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Glutamate receptor agonists modulate [Ca2+]i in isolated rat melanotropes.
Neuroendocrinology. 1995 Aug; 62(2):111-22.N

Abstract

Although glutamate is the predominant excitatory amino acid in the vertebrate central nervous system (CNS) where it affects a variety of physiological processes and pathophysiological states, the role that glutamate receptors may play outside the CNS has not been clearly established. In the present study, the effects of N-methyl-D-aspartate (NMDA), alpha-amino-2,3-dihydro-5-methyl-3-oxo-4-isoxazolepropanoic acid (AMPA) kainate, and metabotropic glutamate receptor agonists and antagonists were investigated on neuroendocrine melanotropes of the rat pars intermedia using single-cell dual-wavelength microfluorometry and the Ca(2+)-sensitive probe, fura-2, to monitor changes in [Ca2+]i. Glutamate induced a rapid, concentration-dependent rise in [Ca2+]i with an EC50 of 24 microM that was Mg(2+)-sensitive and dependent on the presence of extracellular Ca2+. NMDA increased [Ca2+]i in a glycine-dependent manner with an EC50 of 83 microM that was blocked by 1 microM MK-801 and 1 mM Mg2+. The non-NMDA receptor agonists kainate, AMPA, and quisqualate increased [Ca2+]i with an EC50 of 124, 5 and 8 microM, respectively. Responses to kainic acid were blocked by 10 microM CNQX and were shown to be sensitive to Mg2+ and dihydropyridine. AMPA stimulation was the most potent, and glutamate stimulation was the most efficacious at mediating increases in [Ca2+]i. The metabotropic receptor-specific agonist, trans-ACPD, failed to induce a change in [Ca2+]i. The glutamate-induced Ca2+ influx was about half of that elicited by a 50 mM K(+)-induced membrane depolarization and activation of voltage-sensitive Ca2+ channels. These results demonstrate the presence of glutamate receptors on rat melanotropes and suggest that glutamate receptors in the intermediate lobe of the pituitary may provide the excitatory counterbalance to the well-described secretoinhibiting input via dopamine and gamma-aminobutyric acid receptors.

Authors+Show Affiliations

Department of Physiology, University of Michigan Medical School, Ann Arbor 48109, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

8584110

Citation

Giovannucci, D R., and E L. Stuenkel. "Glutamate Receptor Agonists Modulate [Ca2+]i in Isolated Rat Melanotropes." Neuroendocrinology, vol. 62, no. 2, 1995, pp. 111-22.
Giovannucci DR, Stuenkel EL. Glutamate receptor agonists modulate [Ca2+]i in isolated rat melanotropes. Neuroendocrinology. 1995;62(2):111-22.
Giovannucci, D. R., & Stuenkel, E. L. (1995). Glutamate receptor agonists modulate [Ca2+]i in isolated rat melanotropes. Neuroendocrinology, 62(2), 111-22.
Giovannucci DR, Stuenkel EL. Glutamate Receptor Agonists Modulate [Ca2+]i in Isolated Rat Melanotropes. Neuroendocrinology. 1995;62(2):111-22. PubMed PMID: 8584110.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glutamate receptor agonists modulate [Ca2+]i in isolated rat melanotropes. AU - Giovannucci,D R, AU - Stuenkel,E L, PY - 1995/8/1/pubmed PY - 1995/8/1/medline PY - 1995/8/1/entrez SP - 111 EP - 22 JF - Neuroendocrinology JO - Neuroendocrinology VL - 62 IS - 2 N2 - Although glutamate is the predominant excitatory amino acid in the vertebrate central nervous system (CNS) where it affects a variety of physiological processes and pathophysiological states, the role that glutamate receptors may play outside the CNS has not been clearly established. In the present study, the effects of N-methyl-D-aspartate (NMDA), alpha-amino-2,3-dihydro-5-methyl-3-oxo-4-isoxazolepropanoic acid (AMPA) kainate, and metabotropic glutamate receptor agonists and antagonists were investigated on neuroendocrine melanotropes of the rat pars intermedia using single-cell dual-wavelength microfluorometry and the Ca(2+)-sensitive probe, fura-2, to monitor changes in [Ca2+]i. Glutamate induced a rapid, concentration-dependent rise in [Ca2+]i with an EC50 of 24 microM that was Mg(2+)-sensitive and dependent on the presence of extracellular Ca2+. NMDA increased [Ca2+]i in a glycine-dependent manner with an EC50 of 83 microM that was blocked by 1 microM MK-801 and 1 mM Mg2+. The non-NMDA receptor agonists kainate, AMPA, and quisqualate increased [Ca2+]i with an EC50 of 124, 5 and 8 microM, respectively. Responses to kainic acid were blocked by 10 microM CNQX and were shown to be sensitive to Mg2+ and dihydropyridine. AMPA stimulation was the most potent, and glutamate stimulation was the most efficacious at mediating increases in [Ca2+]i. The metabotropic receptor-specific agonist, trans-ACPD, failed to induce a change in [Ca2+]i. The glutamate-induced Ca2+ influx was about half of that elicited by a 50 mM K(+)-induced membrane depolarization and activation of voltage-sensitive Ca2+ channels. These results demonstrate the presence of glutamate receptors on rat melanotropes and suggest that glutamate receptors in the intermediate lobe of the pituitary may provide the excitatory counterbalance to the well-described secretoinhibiting input via dopamine and gamma-aminobutyric acid receptors. SN - 0028-3835 UR - https://www.unboundmedicine.com/medline/citation/8584110/Glutamate_receptor_agonists_modulate_[Ca2+]i_in_isolated_rat_melanotropes_ L2 - https://www.karger.com?DOI=10.1159/000126995 DB - PRIME DP - Unbound Medicine ER -