The effects of N-methyl-D,L-aspartate and gonadotropin-releasing hormone on in vitro growth hormone release in steroid-primed immature rainbow trout, Oncorhynchus mykiss.

In the present study we investigated the effects of 17 beta-estradiol (E2) and 5 alpha-dihydrotestosterone (5 alpha DHT) on the ability of the glutamate agonist, N-methyl-D,L-aspartate (NMA), to stimulate growth hormone (GH) release from perifused pituitary glands of sexually immature rainbow trout (Oncorhynchus mykiss). Two weeks after steroid hormone implantation, pituitary glands were removed from the fish and challenged with NMA (10(-8) M) in a perifusion unit. NMA rapidly and significantly elevated GH release from perifused pituitary fragments taken from all treatment groups, and there was a main effect of in vivo steroid hormone treatment on the in vitro GH response to NMA. To examine the relationship between NMA and gonadotropin-releasing hormone on GH release, pituitaries from E2- and 5 alpha DHT-primed and control fish were exposed to a single pulse of salmon gonadotropin-releasing hormone (sGnRH) which also elicited a significant elevation in GH release from perifused pituitary fragments, although the response in the E2- and 5 alpha DHT-primed fish was significantly smaller (P < 0.05) than that for the NMA challenge. Administration of a specific GnRH antagonist, D-pGlu1,D-Phe2,D-Trp3,6-LHRH, did not affect the GH response to NMA, whereas administration of the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid blocked the GH response to NMA. These data suggest that NMA acts to stimulate GH release directly at the level of the somatotroph, likely through the NMDA receptor and not through increased release of GnRH.