Mechanism of Glutamate-inducedCa2+i Increase in Substantia Gelatinosa Neurons of Juvenile Rats
The Korean Journal of Physiology and Pharmacology
;
: 53-58, 2003.
Article
in English
| WPRIM
| ID: wpr-727619
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Spinal Cord
/
Substantia Gelatinosa
/
Central Nervous System
/
Fura-2
/
N-Methylaspartate
/
Receptors, Glutamate
/
Receptors, Metabotropic Glutamate
/
Receptors, AMPA
/
6-Cyano-7-nitroquinoxaline-2,3-dione
/
Glutamic Acid
Limits:
Animals
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2003
Type:
Article
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