Reversible action of N-methyl aspartate on gonadotrophin neuroregulation

Price, Madelon T.; Olney, John W.; Anglim, Margo; Buchsbaum, Susan

doi:10.1016/0006-8993(79)90880-1

Cited by 24 publications

(6 citation statements)

References 4 publications

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“…N-methyl-DL-aspartate produced a significant elevation of serum LH levels only at the highest dose tested (66 mg/kg SC), a dose previously reported to be neurotoxic (Schainker and Cicero, 1980). The failure of lower doses of NMA to significantly increase serum LH levels may be due to the older age of the rats used in this study compared to those of Price et al (1978Price et al ( , 1979 as discussed by Schainker and Cicero (1980). Of interest is our findings, similar to those of Carillo and Alcantura (1981), that NMA produced no elevation in serum levels of FSH.…”

Section: Effects Of Acute Administration Of Msg and Related Excitatorcontrasting

confidence: 69%

“…These data have been comprehensively reviewed (Olney and Price, 1980). Price et al (1978aPrice et al ( , 1979 reported that SC administration of NMA (15-40 mg/kg) to young male rats produces a significant elevation in serum LH levels. These doses of NMA are considered to be below those required to produce hypothalamic destruction.…”

Section: Effects Of Acute Administration Of Msg and Related Excitatormentioning

confidence: 99%

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Effects of Neurotoxic Excitatory Amino Acids on Neuroendocrine Regulation

Nemeroff

1983

Excitotoxins

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This report surnmarizes the available literature concerning the effects of glutamate and related excitatory amino acids on neuroendocrine function. The majority of investigators in this field have pursued two lines of inquiry: (1) evaluation of the effect of administration of monosodium glutamate (MSG) and related excitotoxic amino acids to neonatal rodents on endocrine regulation in adulthood and (2) assessment of the acute neuroendocrine effects of MSG and related compounds in adult rodents. The use of these compounds as tools in neuroendocrine research is described. KEYWORDSMonosodium glutamate (MSG); n-methyl aspartate (NMA); growth hormone (GH); prolactin (PRL); luteinizing hormone (LH).; follicle-stimulating hormone (FSH); thyrotropin (TSH); hypothalamic releasing hormones; dopamine; acetylcholine.

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Section: Effects Of Acute Administration Of Msg and Related Excitatorcontrasting

confidence: 69%

Section: Effects Of Acute Administration Of Msg and Related Excitatormentioning

confidence: 99%

Effects of Neurotoxic Excitatory Amino Acids on Neuroendocrine Regulation

Nemeroff

1983

Excitotoxins

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“…Stimulation of LH secretion by systemic injections of NMDA or NMA has been reported in both rodents [9,10,14,[22][23][24] and primates [8,15,25] of both sexes. In order to determine the effective i.c.v.…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of GABA<sub>A</sub> and GABA<sub>B</sub> Receptor Agonists on NMDA-Induced and Noradrenaline Induced Luteinizing-Hormone Release in the Ovariectomized Estrogen-Primed Rat

Akema

Kimura²

1993

Neuroendocrinology

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Effects of selective γ-aminobutyric acida (GABAa) and GABAb receptor agonists on noradrenaline (NA)-induced and N-methyl-D-aspartate (NMDA)-induced luteinizing-hormone (LH) secretion were examined in ovariectomized estrogen-primed rats. Experiments were performed in unanesthetized animals bearing chronic intracerebroventricular (i.c.v.) cannulae. Lev. injections of NA or NMD A stimulated LH secretion in animals that had received prior i.c.v. injections of saline. The effects of NA and NMDA were significantly attenuated by a prior i.c.v. injection of phentolamine (a selective α-adrenergic-receptor blocker) and 2-amino-5-phosphonovaleric acid (a selective NMDA receptor antagonist), respectively. NA-induced LH release was also inhibited by i.c.v. injections of either muscimol (a selective GABAa receptor agonist) or baclofen (a selective GABAb receptor agonist). On the other hand, although muscimol inhibited the effect of NMDA, baclofen did not inhibit but slightly augmented the NMDA-induced release of LH. These results support the hypothesis that both GABAa and GABAb receptors are involved in the GABAergic inhibition of LH secretion, and further suggest that they are probably located at different sites in the neural mechanism regulating LH secretion in the female rat.

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“…The results of analogous studies in the rat are inconsistent. In an early investigation of the male, Price et al [14] reported a decrement in the LH response to the 2nd and 3rd subcutaneous injection of NMA, but this finding was not confirmed in the more recent study by Pohl et al [15], who employed an intra venous mode of NMA administration. The failure of repetitive injections of Glu to sustain a train of GnRH discharges cannot be accounted for by a Glu induced ac celeration in the clearance of this amino acid from the circulation.…”

Section: Discussionmentioning

confidence: 76%

Repetitive Injections of L-Glutamic Acid, in Contrast to Those of N-Methyl-D,L-Aspartic Acid, Fail to Elicit Sustained Hypothalamic GnRH Release in the Prepubertal Male Rhesus Monkey (Macaca mulatta)

Medhamurthy

Plant²

1992

Neuroendocrinology

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The purpose of the present study was to examine whether repetitive intravenous injections of L-glutamic acid (Glu), like those of N-methyl-D, L-aspartic acid (NMA), are able to elicit a sustained train of gonadotropin releasing hormone (GnRH) discharges from the hypothalamus of the prepubertal male monkey. In order to utilize pituitary luteinizing hormone (LH) secretion as a bioassay of hypothalamic GnRH release, the responsiveness of the gonadotroph of the prepubertal animals was enhanced prior to the study with a chronic intermittent intravenous infusion of the synthetic decapeptide (0.1 µg/min for 3 min every h). Sequential intravenous injections of Glu (150 mg/kg BW) were administered at 3-hour intervals for 6 or 24 h. Although the first injection of this acidic amino acid elicited a robust discharge of GnRH, subsequent stimulation with Glu resulted in GnRH discharges with progressively decreasing magnitudes, and by the 9th injection Glu-induced GnRH release was abolished. Peak concentrations of circulating Glu following the 1st and 4th Glu injection were indistinguishable (3,959 ± 437 vs. 4,139 ± 72 nmol/ml, respectively). Interestingly, the failure of repetitive intravenous injections of Glu to sustain pulsatile GnRH release was not associated with a loss of responsiveness to NMA administration, nor was it accompanied by a corresponding decrement in Glu induced growth hormone (GH) discharges. As previously demonstrated, repetitive intravenous administration of NMA (2-5 mg/kg BW) every 3 h for 9 h sustained pulsatile GnRH secretion without decrement. A similar intermittent infusion of kainic acid (KA; 1 mg/kg BW every 3 h for 6 h), however, elicited a GnRH response that mimicked that observed in response to intermittent Glu treatment. These findings are consistent with the notion that Glu administered by intravenous injection fails to reach the central N-methyl-D-aspartic acid (NMDA) receptors that mediate the sustained train of GnRH discharges elicited in response to repetitive intravenous injections of NMA. Instead, circulating Glu appears to activate non-NMDA receptors in the vicinity of the median eminence. Repetitive activation of these non-NMDA receptors, in contrast to that of the NMDA receptor, fails to sustain an intermittent discharge of GnRH. The Glu induced GH release, which occurred without decrement, was therefore presumably mediated by NMDA receptors on GH releasing hormone cells in close proximity to the median eminence.

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Reversible action of N-methyl aspartate on gonadotrophin neuroregulation

Cited by 24 publications

References 4 publications

Effects of Neurotoxic Excitatory Amino Acids on Neuroendocrine Regulation

Effects of Neurotoxic Excitatory Amino Acids on Neuroendocrine Regulation

Differential Effects of GABA<sub>A</sub> and GABA<sub>B</sub> Receptor Agonists on NMDA-Induced and Noradrenaline Induced Luteinizing-Hormone Release in the Ovariectomized Estrogen-Primed Rat

Repetitive Injections of L-Glutamic Acid, in Contrast to Those of N-Methyl-D,L-Aspartic Acid, Fail to Elicit Sustained Hypothalamic GnRH Release in the Prepubertal Male Rhesus Monkey (Macaca mulatta)

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