Abstract
Over the past thirty years, a wide variety of chemical transmitter actions on post-synaptic membrane conductances have been identified in nerve and muscle cells. In most transmitter actions that have been studied so far, including that of acetylcholine at the motor end plate, the binding of transmitter leads directly to the opening of an ion channel which is tightly coupled to the receptor, thereby producing the observed postsynaptic potential (psp) (Adams, 1981; Karlin, 1980; see also Chapter 16). Recently, a second class of transmitter actions has been delineated in which the transmitter receptor is not directly coupled to an ion channel. For many of these transmitter effects, the intracellular second messenger cyclic AMP is thought to provide the link between the binding reaction and the change in channel gating (Kandel and Schwartz, 1982; Greengard, 1976; Kupferman, 1980). According to a hypothesis first proposed by Greengard (1981), the binding of transmitter activates a membrane-bound adenylate cyclase, which elevates the intracellular level of cyclic AMP. The increase in cyclic AMP leads to activation of a cyclic-AMP-dependent protein kinase, which then phosphorylates some as yet unidentified protein, which results in a change in the ionic conductance (see Kandel and Schwartz, 1982; Greengard, 1981).
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Camardo, J.S., Siegelbaum, S.A. (1983). Single-Channel Analysis in Aplysia Neurons A Specific K+ Channel Is Modulated by Serotonin and Cyclic AMP. In: Sakmann, B., Neher, E. (eds) Single-Channel Recording. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-7858-1_21
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DOI: https://doi.org/10.1007/978-1-4615-7858-1_21
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