| Research Abstract |
Lordosis reflex is an estrogen-dependent, essential component of the female rat sexual behavior. We examined electrical stimulation effects of the POA on lordosis in the free-moving, estrogen- and progesterone-treated ovariectomized 'rats, which were deprived of septal efferents of the POA by neural transections and compared with those of the ventral tegmental area (VTA). The cut reduced the amount of estrogen needed to elicit maximal lordosis. In spite of the removal of septal inhibition, stimulation of the transected POA caused a prompt and strong suppression of lordosis in response to male mounts with a threshold at 30muA. The optimal frequency was at 50-100 Hz. Lordosis performance returned promptly to the prestimulation level after the termination of current application. The rapid time course d
istinguished the effect from that in the non-deafferented animals, , which occurred slowly and persisted. VTA stimulation at 30muA and 75-125 Hz was as effective as stimulation of the transe
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cted POA to cause a rapid and strong suppression of lordosis. No aversive response accompanied the blockade of lordosis form the POA or VTA. Electrical stimulation of both structures specifically blocked lordosis, without disrupting the proceptive components of the female-sexual behavior. Thus, the POA is an independent and separate entity in the Inhibitory mechanism of lordosis. The exaggerated effect of electrical stimulation in the deafferented animals may result from a desruption of facilitative circuitry-for this reflex by the transection.
In 683 POA neurons, VTA stimulation in urethane-anesthetized rats caused antidromic activation at latencies ranging 1.643.7 ms. Stimulus threshold was as low as 60muA in 106 rats under light urethane anaesthesia. Effects of estrogen, given 5-8 days prior to the recording in a 5-mm Silastic capsule, were compared within each animal group, which consisted of 38 female rats ovariectomized as adults (n=278, n, number of cells), 38 male rats castrated on the day of birth (day 1, NC males) (n=181), and 30 female rats given 1.25 mg testosterone on day 5 and ovariectomized as adults (TP females) (n=224). estrogen significantly increased the antidromic activation threshold in the ovariectomized females (P<0.02, Mann-Whitney U test) and in the NC males (P<0.04). In the former, the prolonged refractory period (P<0.02) and antidromic spike latency (P<0.002) were also detected. In the TP females, no parameter was affected by estrogen. Thus estrogen depressed the excitability of the POA axons in animals which had not been exposed to testosterone during the development.
In animals under urethane anesthesia, antidromic spike latency (range : 2-40 ms) and stimulus threshold (100-1, 500muA) were determined for 371 neurons in the ventromedial hypothalamic nucleus (VMN) following electrical stimulation of the mid-brain central grey In 10 intact (number of neurons, n=71) and 29 orchidectomized male rats, which received either no treatment (10 rats, n=75), testosterone propionate (5 rats, n=75), estradiol benzoate (8 rats, n=77) or dehydrotestosterone (6 rats, n=73). Orchidectomy significantly decreased antidromic activation thresholds. Either hormone was effective to raise the mean threshold to values comparable to that in the intact males. Frequency histograms of the threshold showed that dehydrotestosterone achieved this effects by decreasing the number of cells at a low threshold range, whereas the action of estrogen was not on this fraction of cells. The histogram for the testosterone-treated animals was similar to that in the intact males. The results suggest that different subgroups of VMN neurons with specific sensitivity to metabolites of testosterone project to the central grey, and may govern different aspects of endocrine or affective controls.
Long-term recordings up to 4 days were made from neurons in the POA in free-moving female rats during the copulatory encounter with males by microwire electrodes. We found (1) neurons specifically respond to vaginal stimulation by the male partner, and (2) those with a brief increase in their activity prior to the display of lordosis. Less
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