Abstract
Ca2+ is an important mediator of molecular events in the functioning nerve terminal (1, 2). An increase in cytoplasmic Ca2+ has been shown to regulate a variety of neuronal cell functions, including neurotransmitter release, stimulation of protein phosphorylation, and synaptic morphological changes (3). It is well-established that these events are directly dependent on the entry of extracellular Ca2+ into the presynaptic nerve terminal through specific voltage-gated Ca2+ channels (4,6). The central role of Ca2+ channels in stimulus-secretion coupling mechanisms has led to the extensive investigation of Ca2+ channel function in a wide variety of intact and broken cell preparations (7). Despite extensive electrophysiological characterization of Ca2+ channels in brain, the molecular nature and pharmacological characteristics of this major neuronal Ca2+ channel remain largely unclear.
Keywords
- Neurotransmitter Release
- Presynaptic Nerve Terminal
- Neuronal Cell Function
- Intact Synaptosome
- Break Cell Preparation
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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© 1986 Martinus Nijhoff Publishing, Boston
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DeLorenzo, R.J., Taft, W.C., Andrews, W.T. (1986). Regulation of Voltage-Sensitive Calcium Channels in Brain by Micromolar Affinity Benzodiazepine Receptors. In: Rahamimoff, R., Katz, B. (eds) Calcium, Neuronal Function and Transmitter Release. Topics in the Neurosciences, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2307-5_24
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DOI: https://doi.org/10.1007/978-1-4613-2307-5_24
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