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We have previously shown that cultured LHRH-1 neurons, derived from monkey olfactory placode region, exhibit pulsatile LHRH-1 release at hourly intervals and spontaneous intracellular calcium, [Ca
2+
]
i
, oscillations, which synchronize at a frequency similar to LHRH-1 release. Brief application of estrogen induced a rapid increase in the frequency of [Ca
2+
]
i
oscillations and the frequency of synchronizations. The estrogen-induced frequency of [Ca
2+
]
i
oscillations was mediated by estrogen receptors (ER), whereas the frequency of synchronizations was not mediated by ER. In the present study we further examined the rapid action of estrogen using patch-clamp recording in primate LHRH-1 neurons. Cell-attached patch-clamp recording showed that LHRH-1 neurons exhibited monophasic or biphasic action currents, which were sensitive to an increase in extracellular K
+
and the sodium channel blocker, TTX. The majority (90%) of LHRH-1 neurons showed irregular firing patterns comprised of bursts and irregular beatings of action currents, which further formed a ‘cluster’ firing pattern. Brief application of 17β-estradiol (E
2
, 1 nM) increased the firing frequency and burst duration of LHRH-1 neurons with a latency of 60–120 s for up to 25 min. ICI182,780, an ER antagonist blocked the E
2
-induced increase in the firing activity of LHRH-1 neurons. These results suggest that 1) primate LHRH-1 neurons exhibit complex firing patterns comprised of activities with different time domains, 2) estrogen causes rapid stimulatory action of firing activity, and 3) this estrogen action is mediated by ER in primate LHRH-1 neurons.