A nimal models have indicated that androgenic steroids acting before birth might influence the sexual orientation of adult humans. Here we examine the androgen-sensitive pattern of finger lengths 1 , and find evidence that homosexual women are exposed to more prenatal androgen than heterosexual women are; also, men with more than one older brother, who are more likely than first-born males to be homosexual in adulthood 2 , are exposed to more prenatal androgen than eldest sons. Prenatal androgens may therefore influence adult human sexual orientation in both sexes, and a mother's body appears to 'remember' previously carried sons, altering the fetal development of subsequent sons and increasing the likelihood of homosexuality in adulthood.

No abstract

This review focuses on the effect of gonadal steroid hormones, androgen and estrogen, on dendrites in the adult rat central nervous system (CNS). Four hormone-responsive nuclei are considered: The spinal nucleus of the bulbocavernosus (SNB), the medial nucleus of the amygdala (MeA), the ventromedial nucleus of the hypothalamus (VMN), and the CA1 region of the dorsal hippocampus. Particular emphasis is placed on the mode of hormone action in each nucleus. In the SNB, VMN, and hippocampus, hormones appear to mediate their effects indirectly, via cells other than those that display morphological plasticity. In the MeA, estrogen and/or androgen appears to act primarily on those cells whose dendrites are modulated by the hormone. Importantly, increasing levels of gonadal hormones do not simply result in increases in dendritic parameters. In the VMN, high levels of estrogen associated with proestrus increase dendritic spine density in one subset of cells and reduce spine density in another subset. The pyramidal cells of dorsal CA1 also undergo phasic changes in dendritic spine and synapse density across the estrous cycle. The estrogen-induced excitatory synapses connect with preexisting axonal boutons that also form synapses with other CA1 cells, thereby increasing the divergence of excitatory afferents to dorsal CA1. These findings indicate that gonadal steroids have a profound impact on the morphology of dendrites and patterns of synaptic connectivity. Consequently, the experimental manipulation of hormone levels is a powerful tool to study structure-function relationships in the mammalian brain.

The medial amygdala is important in social behaviors, many of which differ between males and females. The posterodorsal subnucleus of the medial amygdala (MeApd) is particularly sensitive to gonadal steroid hormones and is a likely site for gonadal hormone regulation of sexually dimorphic social behavior. Here we show that the synaptic organization of the MeApd in the rat is sexually dimorphic and lateralized before puberty. With the use of whole-cell voltage-clamp recording and quantitative electron microscopy, we found that, specifically in the left hemisphere, prepubertal males have ϳ80% more excitatory synapses per MeApd neuron than females. In the left but not the right MeApd, miniature EPSC (mEPSC) frequency was significantly greater in males than in females; mEPSC amplitude was not sexually dimorphic. Paired-pulse facilitation of EPSCs, an index of release probability, also was not sexually dimorphic, suggesting that greater mEPSC frequency is caused by a difference in excitatory synapse number. Electron microscopy confirmed that the asymmetric synapse-to-neuron ratio and the total asymmetric synapse number were significantly greater in the left MeApd of males than of females. In contrast to results for excitatory synapses, we found no evidence of sexual dimorphism or laterality in inhibitory synapses. Neither the frequency nor the amplitude of mIPSCs was sexually dimorphic or lateralized. Likewise, the number of symmetric synapses measured with electron microscopy was not sexually dimorphic. These findings show that the excitatory synaptic organization of the left MeApd is sexually differentiated before puberty, which could provide a sexually dimorphic neural substrate for the effects of hormones on adult social behavior.

No abstract