Excitability of female rat central gray cells with medullary projections: changes produced by hypothalamic stimulation and estrogen treatment.

1. Effects of estrogen on the excitability of 74 neurons in the central gray of the mesencephalon (CG) antidromically identified from the medulla were investigated extracellularly in female rats under urethan anesthesia. 2. The mean rate of spontaneous discharge of the identified CG cells was higher in estrogen-treated (2.9 Hz) than in untreated ovariectomized rats (0.3 Hz). In the estrogen-treated preparations, 18.5% of the identified cells had discharge rates exceeding 3.0 Hz, while none were found in this range in the untreated animals. 3. Two types of positive-negative biphasic antidromic spike potentials were distinguished. In one ("fast") the initial positive deflection was completed within 500-700 microseconds, while it took longer than 1 ms in the other ("slow" spikes). Slow spikes had a notch in the rising phase of their initial positive deflection, at which antidromic propagation was often blocked. Mean antidromic spike latency for the fast spikes was 6.8 ms, while the value for the slow spikes was 14.7 ms. 4. In slow spikes, the percentage of successful antidromic spike invasions into the somatodendritic complex remained constant for a long time when the response was elicited by repetitive antidromic stimuli at 0.5 Hz. Antidromic propagation into the somatodendritic complex occurred more frequently in the slow spikes recorded from estrogen-treated preparations (94.2%) than in those of ovariectomized untreated animals (55.7%). 5. Electrical stimulation of the preoptic area (POA) reduced the frequency of successful antidromic propagation into the somatodendritic complex. Stimulation of the ventromedial nucleus of the hypothalamus (VMN) increased it. Conversely, electrolytic lesion of the POA facilitated, while VMN lesion reduced antidromic spike invasion. 6. Thus, excitability of some neurons in the CG is facilitated by estrogen. Similar effects of VMN stimulation and POA lesion suggest that the estrogenic effect could be mediated by these structures. The pattern of effects on these CG neurons is that required for their control of lordosis behavior, an estrogen-dependent postural reflex in female rodents. These cells may modulate medullary reticulospinal cells, which in turn govern the reflex.