Electrophysiological roles of L-type channels in different classes of guinea pig sympathetic neuron
| Autor: | David R. Ireland, Philip J. Davies, Elspeth M. McLachlan, Juan Martinez-Pinna |
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| Přispěvatelé: | Dirección General de Enseñanza Superior e Investigación Científica (España), National Health and Medical Research Council (Australia) |
| Rok vydání: | 1999 |
| Předmět: |
Male
Potassium Channels Nifedipine Physiology Guinea Pigs Action Potentials Superior Cervical Ganglion Tonic (physiology) Membrane Potentials Guinea pig Species Specificity medicine Animals Neurons Communication Ganglia Sympathetic Chemistry business.industry General Neuroscience Calcium Channel Blockers Rats Electrophysiology medicine.anatomical_structure Female Neuron Calcium Channels business Neuroscience |
| Zdroj: | Journal of neurophysiology. 82(2) |
| ISSN: | 0022-3077 |
| Popis: | The electrophysiological consequences of blocking Ca(2+) entry through L-type Ca(2+) 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 Ca(2+) entry with Co(2+) or Cd(2+) 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 Ca(2+)-dependent K(+) conductances (gKCa1 and gKCa2) were reduced markedly in all classes. Addition of 10 microM 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 microM Ni(2+) differed from those of nifedipine. Thus in Ph neurons, Ca(2+) 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 Ca(2+) for activating the various Ca(2+)-activated K(+) conductances are distinct in different types of neuron. This work was supported by the National Health and Medical ResearchCouncil of Australia. D. R. Ireland holds an Australian Postgraduate Award.J. Martinez-Pinna’s travel was supported by funds from the Direccion Generalde Enseñanza Superior, Spain. |
| Databáze: | OpenAIRE |
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