Neurotransmitters release mechanisms

With TMS, a brief but powerful electric current is passed through a small coil held against the scalp of a conscious patient. This generates a powerful local magnetic field which passes unimpeded through the skull and induces a weaker, less focused electric current within the brain. Due to the non-invasive nature of this method, the important physiological effects of TMS are likely to be a consequence of the density of the electric current and the electric field which is induced in the cortex. It is believed that the induced electrical fields cause neuronal depolarization which changes the neurotransmitter release mechanisms. 

Neuyen VH, Ingram SL, Kassiou M, Christie MJ (1998) cr-Binding site ligands inhibit K currents in rat locus coeruleus neurons in vitro, Eur J Pharmacol 361 157-163 NichoUs DG, Sanchez-Prieto J (1998) Neurotransmitter release mechanism. In Anne Stephenson F, Turner AJ (eds) Frontiers in neurobiology 3 Amino acid neurotransmission, Portland Press, London, pp 1-24... 

Dunant, Y (1994) Hormone and neurotransmitters release four mechanisms of secretion. Cell Biol. Int. 18 327-336. 

Greengard, P, Benfenati, F and Valtorta, F (1994) Synapsin I, an active-binding protein regulating synaptic vesicle traffic in the nerve terminal. In Molecular and Cellular Mechanisms of Neurotransmitter Release (Eds Starjne, L, Greengard, P, Grillner, S, Hokfelt, T and Ottoson, D), Raven Press, New York, pp. 31 5. 

Sihra, TS and Nichols, RA (1993) Mechanisms in the regulation of neurotransmitter release from brain nerve terminals current hypothesis. Neurochem. Res. 18 37-58. 

Sulzer, D., Sonders, M.S., Poulsen, N.W., Galli, A. Mechanisms of neurotransmitter release by amphetamines a review. Prog. Neurobiol. 75 406, 2005. 

Steinhardt, R.A., Bi, G. and Alderton, J.M. (1994) Cell membrane resealing by a vesicular mechanism similar to neurotransmitter release. Science 263, 390-393. 

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... 

The exact mechanisms by which BDNF enhances the induction of LTP remain obscure. Nevertheless, both pre-and postsynaptic mechanisms appear to be possible. As mentioned above, BDNF elevates presynaptic cytosolic calcium level and thus increases vesicular neurotransmitter release. When a postsynaptic neuron is injected with a Trk tyrosine kinase inhibitor (K252a), BDNF-augmented LTP is curtailed this suggests that a postsynaptic mechanism is adopted by BDNF in the manifestation of LTP. It has been postulated that neurotrophins may act as... 

A second type of NMDA-receptor-independent LTP exists in the mossy-fiber pathway at the dentate granule cell-to-CA3 pyramidal cell synapse [19]. This form of LTP, termed mossy fiber-CA3 LTP, is believed to involve PKA activation in the presynaptic cell which leads to increased neurotransmitter release. However, the exact induction mechanism is not yet clear. 

Penile erection occurs by relaxation of the smooth muscle of the corpus cavernosum, increasing blood flow into the penis and producing erection and rigidity. In a parallel fashion, vaginal pressure stimulation increases blood velocity and flow into clitoral arteries (Lavoisier et al. 1995). Cavernosal vasodilation is accomplished by neurotransmitters released from the cavernosal nerve and endothelial cells. One of the most important transmitters in this cascade is nitric oxide (NO), which induces synthesis of cyclic GMP from guanylate cyclase (Rajfer et al. 1992). Thus, ginkgo s vascular mechanisms could be responsible for some of the putative sexual effects. 

In addition to the physiological process of autoinhibition, another mechanism of presynaptic inhibition has been identified in the peripheral nervous system, although its precise relevance to the brain is unclear. In the dorsal horn of the spinal cord, for example, the axon terminal of a local neuron makes axo-axonal contact with a primary afferent excitatory input, which leads to a reduction in the neurotransmitter released. This is due to the local neuron partly depolarizing the nerve terminal, so that when the axon potential arrives, the change induced is diminished, thereby leading to a smaller quantity of transmitter being released. In the brain, it is possible that GABA can cause presynaptic inhibition in this way. 

C. The purpose of this question is to clarify the cellular mechanism of analgesia produced by morphine. First, morphine blocks the transmission of nociceptive impulses. In that case, the relevant question is how nociceptive impulses are transmitted via the release of pronociceptive neurotransmitters. The question then is to determine which intracellular process favors a block of release of neurotransmitters. The correct answer is C because calcium is required for neurotransmitter release. Blocking potassium efflux and increasing calcium channel phosphorylation produce functional depolarization and neurotransmitter release. Opioids are coupled to Gj (inhibitory proteins) that decrease cAMP. 

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