%0 Journal Article
%T Mediation by calcium/calmodulin-dependent protein kinase II of suppression of GABAAreceptors by NMDA<br>
%A WANG Dianshi Lü
%A Hui XU Tianle
%A <br>
%J 中国科学C辑(英文版)
%D 2000
%I Springer
%X 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 (V H ) of  40 mV in SDCN neurons. The selective NMDA receptor antagonist, D-2-amino-5-phosphonovaleric acid (APV, 100 γmol/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 μmol/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 suppression of Igaba by NMDA application; (iii) the suppression of IGAba by NMDA was inhibited by KN-62, a calcium/calmodulin-dependent protein kinase II (CaMKII) inhibitor. These results indicated that the inhibition of GABA response by NMDA is Ca2+-dependent and CaMKII is involved in the process of the Ca2+-dependent inhibition.
%K sacral dorsal commissural nucleus
%K N-methyl-D-aspartate receptor
%K γ
%K -aminobutyric acid receptor
%K calcium/calmodulin-dependent protein kinase II
%K cross talk<br>
%U http://www.alljournals.cn/get_abstract_url.aspx?pcid=90BA3D13E7F3BC869AC96FB3DA594E3FE34FBF7B8BC0E591&jid=180CF3A72E750F3261A8A60EDC957784&aid=73EDAC7840115E05&yid=9806D0D4EAA9BED3&vid=BE33CC7147FEFCA4&iid=B31275AF3241DB2D&sid=04FC77FB58A9B53A&eid=A0C7970CD30381EA&journal_id=1674-7305&journal_name=ScienceChina.Lifesciences&referenced_num=0&reference_num=17