Cytosolic phospholipase A2 alpha/arachidonic acid pathway mediates depolarization-induced suppression of excitation at cerebellar parallel fiber-Purkinje cell synapses
作者单位：Department of NeurobiologyKey Laboratory of Medical Neurobiology of Ministry of HealthZhejiang Province Key Laboratory of NeurobiologyZhejiang University School of Medicine Neuroscience Care UnitThe Second Affiliated Hospital of Zhejiang University School of Medicine
会议名称：《中国神经科学学会第十届全国学术会议》
会议日期：2013年
学科分类：0710[理学-生物学] 07[理学] 071006[理学-神经生物学]
关 键 词：DSE cPLA2α arachidonic acid Purkinje cell parallel fiber
摘 要：Objective Depolarization-induced suppression of excitation(DSE) at parallel fiber to Purkinje cell synapses is an endocannabinoid-mediated short-term retrograde *** Ca elevation is critical for the endocannabinoid production and ***,what biochemical pathways are evoked by elevated Ca and are involved in the synthesis and release of endocannabinoids is not *** the present study,we aimed to elucidate the mechanisms by which the brief depolarization induces DSE at parallel fiber to Purkinje cell *** Using slice whole-cell patch-clamp combined with pharmacological applications,electrophysiological experiments were developed at parallel fiber-Purkinje cell *** In the present work,we measured DSE at parallel fiber-Purkinje cell synapses in wild type and phospholipase A alpha(cPLA) knock-out *** data showed that DSE is inhibited in cPLA knock-out mice,which can be rescued by the bath application of arachidonic acid,which is freed from phospholipids by *** also show that DSE at parallel fiber-Purkinje cell synapses is blocked by internal K,but not affected by the antagonists of purinergic P2X7 receptor(P2X7R),protein kinase C(PKC) and cAMP-dependent protein kinase(PKA).Conclusion Our data showed that cPLA/arachidnoic acid pathway is required for DSE *** data first suggest a novel mechanism for the brief depolarization-induced DSE at parallel fiber to Purkinje cell *** also show that DSE at this synapse is blocked by internal K,but not affected by the ectopic activation of P2X7R and presynaptic PKC and PKA.