EFFECTS OF EXCITATORY AMINO-ACID RECEPTOR AGONISTS AND ANTAGONISTS ONTHE SECRETION OF MELATONIN, LUTEINIZING-HORMONE AND PROLACTIN IN THE RAM

To assess the role of excitatory amino acids (EAA) as neurotransmitter s in the transmission of light information from the retina to the pine al gland, we have determined whether the systemic injection of EAA ago nists in Soay rams will mimic the suppressive effect of light on the s ecretion of melatonin, and whether pretreatment of rams with EAA antag onists will block this effect. In addition, the efficacy of the drugs in affecting neuroendocrine systems was investigated by measuring the changes in the secretion of luteinizing hormone (LH) and prolactin. In jections of the EAA receptor agonist, NMDA (N-methyl-D,L-aspartate: 4. 0 mg/kg iv), and the non-NMDA type EAA receptor agonist, AMPA -alpha-a mino-3-hydroxy-5-methylisoxazole-propionic acid: 0.2 mg/kg iv) given a t night to rams exposed to long days (16 h light: 8 h darkness), cause d no change in the blood plasma concentrations of melatonin. The treat ments induced an acute increase in the concentrations of LH, and NMDA, but not AMPA, caused a sustained increase in the concentrations of pr olactin. Injections of the specific NMDA-type receptor antagonist, CGP (CGP 37849: 1.0 mg/kg iv) and the non-NMDA-type receptor antagonist, DNQX (6,7 Dinitroquinoxaline-2,3-dione: 0.5 mg/kg iv), given prior to a 1-h light period at night, in rams under long days, caused no change in the light-induced decrease in blood plasma concentrations of melat onin. The drug treatments had no effect on the plasma concentrations o f LH, but CGP, and not DNQX, stimulated an acute increase in the plasm a concentrations of prolactin. These results provide support for the h ypothesis that EAA mechanisms operate in the hypothalamus to regulate the release of peptides and catecholamines which control the secretion of LH and prolactin from the pituitary gland; different sub-types of EAA receptors are involved in the control of the two pituitary hormone s. The failure of the treatments to affect the secretion of melatonin may indicate that EAA receptor activation is not involved in the photi c relay to the pineal gland, or may merely reflect the inability of th e drugs to penetrate into the retina/SCN/pineal neural circuits to pro duce a response.