A-CURRENT MODIFIES THE SPIKE OF C-TYPE NEURONS IN THE RABBIT NODOSE GANGLION

1. In the rabbit nodose ganglion, C-type fibre neurones (C neurones) c an be divided into two subtypes according to their after-hyperpolarizi ng potential (AHP) i.e. those with a fast AHP only and those with a fa st AHP and a subsequent slow AHP produced by a slow calcium-dependent potassium current. In addition eve have shown that some C neurones can be divided into two groups according to the effect of membrane hyperp olarization on their spikes i.e. type 1 in which duration and amplitud e do not change and type 2 in which duration and amplitude decrease si gnificantly. 2. In the present report we studied the effect of A-curre nt (I-A) on spike duration, amplitude and slow AHP using intracellular recording techniques. 3. To detect the presence of I-A, we first appl ied a series of increasing rectangular hyperpolarizing pulses to remov e I-A inactivation and then a short depolarizing pulse to trigger a sp ike. In type 1 C neurones the lag time of the spike in relation to hyp erpolarization remains constant whereas in type 2 C neurones the spike only appears after I-A inactivation and lag time in relation to hyper polarization is lengthened. Thus, type 2 C neurones have an I-A while type 1 C neurones do not. The fact that addition of cadmium did not ch ange the lag time in type 2 C neurones shows that the I-A is not calci um dependent. 4. Nodose neurones can be orthodromically activated by s timulation of the vagal peripheral process. In this way, after a hyper polarizing pulse, I-A can be fully activated by the orthodromic spike itself. Under these conditions it is possible to analyse the effects o f I-A on the spike. This was done by increasing either the hyperpolari zing potential, pulse duration, or the delay of the spike after the en d of the pulse. We observed that maximum I-A inactivation removal was always associated with the lowest duration and amplitude of the spike. 5. When I-A inhibitors, 4-aminopyridine (4-AP) or catechol, were appli ed to type 2 C neurones, the delay of the spike after the hyperpolariz ation-depolarization test was no longer observed. In addition 4-AP abo lished the shortening of the duration of the spike induced by steady h yperpolarization. 6. In type 2 C neurones with slow AHP, the I-A-relat ed decrease in spike duration was associated with a disappearence of t he slow AHP. This indicates that I-A decreases the calcium influx duri ng the spike. 7. In conclusion, since I-A regulates the amplitude and duration of the spike in prehyperpolarized cells, it is logical to ass ume that I-A is able to regulate the calcium influx into the cell. If this mechanism occurs at axon terminals, it could interfere with trans mitter release and thus modulate synaptic transmission.