Introduction

Gonadal steroid hormone receptors are ligand-activated transcription factors that are part of a complex superfamily of such factors (Evans 1988). These receptors alter the transcription of genes containing specific promoter or enhancer sequences. In this way, estrogen, acting through the estrogen receptor (ER), alters the transcription of genes in the cells where the receptors are found.

Neurons that contain gonadal steroid hormone receptors are a key to the mechanisms through which these hormones govern the behavioral and neuroendocrine processes underlying reproduction (Morrell et al. 1975; Morrell and Pfaff 1983). A complex and only partly understood cascade of events occurs subsequent to the genomic regulation initiated by these ligand-activated transcription factors (Yamamoto 1985). The presence of gonadal steroid hormone receptors in neurons has been documented by means of steroid hormone autoradiography, biochemical assays for binding, and immunocytochemistry (Blaustein and Olster 1989; DonCarlos et al. 1991; Giordano et al. 1991; Morrell et al. 1992). Now the tools of molecular biology provide a means of investigating the mRNA from which gonadal steroid hormone receptors are translated.

The differential sensitivity of brain regions to steroid hormones is based on the combination of the regional location of neurons containing these receptors, the number of neurons containing the receptors per brain region, and the number of receptors per neuron. The degree of sensitivity to steroid hormones is not a static property of the brain as there is increasing evidence that the endocrine and behavioral status of the adult mammal can govern the sensitivity of brain regions to steroid hormones by regulating either the number of neurons expressing the receptors or the amount of receptor per neuron (Hnatczuk et al. 1994; Koch and Ehret 1989; Pearson et al. 1993; Simerly and Young 1991).