The present series of studies was undertaken to determine the effects of peripherally and centrally administered alpha-melanocyte stimulating hormone (MSH) on lordosis and to investigate some of the mechanisms underlying these effects. The results of Experiments 1-5 (Section I) indicated that, when confounding factors were minimized, peripherally administered MSH facilitated receptivity. Centrally administered MSH was found to produce both a long and a short term inhibitory effect. Experiment 6 (Section II) tested the hypothesis that the facilitatory action of peripherally administered MSH was due to an MSH-induced release of progesterone or some other facilitatory adrenal steroid. Results indicated that, while adrenalectomy per se did not inhibit lordosis, it blocked the facilitatory action of MSH, supporting the hypothesis. In Experiments 7-9 (Section III), the role of estrogen and progesterone in the inhibitory actions of MSH was examined. The results of these studies suggested that both estrogen and progesterone are necessary for the short term inhibitory action of MSH. However, the long term inhibitory action of MSH appears to be due, in part, to an MSH-induced decrease in the availability of cytoplasmic progestin receptors. In Experiments 10-15 (Section IV), the role of serotonin in the production of the inhibitory actions of MSH was examined. Parachlorophenyl-alanine (PCPA), a serotonin depletor, was found to prevent the long term inhbitory action of MSH. In addition, the inhibitory effects of PCPA or pirenperone, a serotonin type II receptor antagonist, did not summate with the inhibitory action of MSH. This suggested that serotonin type II receptors were involved in the production of the inhibitory actions of MSH. In Experiment 12, quipazine, a serotonin type II agonist, was found to attenuate fully the short term Inhibitory action of MSH. However, quipazine did not fully attenuate the long term inhibitory action of MSH, suggesting that the short and long term inhibitory actions of MSH are mediated through different mechanisms. This possibility was supported by the results of Experiment 13, which indicated that 20 ng MSH produced a long term, but not a short term, inhibitory effect. The results of Experiment 14 indicated that subthreshold doses of pirenperone and of MSH, when administered together, would inhibit receptivity. Experiment 15 indicated that this inhibition could be attenuated by quipazine. Thus, the following conclusions can be drawn: 1) the facilitatory action of peripherally administered MSH is probably mediated by an MSH-induced release of progesterone from the adrenals, 2) the short term inhibitory action of MSH is mediated, to a large extent, by an MSH-induced decrease in serotonin type II activity, and 3) the long term inhibitory action of MSH is mediated, in part, by an MSH/serotonin-induced decrease in the availability of progestin receptors. In addition, it was hypothesized that: 1) progesterone acts in the MRF to increase serotonin type II activity. Thus, MSH-induced decreases in serotonin type II activity and in progestin receptors probably occur at this location, and 2) estrogen acts in the AH-POA to decrease serotonin type I activity. Therefore, any actions of MSH on serotonin type I activity or on estrogen receptors is likely to occur in this region. Finally, it was suggested that MSH plays a role in the induction and maintenance of pseudopregnancy, thereby providing MSH with a functional role in the regulation of receptive states. / Arts, Faculty of / Psychology, Department of / Graduate

Thesis (Ph.D.)--University of Florida, 2004. / Typescript. Title from title page of source document. Document formatted into pages; contains 142 pages. Includes Vita. Includes bibliographical references.