Absence of gaba type a signaling in adult medial

• 作 者: De-GuangWANG[1]Tian-LeXU[2]
• 机 构: Department of Human Anatomy, Xuzhou Medical College, Xuzhou 221002
• 出 处: 中国神经科学学会第四次会员代表大会暨第七届全国学术会议(The 7th Biennial Meeting and the
• 发表日期: 2007年期

　　Neural inhibition in the brain is mainly mediated by onotropic GABA type A receptors.Apart from the GABA type receptors,both K-C1 cotransporter isoform 2 and the GABA-synthesizing enzyme,glutamic acid decarboxylase,are essential determinants for GABA type A receptor-mediated inhibition.By using immunofluorescent staining,we observed that K-Cl cotransporter isoform 2,GABA type A receptor 2/3 subunits and a presynaptically localized glutamic acid decarboxylase isoform,glutamic acid decarboxylase 65,were all absent in adult Sprague-Dawley rat medial habenular nucleus,while immunopositive staining for glutamic acid decarboxylase 67,GABA and GABA type B receptor type 2 subunit were present in the medial habenular nucleus.Consistent with the lack of GABA type A signaling as detected by immunohistochemistry,GABA (100 μM) evoked no measurable currents in the medial habenular nucleus but induced bicuculline-sensitive currents in the lateral habenular nucleus and in the CA1 area of hippocampus.