Meeting Abstract

S10.7  Tuesday, Jan. 6  Regulation of Vertebrate Reproduction by GnRH and GnIH BENTLEY, GE*; UBUKA, T; MCGUIRE, NL; CALISI, RM; PERFITO, MN; TSUTSUI, K; WINGFIELD, JC; Univ. of California, Berkeley; Univ. of California, Berkeley; Univ. of California, Berkeley; Univ. of California, Berkeley; Univ. of California, Berkeley; Waseda University, Japan; Univ. of California, Davis gb7@berkeley.edu

Our initial studies on gonadotropin-inhibitory hormone (GnIH) focused on the avian anterior pituitary as the only physiological target of GnIH, and we now have several lines of evidence that GnIH directly inhibits pituitary gonadotropin synthesis and release in birds and mammals. Our histological studies on projections from hypothalamic GnIH neurons subsequently implied direct actions of GnIH within the brain. GnIH axons and terminals are present in multiple brain areas in birds, and GnIH receptor is expressed on GnRH (gonadotropin-releasing hormone)-I and II neurons. Thus, GnIH can act directly on GnRH-I and II neurons to regulate reproductive physiology and behavior. Our data imply that hypothalamic GnIH content is increased by stress, and thus might be a modulator of stress-induced reproductive dysfunction. Similar histological and functional data have since been gathered in mammals. In addition to actions on the GnRH system and on the pars distalis via the median eminence, we have demonstrated the presence of GnIH and its receptor in avian and primate gonads. One of the actions of GnIH in the gonads is to modulate production of gonadal steroids directly. In sum, our data indicate that GnIH is responsive to external stimuli and is an important modulator of reproductive function at the level of the GnRH neuron, the gonadotrope and the gonads.