The Stimulatory Action of the Glutamate Agonist, N-Methyl-Aspartate, on Luteinizing Hormone Release in the Cockerel with Immunocytochemical Observations on Its Mode of Action

Abstract

Bolus intravenous injections of 5–40 mg/kg body weight of the glutamate agonist, N-methlyl-aspartate (NMA), induced an immediate increase in the concentration of plasma luteinizing hormone (LH) in juvenile (8–10 week old) cockerels. The concentration of plasma LH returned to baseline values within 30 minutes. The NMA treatment resulted in the appearance of the product of an immediate-early gene, c-fos, localized immunocytochemically in cell nuclei in the preoptic, periventricular and basal hypothalamus. Although fos-immunoreactivity occurred in cell bodies close to gonadotropin releasing hormone-I (GnRH-I) perikarya, double immunocytochemical labeling demonstrated that the NMA treatment did not induce fos expression in GnRH-I neurons. Potential sites of action of NMA in releasing GnRH-I and LH were explored immunocytochemically. Perikarya, immunoreactive for N-methyl-D-aspartate (NMDA) receptor, were detected throughout the hypothalamus and were particularly prominent in the supraoptic and paraventricular nuclei, but none were observed in the the vicinity of GnRH-I neurons. Immunoreactive fibers were abundant throughout the hypothalamus, including the internal zone of the median eminence. Many were found in the vicinity of GnRH-I cell bodies, suggesting the possibility of direct contact. The presence of NMDA receptor was also demonstrated in the cephalic lobe of the anterior pituitary. These observations provide evidence for the first time in a bird, that LH release is stimulated by an excitatory amino acid. Apparently, the action of NMA does not involve expression of c-fos or NMDA-like receptors in GnRH-I neurons.