N-Methyl-D-Aspartate Treatment Increases Circulating Adrenocorticotropin and Luteinizing Hormone in the Rat*

Farah, John M.; Rao, Tadimeti S.; Mick, Stephen J.; Coyne, Katherine; Iyengar, Smriti

doi:10.1210/endo-128-4-1875

Cited by 80 publications

(37 citation statements)

References 34 publications

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“…However, the existence of glutamate receptors in hypothalamic areas related to TSH [17], and the increase of TSH levels after central administration of glutamate receptor agonists, which was abolished by glutamate receptor antagonists coadministration (data not shown, preliminary studies), seems to suggest that the action of EAAs may occur at brain level. The increase in LH, ACTH or GH secretion induced by administration of EAAs is widely accepted to occur both in vivo and in vitro studies with actions leading to an increased release of hypothalamic hormones from the hypothalamus [18, 19]. Both NMDA and non-NMDA glutamate receptors were involved in the action of EAAs controlling the release of GnRH [20, 21], CRH [5, 22]or GHRH [23, 24].…”

Section: Discussionmentioning

confidence: 99%

Effect of Excitatory Amino Acids on Serum TSH and Thyroid Hormone Levels in Freely Moving Rats

Alfonso

Durán²,

Arufe³

2000

Horm Res Paediatr

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The actions of glutamate (L-Glu), and glutamate receptor agonists on serum thyroid hormones (T4 and T3) and TSH levels have been studied in conscious and freely moving adult male rats. The excitatory amino acids (EAA), L-Glu, N-methyl-D-aspartate (NMDA), kainic acid (KA) and domoic acid (Dom) were administered intraperitoneally. Blood samples were collected through a cannula implanted in the rats jugular 0–60 min after injection. Thyroid hormone concentrations were measured by enzyme immunoassay, and thyrotrophin (TSH) concentrations were determined by radioimmunoassay. The results showed that L-Glu (20 and 25 mg/kg) and NMDA (25 mg/kg) increased serum thyroxine (T4), triiodothyronine (T3) and TSH concentrations. Serum thyroid hormone levels increased 30 min after treatment, while serum TSH levels increased 5 min after i.p. administration, in both cases serum levels remained elevated during one hour. Injection of the non-NMDA glutamatergic agonists KA (30 mg/kg) and Dom (1 mg/kg) produced an increase in serum thyroid hormones and TSH levels. These results suggest the importance of EAAs in the regulation of hormone secretion from the pituitary-thyroid axis, as well as the importance of the NMDA and non-NMDA receptors in this stimulatory effect.

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Section: Discussionmentioning

confidence: 99%

Effect of Excitatory Amino Acids on Serum TSH and Thyroid Hormone Levels in Freely Moving Rats

Alfonso

Durán²,

Arufe³

2000

Horm Res Paediatr

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“…Systemic administration of NMDA also stimulates the release of ACTH in adult rats [11, 12, 27], even though NMDA does not cross the blood-brain barrier readily. Studies using hypothalamic explants showed that NMDA can increase AVP release but not CRH [28, 29].…”

Section: Discussionmentioning

confidence: 99%

“…Excitatory amino acids, such as glutamate and aspartate, have been implicated in the regulation of hormone release from the anterior pituitary [10]and NMDA has been shown to stimulate the release of ACTH in adult animals [11, 12]. Recently, Brooks and Howe [13]reported that administration of NMDA to the ovine fetus elicited a significant increase in plasma ACTH and luteinizing hormone that was completely abolished by the NMDA antagonist CGP37849.…”

Section: Introductionmentioning

confidence: 99%

The Role of N-Methyl-D-Aspartate Receptors in the Release of Adrenocorticotropin by Dynorphin A<sub>1–13</sub>

Szeto¹,

Soong²,

Wu³

1999

Neuroendocrinology

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We previously reported that dynorphin A_1–13 evokes a significant increase in plasma adrenocorticotropin (ACTH) after intravenous administration in the ovine fetus. This response was not sensitive to naloxone and was regulated differently from the response to U50,488H, a selective ĸ-opioid agonist. NMDA appears to play a role in many of the nonopioid actions of dynorphin. We therefore hypothesized that dynorphin A_1–13 may release ACTH via N-methyl-D-aspartate (NMDA) receptors. To test this hypothesis, we have compared the ACTH response to dynorphin A_1–13 and NMDA in the chronically-instrumented ovine fetus. Our data show that both dynorphin A_1–13 (0.5 mg/kg) and NMDA (4 mg/kg) induced a significant release of immunoreactive ACTH in the late-term ovine fetus. The ACTH response to NMDA was of a smaller magnitude, but of longer duration, when compared to dynorphin A_1–13. The response to both dynorphin A_1–13 and NMDA was significantly attenuated by pretreatment with the noncompetitive NMDA antagonist, MK-801, but was not affected by antagonists of corticotropin-releasing hormone and arginine vasopressin. Finally, the ACTH response to both dynorphin A_1–13 and NMDA were inhibited by dexamethasone. The results of this study indicate a role for NMDA receptors in the action of dynorphin A_1–13, and suggest that NMDA may act directly at the level of the pituitary to release ACTH without the involvement of hypothalamic secretagogues.

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“…Pharmacological studies have shown that exogenous excitatory amino acids (EAA) are potent modulators of prolactin (PRL) and adrenocorticotropin (ACTH) secretion. Thus, administration of glutamate receptor agonists, particularly in high doses, is followed by a rapid rise in PRL [3, 4, 5, 6]and ACTH levels [7, 8, 9, 10, 11]. There are only few data indicating a role of endogenous EAA [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Simultaneous Blockade of Two Glutamate Receptor Subtypes (NMDA and AMPA) Results in Stressor-Specific Inhibition of Prolactin and Corticotropin Release

1999

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Many neurons express simultaneously two or more isotypes of glutamate receptors, so that pharmacological modulation of more than one receptor may be necessary to reveal the role of glutamate in mediating physiological processes. The present studies were aimed at evaluating involvement of endogenous glutamate in triggering plasma prolactin (PRL) and adrenocorticotropic hormone (ACTH) levels in response to three different stress stimuli (footshock, immobilization and ether stress). Blockade of glutamate receptor subtypes was achieved by the administration of the NMDA antagonist dizocilpine (MK-801, 0.2 mg/kg) and the selective AMPA antagonist GYKI 52466 (10 mg/kg). Rats were pretreated for 4–5 days and then exposed to stressful stimulation. Basal hormone levels were not affected by the antagonists. In male rats, combined, but not separate blockade of NMDA and AMPA/kainate subtypes of glutamate receptors prevented the rise in plasma PRL in response to footshock stress. In female rats, footshock-induced PRL release was inhibited even by separate blockade of NMDA receptors by dizocilpine, suggesting that the PRL system of females is more sensitive to the effect of NMDA antagonists than that of males. None of the treatments affected PRL release during immobilization or ether stress. Simultaneous blockade of NMDA and AMPA receptor subtypes resulted in a mild inhibition of immobilization-induced ACTH release without any effect on ACTH response to footshock or ether stress. The data suggest that involvement of glutamatergic pathways in neuroendocrine response during stress is selective for discrete stress stimuli and stress hormones. In addition a concerted action of glutamate on both NMDA and non-NMDA receptor subtypes is involved in the control of PRL release during footshock stress.

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N-Methyl-D-Aspartate Treatment Increases Circulating Adrenocorticotropin and Luteinizing Hormone in the Rat*

Cited by 80 publications

References 34 publications

Effect of Excitatory Amino Acids on Serum TSH and Thyroid Hormone Levels in Freely Moving Rats

Effect of Excitatory Amino Acids on Serum TSH and Thyroid Hormone Levels in Freely Moving Rats

The Role of N-Methyl-D-Aspartate Receptors in the Release of Adrenocorticotropin by Dynorphin A<sub>1–13</sub>

Simultaneous Blockade of Two Glutamate Receptor Subtypes (NMDA and AMPA) Results in Stressor-Specific Inhibition of Prolactin and Corticotropin Release

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