Search

Female sexual behavior in rodents, termed lordosis, is controlled by facilitatory and inhibitory systems in the brain. It has been well demonstrated that a neural pathway from the ventromedial hypothalamic nucleus (VMN) to the midbrain central gray (MCG) is essential for facilitatory regulation of lordosis. The neural pathway from the arcuate nucleus to the VMN, via the medial preoptic nucleus, in female rats mediates transient suppression of lordosis, until female sexual receptivity is induced. In addition to this pathway, other regions are involved in inhibitory regulation of lordosis in female rats. The lordosis-inhibiting systems exist not only in the female brain but also in the male brain. The systems contribute to suppression of heterotypical sexual behavior in male rats, although they have the potential ability to display lordosis. The lateral septum (LS) exerts an inhibitory influence on lordosis in both female and male rats. This review focuses on the neuroanatomy and sex differences of the lordosis-inhibiting system in the LS. The LS functionally and anatomically links to the MCG to exert suppression of lordosis. Neurons of the intermediate part of the LS (LSi) serve as lordosis-inhibiting neurons and project axons to the MCG. The LSi-MCG neural connection is sexually dimorphic, and formation of the male-like LSi-MCG neural connection is affected by aromatized testosterone originating from the testes in the postnatal period. The sexually dimorphic LSi-MCG neural connection may reflect the morphological basis of sex differences in the inhibitory regulation of lordosis in rats.

Neurons in the lateral septum (LS) with projecting axons to the midbrain central gray (MCG) exert an inhibitory influence on lordosis. The number of such neurons is greater in female than in male rats. In this experiment, effects of neonatal estrogen on the density of the LS-MCG connections and on lordosis behavior were examined in female rats. On postnatal day 4 (day 0 = day of birth), females were injected subcutaneously with 50 or 100 μg estradiol benzoate (EB) or oil. On postnatal day 60, females and control males were gonadectomized. Behavioral tests were carried out after the implantation of silicone tubes containing estradiol. Lordotic activities in both males and EB-treated females were lower than in oil-treated females. After completing the behavioral tests, the animals were injected with Fluoro-Gold (FG), a retrograde tracer, into the right-side MCG and the number of FG-labeled neurons in the LS was measured. In all groups, the right-side LS ipsilateral to the FG injection had more FG-labeled neurons than the left-side LS. The number of FG-labeled neurons in the LS of oil-treated females was larger than that of males on both right and left sides. In the females treated with 100 μg EB (EB100), the number of FG-labeled neurons was comparable with that of males and lower than that of oil-treated females. The number of FG-labeled neurons in the EB50 females was also lower than that in oil-treated females, but tended to be larger than that observed in the EB100 group. These results indicate that neonatal estrogen decreases both lordotic activity and the density of the LS-MCG neural connections in female rats.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The goal of this study was to determine, by combining retrograde fluorescent tract tracing with double immunocytochemistry, whether neurons immunoreactive (IR) for both progesterone receptors (PR) and somatostatin (SOM) in the guinea-pig ventrolateral nucleus (VL) send their axons directly to the midbrain. Unilateral microinjections of true blue (TB) fluorescent dye were made into the midbrain central gray (MCG) of ovariectomized animals primed with estradiol to induce PR and injected intracerebroventricularly with colchicine to visualize SOM-IR neurons. The highest number of PR/SOM-IR neurons in the VL that projected to the midbrain was found when the fluorescent retrograde tracer was confined to the lateral region of the MCG at the mid-rostrocaudal level. More specifically, 29% of the progesterone target neurons containing SOM detected in the VL projected directly to the midbrain, accounting for 7% of the PR-IR neurons and for 9% of the SOM-IR neurons. These triple-labeled cells were found throughout the extent of the VL. Double-labeled cells also sent axons to the MCG and were either PR-IR (14%) or SOM-IR (12%). These results provide morphological evidence that a subset of the PR-IR neurons expressing SOM in the VL have long projections to the midbrain and suggest that the SOM system may modulate neural circuits involved in the regulation of steroid-influenced behaviors and neuroendocrine functions. [ABSTRACT FROM AUTHOR]