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Presynaptic Modulation of Peripheral Nitrergic Neurotransmission

  • Chapter
Nitric Oxide and Free Radicals in Peripheral Neurotransmission

Part of the book series: Nitric Oxide in Biology and Medicine ((NOBM,volume 2))

  • 63 Accesses

Abstract

Through the work of authors such as K. Starke and S. Langer, the concept of presynaptic modulation of the release of classic neurotransmitters such as noradrenaline, acetylcholine, and dopamine has developed (Langer, 1981,Starke, 1981,Starke et al., 1989). In both the central and peripheral nervous system, the release of these neurotransmitters can, indeed, be regulated via presynaptic receptors on the axon terminals. Modulation can be exerted by the neuron’s own neurotransmitter via presynaptic autoreceptors or by other neurotransmitters or locally produced substances via presynaptic heteroreceptors. In general, stimulation of presynaptic receptors will lead to inhibition of transmitter release; via presynaptic autoreceptors the transmitter is thus able to exert negative feedback on the axon terminals from which it is released. Presynaptic facilitation has also been described, such as via presynaptic [3-receptors on peripheral noradrenergic nerve endings. Classic neurotransmitters are stored in vesicles in the axon terminals, and when the terminals are depolarized by an action potential, an influx of calcium through voltage-gated calcium channels will occur, which is the trigger for the process of exocytosis of the vesicles and the release of neurotransmitter into the synaptic cleft. The calcium channels and the release mechanism must be localized close to each other and might be part of a multimolecular entity (Stanley, 1997). The principal mechanism by which presynaptic receptors inhibit neurotransmitter release is through inhibition, often via a G protein, of the voltage-gated calcium channels, leading to a decrease in electrosecretory coupling (Starke et al., 1989,Stjarne, 1989). The inverse relation between the intensity of nerve activation and the effectiveness of presynaptic receptors to inhibit transmitter release might be due to the increasing intracellular calcium concentration upon high stimulation intensity (Duckles and Budai, 1990).

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Authors
  1. R. A. Lefebvre
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Editors and Affiliations

  1. Department of Physiology and Pharmacology The Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, NY, 10031, USA

    Stanley Kalsner Ph.D.

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Lefebvre, R.A. (2000). Presynaptic Modulation of Peripheral Nitrergic Neurotransmission. In: Kalsner, S. (eds) Nitric Oxide and Free Radicals in Peripheral Neurotransmission. Nitric Oxide in Biology and Medicine, vol 2. Birkhäuser, Boston, MA. https://doi.org/10.1007/978-1-4612-1328-4_10

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  • DOI: https://doi.org/10.1007/978-1-4612-1328-4_10

  • Publisher Name: Birkhäuser, Boston, MA

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