To assess the role of excitatory amino acids (EAA) as neurotransmitters in the transmission of light information from the retina to the pineal gland, we have determined whether the systemic injection of EAA agonists in Soay rams will mimic the suppressive effect of light on the secretion of melatonin, and whether pretreatment of rams with EAA antagonists 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. Injections fo the EAA receptor agonist, NMDA (N-methyl-D,L-aspartate: 4.0 mg/kg iv), and the non-NMDA type EAA receptor agonist, AMPA (DL-alpha-amino-3-hydroxy-5-methylisoxazole-propionic acid: 0.2 mg/kg iv) given at night to rams exposed to long days (16 h light: 8 h darkness), caused no change in the blood plasma concentrations of melatonin. The treatments induced an acute increase in the concentrations of LH, and NMDA, but not AMPA, caused a sustained increase in the concentrations of prolactin. 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 melatonin. The drug treatments had no effect on the plasma concentrations of LH, but CGP, and not DNQX, stimulated an acute increase in the plasma concentrations of prolactin. These results provide support for the hypothesis 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 hormones. The failure of the treatments to affect the secretion of melatonin may indicate that EAA receptor activation is not involved in the photic relay to the pineal gland, or may merely reflect the inability of the drugs to penetrate into the retina/SCN/pineal neural circuits to produce a response.