Electrophysiological roles of L-type channels in different classes of guinea pig sympathetic neuron

The electrophysiological consequences of blocking Ca2+ entry through L-type Ca2+ channels have been examined in ph as:ic (Ph), tonic (T), and long-aft erhyperpolarizing (LAH) neurons of intact guinea pig sympathetic ganglia is olated in vitro. Block of Ca2+ entry with Co2+ Or Cd2+ depolarized T and LA H neurons, reduced action potential (AP) amplitude in Ph and LAH neurons, a nd increased AP half-width in Ph neurons. The afterhyperpolarization (AHP) and underlying Ca2+-dependent K+ conductances (gKCa1 and gKCa2) were reduce d markedly in all classes. Addition of 10 mu M nifedipine increased input r esistance in LAH neurons, raised AP threshold in Ph and LAH neurons, and ca used 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 a ll classes; the slower conductance, gKCa2, which underlies the prolonged AH P in LAH neurons, was reduced by 40%. Surprisingly, AHP half-width was leng thened by nifedipine in a proportion of neurons in all classes; despite thi s, neuron excitability was increased during a maintained depolarization. Ni fedipine'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 mod ify transient outward currents of the A or D types. The effects of 100 mu M Ni2+ differed from those of nifedipine. Thus in Ph neurons, Ca2+ entry thr ough L-type channels during a single action potential contributes to activa tion of K+ conductances involved in both the AP and AHP, whereas in T and L AH 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 whi ch L-type channels are selectively coupled to SK channels. We conclude that the sources of Ca2+ for activating the various Ca2+-activated K+ conductan ces are distinct in different types of neuron.