Thyrotropin-releasing hormone (TRH) attenuates glutamate-stimulated increases in calcium in primary neuronal cultures

• Published in: Brain research 1996-08, Vol.730 (1-2), p.143-149
• Main Authors: KOENIG, M. L, YOURICK, D. L, MEYERHOFF, J. L
• Format: Article
• Language: English
• Subjects: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid - pharmacology; Animals; Biological and medical sciences; Calcium - metabolism; Calcium Channels - physiology; Cells, Cultured; Cycloleucine - analogs & derivatives; Cycloleucine - pharmacology; Electrophysiology; Fundamental and applied biological sciences. Psychology; Glutamic Acid - pharmacology; Intracellular Membranes - metabolism; Ion Channel Gating; Isolated neuron and nerve. Neuroglia; N-Methylaspartate - pharmacology; Neurons - metabolism; Rats - embryology; Thyrotropin-Releasing Hormone - pharmacology; Vertebrates: nervous system and sense organs
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(96)00433-7

Thyrotropin-releasing hormone (TRH) has been found to be widely distributed in the mammalian central nervous system. Further, the concentration of the tripeptide increases following seizure activity, and TRH is known to have anticonvulsant effects. We have investigated the possibility that the anticonvulsant activity of TRH may be due, at least in part, to an attenuation of the glutamate-stimulated increases in intraneuronal Ca2+ ([Ca]i) that occur with epileptic activity. We find that the tripeptide does not itself excite neurons and that it is able to significantly reduce glutamate-stimulated increases in [Ca]i in cultured neurons derived from fetal rat forebrain. Increases in the concentration of TRH following seizure activity may represent an endogenous homeostatic mechanism for reducing glutamate-induced elevations in intraneuronal Ca2+.