Excitatory amino acids have been known to increase pituitary secretion of LH in vivo and are probably involved in the neuroendocrine regulation of the hypothalamic-pituitary-gonadal axis. We have found that systemic administration of the excitatory amino acid agonist N-methyl-D-aspartate (NMDA) evokes a transient and profound increase in circulating levels of ACTH as well. Treatment of adult male Long-Evans rats with NMDA (30 mg/kg, sc) maximally increased plasma ACTH and immunoreactive beta-endorphin from 7-15 min after injection, and levels of both remained significantly elevated until 60 min into the time course. Corresponding increases in corticosterone were observed 15 and 30 min after treatment, while LH, similar to other pituitary hormones, was increased from 7-30 min after NMDA. Stimulation of the pituitary-adrenal and pituitary-gonadal neuroendocrine axes by NMDA was monitored in subsequent studies by plasma ACTH and LH, respectively; both were increased in a dose-related manner after the administration of 3-60 mg/kg NMDA, although stimulation of ACTH (800%) was more pronounced than that of LH (200%). The increases in ACTH and LH due to NMDA were inhibited by pretreatment with the competitive NMDA antagonist (+/-)3-(2-carboxypiperazin-4- yl)propyl-1-phosphonic acid, CPP (6 and 10 mg/kg, ip, for 21 min); by contrast, dexamethasone pretreatment (50 micrograms/kg, ip, for 4 h) blocked only the NMDA-evoked increase in circulating ACTH. These findings indicate that an NMDA receptor mechanism might be involved in the acute activation of the hypothalamic-pituitary-adrenal axis in the rat.

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A pharmacologic approach was used to examine the possible role of dopamine neurons in the regulation of pituitary beta-endorphin-like immunoreactivity (beta-END-LI) secretion in the rat. Blockade of dopamine receptors by haloperidol or pimozide treatment evoked dose- and time-related increases in plasma levels of beta-END-LI. Physical immobilization increased circulating beta-END-LI six-fold and pretreatment with dopamine receptor agonists (bromocriptine or pergolide) significantly attenuated this rise without affecting plasma beta-END-LI levels in non-stressed animals. Dopaminergic drugs and immobilization produced similar effects on circulating PRL as on beta-END-LI. However, the magnitude of change in levels of PRL was generally greater than the change in beta-END-LI. The present findings suggest that dopaminergic neurons inhibit the release of pituitary beta-END-LI as well as PRL in the rat.

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In order to characterize the properties of tuberohypophysial dopaminergic neurons which terminate in the intermediate (IL) and neural (NL) lobes of the pituitary gland a technique was developed which permitted the selective dissection of the rat pituitary into its three distinct lobes (NL, IL and anterior lobe, AL). The success of the dissection was evaluated histologically and biochemically by measuring the distribution of peptide hormones characteristic of the dissected regions. As would be predicted, prolactin was found almost exclusively in the AL, arginine-vasopressin in the NL and α-melanotropin in the IL. Over two-thirds of total immunoreactive β-endorphin was located in the IL and less than 30% was found in the AL. The concentration of dopamine (DA) was greater in the IL than in the NL, but the rate of turnover of the amine was approximately the same suggesting that the basal activity of tuberohypophysial DA neurons is similar in both regions. On the other hand, the turnover of DA in the IL, but not NL, was increased following the administration of a DA antagonist (haloperidol) and decreased following a DA agonist (bromocriptine). Thus, the activity of DA neurons terminating in the IL is regulated, at least in part, by DA receptor-mediated mechanisms and in this regard these neurons resemble DA neurons terminating in the nucleus accumbens and striatum. Since DA turnover in NL was not altered by the administration of haloperidol or bromocriptine it is proposed that these neurons lack DA receptor-mediated regulatory mechanisms and thus resemble tuberoinfundibular DA neurons terminating in the median eminence.