Modulation of a Specific Potassium Channel in Sensory Neurons of Aplysia by Serotonin and cAMP-dependent Protein Phosphorylation

  1. J.S. Camardo,
  2. M.J. Shuster,
  3. S.A. Siegelbaum, and
  4. E.R. Kandel
  1. Center for Neurobiology and Behavior, Columbia University, College of Physicians and Surgeons and The New York State Psychiatric Institute, New York, New York 10032

This extract was created in the absence of an abstract.

Excerpt

One of the important developments in the study of synaptic transmission has been the discovery that neurotransmitters produce a wide range of electrical signals by interacting with different types of ionic channels. Since 1950, it has been well established that chemical transmitters elicit short-lived postsynaptic potentials, such as the end-plate potential produced by acetylcholine (ACh) in skeletal muscle (Katz 1966; Sakmann et al., this volume). Here, ACh activates a channel that opens only in the presence of the transmitter and therefore does not normally contribute to the resting or active electrical properties of the cell (Neher and Sakmann 1976). Recently, however, transmitters have been found to exert long-lasting effects on some neurons by modulating channels that contribute to the resting potential, the action potential, or the passive membrane properties (for review, see Kehoe and Marty 1980; Siegelbaum and Tsien 1983). Modulation of these channels can dramatically change the electrophysiological behavior...

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