海馬CA１錐体細胞におけるNMDA受容体を介したプラトー電位に伴うカルシウム上昇

抄録

Extra-synaptic NMDA-receptor (NMDA-R) -mediated plateau potential can be induced either by synaptic stimulation in the presence of glutamate transporter antagonist TBOA or by iontophoresis of glutamate in hippocampal CA1 pyramidal neurons (Suzuki et al., 2007, submitted). To investigate if the NMDA-R-mediated plateau potentials is accompanied by a rise in [Ca ²⁺]_i, we performed whole-cell recordings and Ca²⁺ imagings simultaneously from single CA1 pyramidal neurons in hippocampal slices. Neurons were loaded with Ca²⁺ indicator Fluo-4 (100μM). NMDA-R-mediated plateau potentials were induced by repetitively stimulating Schaffer collaterals or by applying glutamate iontophoretically in the presence of 10μM CNQX and 50μM DL-APV. Substantial increase in [Ca²⁺]_i accompanying the plateau potential was detected both at the dendrite and the soma. When TBOA was present, a slow rise in [Ca²⁺]_i was detected near the soma after the end of the plateau potentials. After adding Cd²⁺ and antagonists for metabotropic glutamate receptors, most of the Ca²⁺ rise was suppressed, leaving small but substantial Ca²⁺ rise in the dendrites. This Ca²⁺ elevation was abolished by applying 30μM 5,7-dCK, an antagonist for the glycine binding site of the NMDA-R. Our results show that the NMDA-R-mediated plateau potential is accompanied by substantial Ca²⁺ elevation mainly due to Ca²⁺ entry from voltage-gated Ca²⁺ channels and partly due to Ca²⁺ entry from NMDA-R channels. [J Physiol Sci. 2008;58 Suppl:S128]