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Presynaptic inhibition of elicited neurotransmitter release

MPG-Autoren
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Wu,  Ling-Gang
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

Externe Ressourcen

http://dx.doi.org/10.1016/S0166-2236(96)01015-6
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http://www.sciencedirect.com/science/article/pii/S0166223696010156/pdfft?md5=32515774ffce1af1a9e673cf9dac6a6e&pid=1-s2.0-S0166223696010156-main.pdf
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Zitation

Wu, L.-G., & Saggau, P. (1997). Presynaptic inhibition of elicited neurotransmitter release. Trends in Neurosciences, 20(5), 204-212. doi:10.1016/S0166-2236(96)01015-6.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0024-CEFF-0
Zusammenfassung
Activation of presynaptic receptors for a variety of neurotransmitters and neuromodulators inhibits transmitter release at many synapses. Such presynaptic inhibition might serve as a means of adjusting synaptic strength or preventing excessive transmitter release, or both. Previous evidence showed that presynaptic modulators inhibit Ca2+ channels and activate K+ channels at neuronal somata. These modulators also inhibit spontaneous transmitter release by mechanisms downstream of Ca2+ entry. The relative contribution of the above mechanisms to the inhibition of elicited release has been debated for a long time. Recent evidence at synapses where the relationship between transmitter release and presynaptic Ca2+ influx has been well characterized suggests that inhibition of presynaptic voltage-dependent Ca2+ channels plays the major role in presynaptic inhibition of elicited neurotransmitter release. In addition, modulation of the release machinery might contribute to inhibition of elicited release