Intracellular recordings were obtained in vitro from oxytocin and vasopressin neurones from dioestrous and lactating female rats. Oxytocin neurones were characterized under current clamp by the expression of a depolarization-activated, sustained outward rectification (SOR) and a rebound depolarization (RD). 2. An increment in extracellular K+ shifted the expression of the SOR and RD towards a more depolarized membrane potential, indicating that the mechanisms underlying these events are dependent on extracellular potassium. 3. The SOR and RD were blocked by external tetraethylammonium (10 mM) and Ba2+ (0.1-0.5 mM). Cs+ (2 mM) blocked the hyperpolarization-activated inward rectification without affecting the expression of the SOR and RD. 4. The SOR was not affected by 4-aminopyridine (6 mM). However, the rebound amplitude was significantly enhanced, indicating that the activation of a transient outward current interacts with the expression of the rebound. 5. Iberiotoxin (100 nM) and apamin (50 nM), toxins known to block some calcium-dependent potassium conductances, did not affect the expression of the SOR and RD. 6. The SOR and RD were significantly reduced by Cd2+ (0.5 mM) but not by Ni2+ (0.25 mM). 7. Muscarine (10 microM) did not affect the SOR or the RD. 8. These results indicate that the SOR and RD depend upon a depolarization-activated, sustained outward potassium current, which might be calcium dependent. A current with these characteristics has never been described before in the magnocellular system. Voltage-clamp experiments are needed to completely characterize this potassium conductance selectively expressed by oxytocin neurones.
