Calcium-Activated Potassium Channels in Presynaptic Nerve Terminals

  • D. K. Bartschat
  • M. P. Blaustein
Part of the Topics in the Neurosciences book series (TNSC, volume 1)


In their classical study of excitability in squid axons, Hodgkin and Huxley (cf. Hodgkin, 1967) showed that the nerve action potential could be explained by selective, transient sodium (Na) and potassium (K) conductance changes that were explicitly described by sets of voltage- and time-dependent parameters. Subsequent work on a wide variety of excitable cells has revealed that, in contrast to Na conductances, a number of K conductances do not conform to the simple voltage- and time-dependent mechanism that occurs in squid axons. For example, in many types of cells, some K conductances are activated by a rise in the calcium (Ca) activity in the cytoplasm (cf. Meech, 1978). Also, in some cells, K conductances may be modulated by intracellular cyclic nucleo- tides, for example, as a consequence of neurotransmitter action (Castelluci et al., 1980; De Peyer et al., 1982). Klein and Kandel (1980) have demonstrated that inactivation of a specific K conductance, due to transmitter action on presynaptic neurons in Aplvsia. may have profound behavioral effects. In addition, it has been suggested that the complex schizophrenia-like syndrome elicited by phencyclidine intoxication in man and animals may involve block of a specific class of presynaptic K channels in the central nervous system (CNS) (Albuquerque et al., 1981; Bartschat and Blaustein, 1984c).


Excitable Cell Mammalian Central Nervous System Quinine Sulfate Presynaptic Nerve Terminal Squid Axon 
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Copyright information

© Martinus Nijhoff Publishing, Boston 1986

Authors and Affiliations

  • D. K. Bartschat
    • 1
  • M. P. Blaustein
    • 1
  1. 1.Department of PhysiologyUniversity of Maryland School of MedicineBaltimoreUSA

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