Functions synaptic vesicle release

Neurons constitute the most striking example of membrane polarization. A single neuron typically maintains thousands of discrete, functional microdomains, each with a distinctive protein complement, location and lifetime. Synaptic terminals are highly specialized for the vesicle cycling that underlies neurotransmitter release and neurotrophin uptake. The intracellular trafficking of a specialized type of transport vesicles in the presynaptic terminal, known as synaptic vesicles, underlies the ability of neurons to receive, process and transmit information. The axonal plasma membrane is specialized for transmission of the action potential, whereas the plasma... 

Specific membrane components must be delivered to their sites of utilization and not left at inappropriate sites [3]. Synaptic vesicles and other materials needed for neurotransmitter release should go to presynaptic terminals because they serve no function in an axon or cell body. The problem is compounded because many presynaptic terminals are not at the end of an axon. Often, numerous terminals occur sequentially along a single axon, making en passant contacts with multiple targets. Thus, synaptic vesicles cannot merely move to the end of axonal MTs. Targeting of synaptic vesicles thus becomes a more complex problem. Similar complexities arise with membrane proteins destined for the axolemma or a nodal membrane. 

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. 

Neurons synthesize acetylcholine from choline, which is obtained from the diet, and from acetyl groups that originate in mitochondria from the metabolism of sugar. Here is yet another example of the importance of sugar for your brain s normal function. The synthesis of acetylcholine occurs within the cytoplasm of your neurons, and the product is stored in synaptic vesicles, those small round packets that neurons release to communicate with each other. Neurons pay a lot of attention to the shelf life of their neurotransmitters they prefer to release the most recently produced neurotransmitter molecules first. As you can see, neurons do not behave like your local grocer they do... 

Rizo J, Chen X, Arac D (2006) Unraveling the mechanisms of synaptotagmin and SNARE function in neurotransmitter release. Trends Cell Biol 16 339-50 Rizo J, Sudhof TC (2002) Snares and Muncl8 in synaptic vesicle fusion. Nat Rev Neurosci 3 641-53... 

Aristotle (350 B.C.) History of Animals. In Barnes J (ed) The complete works of Aristotle The revised Oxford translation, 1984, Princeton, Princeton University Press Ashton AC, Rahman MA, Volynski KE et al (2000) Tetramerisation of a-latrotoxin by divalent cations is responsible for toxin-induced non-vesicular release and contributes to the Ca2+-dependent vesicular exocytosis from synaptosomes. Biochimie 82 453-68 Ashton AC, Volynski KE, Lelianova VG et al (2001) a-Latrotoxin, acting via two Ca2+-dependent pathways, triggers exocytosis of two pools of synaptic vesicles. J Biol Chem 276 44695-703 Auger C, Marty A (1997) Heterogeneity of functional synaptic parameters among single release sites. Neuron 19 139-50... 

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