The Journal of Neurophysiology Vol. 82 No. 2 August 1999, pp. 818-828
Copyright ©1999 by the American Physiological Society

Electrophysiological Roles of L-Type Channels in Different Classes of Guinea Pig Sympathetic Neuron

Prince of Wales Medical Research Institute, University of New South Wales, Randwick, New South Wales 2031, Australia

Davies, Philip J., David R. Ireland, Juan Martinez-Pinna, and Elspeth M. McLachlan. Electrophysiological Roles of L-Type Channels in Different Classes of Guinea Pig Sympathetic Neuron. J. Neurophysiol. 82: 818-828, 1999. The electrophysiological consequences of blocking Ca²⁺ entry through L-type Ca²⁺ channels have been examined in phasic (Ph), tonic (T), and long-afterhyperpolarizing (LAH) neurons of intact guinea pig sympathetic ganglia isolated in vitro. Block of Ca²⁺ entry with Co²⁺ or Cd²⁺ depolarized T and LAH neurons, reduced action potential (AP) amplitude in Ph and LAH neurons, and increased AP half-width in Ph neurons. The afterhyperpolarization (AHP) and underlying Ca²⁺-dependent K⁺ conductances (gKCa1 and gKCa2) were reduced markedly in all classes. Addition of 10 µM nifedipine increased input resistance in LAH neurons, raised AP threshold in Ph and LAH neurons, and caused a small increase in AP half-width in Ph neurons. AHP amplitude and the amplitude and decay time constant of gKCa1 were reduced by nifedipine in all classes; the slower conductance, gKCa2, which underlies the prolonged AHP in LAH neurons, was reduced by 40%. Surprisingly, AHP half-width was lengthened by nifedipine in a proportion of neurons in all classes; despite this, neuron excitability was increased during a maintained depolarization. Nifedipine's effects on AHP half-width were not mimicked by 2 mM Cs⁺ or 2 mM anthracene-9-carboxylic acid, a blocker of Cl channels, and it did not modify transient outward currents of the A or D types. The effects of 100 µM Ni²⁺ differed from those of nifedipine. Thus in Ph neurons, Ca²⁺ entry through L-type channels during a single action potential contributes to activation of K⁺ conductances involved in both the AP and AHP, whereas in T and LAH neurons, it acts only on gKCa1 and gKCa2. These results differ from the results in rat superior cervical ganglion neurons, in which L-type channels are selectively coupled to BK channels, and in hippocampal neurons, in which L-type channels are selectively coupled to SK channels. We conclude that the sources of Ca²⁺ for activating the various Ca²⁺-activated K⁺ conductances are distinct in different types of neuron.