N-Methyl-D, L-aspartic acid (NMA), an agonist of IV-methyl-D-as- increase in PRL secretion. To determine if NMA treatment alone could partate (NMDA) excitatory amino acid receptors, stimulates the secre- induce cFos expression in LHRH neurons, diestrous rats were treated tion of LH by increasing the release of LHRH. During proestrus, with NMA by either systemic (40 mg/kg BW; four injections, 10 min LHRH neurons express cFos in association with the LH surge. To apart) or third ventricular (2 μg in 2 ß\; four injections, 10 min apart) determine the involvement of NMDA receptors in the activation of injections. NMA administration (regardless of the route of administra- LHRH neurons on proestrus, we treated animals with an NMDA tion) caused an increase in LH secretion and significant cFos expres-receptor blocker, MK-801. Treatment with MK-801 (0.3 mg/kg, sc) at sion in many regions of the brain, including sites where the LHRH 1130 h blocked both the LH and PRL surges and cFos expression in perikarya are concentrated. However, neither systemic nor intraven- LHRH neurons. These data suggest that NMDA receptors are involved tricular administration of NMA induced cFos expression in LHRH in the regulation of LHRH neuronal activation during the LH surge. neurons. Thus, even though NMA results in increased activity of neurons and increase LH secretion, but it did result in an We then determined whether NMA treatment could restore LH secre- LHRH neurons, as evidenced by increased LH secretion, NMDA tion and cFos expression in LHRH neurons in animals whose endoge- receptor activation alone appears to be insufficient to induce cFosnous proestrous LH surges were blocked with pentobarbital. In the expression in the LHRH neurons.
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