occurs in virtually all eukaryotic cells 168 A variety of methods have been developed to study exocytosis 169 The neuromuscular junction is a well defined structure that mediates the presynaptic release and postsynaptic effects of acetylcholine 170 Quantal analysis defines the mechanism of release as exocytosis 172 Ca2+ is necessary for transmission at the neuromuscular junction and other synapses and plays a special role in exocytosis 174 Presynaptic events during synaptic transmission are rapid, dynamic and interconnected 175... 

Van der Kloot, W. and Molgo, J. Quantal acetylcholine release at the vertebrate neuromuscular junction. Physiol. Rev. 74 898-991,1994. 

Neuromuscular transmission involves the events leading from the liberation of acetylcholine (ACh) at the motor nerve terminal to the generation of end plate currents (EPCs) at the postjunctional site. Release of ACh is initiated by membrane depolarization and influx of Ca++ at the nerve terminal (Fig. 28.1). This leads to a complex process involving docking and fusion of synaptic vesicles with active sites at the presynaptic membrane. Because ACh is released by exocytosis, functional transmitter release takes place in a quantal fashion. Each quantum corresponds to the contents of one synaptic vesicle (about 10,000 ACh molecules), and about 200 quanta are released with each nerve action potential. 

Scholz KP, Miller RJ (1992) Inhibition of quantal transmitter release in the absence of calcium influx by a G protein-linked adenosine receptor at hippocampal synapses. Neuron 8 1139-50 Seddik R, Schlichter R, Trouslard J (2006) Modulation of GABAergic synaptic transmission by terminal nicotinic acetylcholine receptors in the central autonomic nucleus of the neonatal rat spinal cord. Neuropharmacology 51 77... 

The nerve fibers in the cochlea can be classified as afferent fibers (toward the brain) or efferent fibers (toward the periphery). The afferent fibers that terminate on IHCs constitute approximately 90-95% of all afferent fibers in the cochlea. These afferent fibers originate from type I ganglion cells and are coated with a thick myelin sheath. Each fiber is connected to only one IHC, but each IHC is innervated by 2-10 individual afferent fibers. The principal neurotransmitter released by IHCs, glutamate, activates the afferent fibers in a quantal manner. The remaining 5-10% of afferent fibers are connected to OHCs and are unmyelinated. They originate from type II ganglion cells. Each afferent fiber is highly branched and is connected to 6-100 OHCs. OHCs are innervated mainly by efferent fibers, which are derived from the medial olivocochlear bundle. Efferent fibers release acetylcholine (ACh) as their principal neurotransmitter. Each OHC is in contact with 2-5 efferent synaptic boutons at its base. IHCs receive axodendritic efferent innervation onto afferent fibers from the lateral olivocochlear bundle (reviewed by Raphael and Altschuler, 2003). 

The nature of the feedback inhibitory signal has yet to be elucidated. IGF-II mRNA content is very low in mature innervated muscle. Both quantal and non-quantal leakage release of acetylcholine (Katz and Miledi, 1977) may help suppress IGF-II gene expression. On the other hand, other events, such as those associated with muscle contraction, might produce an inhibitory signal. 

Girard, E. et al., Gambierol markedly enhances evoked quantal acetylcholine release from motor nerve terminals at vertebrate skeletal neuromuscular junctions, in 15th World Congress on Animal, Plant and Microbial Toxins, 1ST, Eds., International Society on Toxinology, Glasgow, Scotland, 2006. 

Cholinergic neurons. Neurons in which choline acetyltransferase synthesizes acetylcholine, accumulates it in synaptic vesicles and releases it, upon depolarization, in the quantal mode. Those neurons located in the septal/ subcortical and cortical regions of the brain are responsible for cognitive and memory functions. Cholinergic motor neurons of anterior horns of medulla oblongata form neuro-muscular synapses responsible for voluntary movements of striated muscles. 

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