STEROID IMPRINTING AND MODULATION OF SEXUAL DIMORPHISM IN THE LUTEINIZING-HORMONE-RELEASING HORMONE NEURONAL SYSTEM

1. Sex differences in the control of gonadotropin secretion and reprod uctive functions are a distinct characteristic in all mammalian specie s, including humans. Ovulation and cyclicity are among the most distin ct neuroendocrine markers of female brain differentiation, along with sex behavioral traits that are also evident in different species. 2. T he luteinizing hormone-releasing hormone (LHRH) neuronal system is the prime regulator of neuroendocrine events leading to ovulation and hor monal changes during the menstrual cycle and, as such, is the potentia l site where many of these sex differences may be expressed or, at the very least, integrated. However, until recently, no significant diffe rences were seen in LHRH neurons between male and female brains, inclu ding cell number, pattern of distribution, and expression of message o r peptide (LHRH) levels. 3. Recently, we reported that galanin (GAL), a brain-gut peptide, is coexpressed in LHRH neurons and that this coex pression is sexually dimorphic. When GAL is used as a marker for this neuronal system, it is clear that estradiol as well as progesterone pr ofoundly affects the message and expression of the peptide and that th is regulation, at least in rodents, is neonatally predetermined by gon adal steroid imprinting. 4. Changes in GAL expression and message can also be seen at puberty, during pregnancy and lactation, and in aging, all situations that affect the function of the LHRH neuronal system. Using an immortalized LHRH neuronal cell line (GT1) we have recently o bserved that these neurons express estrogen receptor (ER) and GAL and that estradiol can increase the expression of GAL, indicating function al activation of the endogenous ER.