Korean J Physiol Pharmacol.
2003 Apr;7(2):53-58.
Mechanism of Glutamate-induced[Ca2+]i Increase in Substantia Gelatinosa Neurons of Juvenile Rats
- Affiliations
-
- 1Department of Physiology, College of Medicine, Kangwon National University, Chunchon, Korea. sangjkim@kangwon.ac.kr
- 2Department of Physiology, Seoul National University College of Medicine, Seoul, Korea.
Abstract
- The glutamate receptors (GluRs) are key receptors for modulatory synaptic events in the central nervous system. It has been reported that glutamate increases the intracellularCa (2+) concentration ([Ca2+]i) and induces cytotoxicity. In the present study, we investigated whether the glutamate-induced[Ca2+]i increase was associated with the activation of ionotropic (iGluR) and metabotropic GluRs (mGluR) in substantia gelatinosa neurons, using spinal cord slice of juvenile rats (10~21 day) .[Ca2+]i was measured using conventional imaging techniques, which was combined with whole-cell patch clamp recording by incorporating fura-2 in the patch pipette. At physiological concentration of extracellularCa (2+), the inward current and[Ca2+]i increase were induced by membrane depolarization and application of glutamate. Dose-response relationship with glutamate was observed in bothCa (2+) signal and inward current. The glutamate-induced[Ca2+]i increase at holding potential of 70 mV was blocked by CNQX, an AMPA receptor blocker, but not by AP-5, a NMDA receptor blocker. The glutamate-induced[Ca2+]i increase inCa (2+) free condition was not affected by iGluR blockers. A selective mGluR (group I) agonist, RS-3, 5-dihydroxyphenylglycine (DHPG), induced[Ca2+]i increase at holding potential of 70 mV in SG neurons. These findings suggest that the glutamate-induced[Ca2+]i increase is associated with AMPA-sensitive iGluR and group I mGluR in SG neurons of rats.