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Using nystatin-perforated whole-cell recording configuration, the modulatory effect of N-methyl-D-aspartate (NMDA) on γ-aminobutyric acid (GABA)-activated whole-cell currents was investigated in neurons freshly dissociated from the rat sacral dorsal commissural nucleus (SDCN). The results showed that: (i) NMDA suppressed GABA- and muscimol (Mus)-activated currents (IGABA and IMUS), respectively in the Mg2+-free external solution containing 1 μmol/L glycine at a holding potential (VH) of -40 mV in SDCN neurons. The selective NMDA receptor antagonist, D-2-amino-5-phosphonovaleric acid (APV, 100 μmol/L), inhibited the NMDA-evoked currents and blocked the NMDA-induced suppression of IGABA; (ii) when the neurons were incubated in a Ca2+-free bath or pre-loaded with a membrane-permeable Ca2+ chelator, BAPTA AM (10 nmol/L), the inhibitory effect of NMDA on IGABA disappeared. Cd2+ (10 μmol/L) or La3+(30 μmol/L), the non-selective blockers of voltage-dependent calcium channels, did not affect the suppressio
Using nystatin-perforated whole-cell recording configuration, the modulatory effect of N-methyl-D-aspartate (NMDA) on γ-aminobutyric acid (GABA) -activated whole-cell currents was investigated in neurons freshly dissociated from the rat sacral dorsal commissural nucleus (SDCN). The results showed that: (i) NMDA suppressed GABA- and muscimol (Mus) -activated currents (IGABA and IMUS), respectively in the Mg2 + -free external solution containing 1 μmol / L glycine at a holding potential VH) of -40 mV in SDCN neurons. The selective NMDA receptor antagonist, inhibited the NMDA-evoked currents and blocked the NMDA-induced suppression of IGABA (APV, 100 μmol / L) ; (ii) when the neurons were incubated in a Ca2 + -free bath or pre-loaded with a membrane-permeable Ca2 + chelator, BAPTA AM (10 nmol / L), the inhibitory effect of NMDA on IGABA disappeared. Cd2 + L) or La3 + (30 μmol / L), the non-selective blockers of voltage-dependent calcium channels, did not aff ect the suppressio