Pharmacological sensitivities of two afterhyperpolarizations in rat optic nerve

Optic nerves were removed from 4-8-week-old rats and studied in a modified sucrose gap chamber in order to examine the pharmacological sensitivities of two afterhyperpolarizations (AHPs), an early and a late one. The peak latency of the early AHP, which occurred immediately after the action potential, was 6-12 ms, and its duration was 44-75 ms. The early AHP was present at resting potential in about 75% of recorded nerves. In the nerves in which an early AHP was not present at resting potential, an AHP was present during delivery of constant current depolarization through the sucrose gap. The early AHP was increased in amplitude by depolarization of the nerve, decreased in amplitude or reversed in polarity by hyperpolarization, was not affected by tetraethylammonium (TEA) or Co2+, and was obliterated by 4-aminopyridine (4-AP) concomitant with action potential broadening. The late AHP followed a broadened action potential in the presence of the potassium channel blocker 4-AP. Its peak latency ranged from 112 to 254 ms and its duration from 336 to 710 ms. It was increased in amplitude with repetitive stimulation, was reversibly obliterated by TEA, but was not significantly altered by Co2+, Cd2+, Ca2+ removal, charybdotoxin or apamin. The results demonstrate the presence of two AHPs mediated by pharmacologically distinct potassium conductances in rat optic nerve, neither of which is calcium-dependent.