CALCIUM-DEPENDENT CHLORIDE CURRENT-INDUCED BY AXOTOMY IN RAT SYMPATHETIC NEURONS

1. Seven to ten days after sectioning their axons, rat sympathetic neu rons were studied using intracellular recording techniques in an in vi tro preparation of the superior cervical ganglion. 2. In 75% of axotom ized cells, an after-depolarization (ADP) was observed following spike firing or depolarization with intracellular current pulses. Discontin uous single-electrode voltage-clamp techniques were employed to study the ADP. When the membrane potential was clamped at the resting level just after an action potential, a slow inward current was recorded in cells that showed an ADP. 3. In the presence of TTX and TEA, inward pe aks and outward currents were recorded during depolarizing voltage jum ps, followed by slowly decaying inward tail currents accompanied by la rge increases in membrane conductance. The inward peak and tail curren ts activated between -10 and -20 mV and reached maximum amplitudes aro und 0 mV. With depolarizing jumps to between +40 and +50 mV, net outwa rd currents were recorded during the depolarizing jumps but inward tai l currents were still activated. 4. In the presence of the Ca2+ channe l blocker cadmium, or when Ca2+ was substituted by Mg2+, the ADP disap peared. In voltage-clamped cells, cadmium blocked the inward tail curr ents. The reversal potential for the inward tail current was approxima tely -15 mV. Substitution of the extracellular NaCl by sucrose or sodi um isethionate increased the amplitude of the inward tail current, and displaced its equilibrium potential to more positive values. Changes in extracellular [K+] did not appreciably affect the inward tail curre nt amplitude or equilibrium potential. Niflumic acid, a blocker of chl oride channels activated by Ca2+, almost completely blocked the tail c urrent. 5. No ADPs were observed in non-axotomized neurons, and when d epolarizing pulses were applied while in voltage clamp no inward tail currents were evoked in these normal cells. 6. It is concluded that ax otomy of sympathetic ganglion cells produces the appearance of a Ca2+- dependent chloride current responsible for the ADP observed following spike firing.