2-aminoethoxydiphenyl borate or lanthanum potentiates transient receptor potential-like channels in rat CA1 hippocampal neurons
2-aminoethoxydiphenyl borate or lanthanum potentiates transient receptor potential-like channels in rat CA1 hippocampal neurons
摘要
Abstract
Expression of transient receptor potential(TRP)channels is widespread with transcripts distributed throughout the brain.All TRP channel subunits are activated following phospholipase C activation and form cation-selective ion channels.Previous studies examining the existence of TRP channels in hippocampal CA1 pyramidal neurons were based on cultured neurons.Therefore,their relevance for living tissue remains unclear.In the present study,patch-clamp recordings were conducted from CA1 pyramidal neurons in hippocampal slices from 7-day-old rats.Whole-cell currents were obtained from CA1 hippocampal neurons with potentiation effects of 2-aminoethoxydiphenyl borate and lanthanum,revealing that recorded experimental currents were characteristic TRP-like channel currents.Identification of rat hippocampal mRNA transcripts of TRPC4,TRPC5,TRPV1,TRPV2,and TRPV3 channels further verified the expression of characteristic TRP-like channels on rat CA1hippocampal neurons.关键词
transient receptor potential-like channel/CA1 hippocampal neuron/2-aminoethoxydiphenyl borate/lanthanum/patch-clampKey words
transient receptor potential-like channel/CA1 hippocampal neuron/2-aminoethoxydiphenyl borate/lanthanum/patch-clamp分类
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Fengpeng Sun,Tian-ming Gao..2-aminoethoxydiphenyl borate or lanthanum potentiates transient receptor potential-like channels in rat CA1 hippocampal neurons[J].中国神经再生研究（英文版）,2010,5(18):1378-1383,6.基金项目
This study was supported by the Medical Scientific Research Foundation of Guangdong Province (Effects of TRPs channel on neuron death following cerebral ischemia), No. A2006372 （Effects of TRPs channel on neuron death following cerebral ischemia）
the National Natural Science Foundation of China (Mechanism of Caspase non-dependent neuronal apoptosis following ischemic cerebral injury), No. U0632007 （Mechanism of Caspase non-dependent neuronal apoptosis following ischemic cerebral injury）
the Natural Science Foundation of Guangdong Province (Basic research of new strategies for treatment of ischemic stroke), No. 9351051501000003 （Basic research of new strategies for treatment of ischemic stroke）
the Major Program of Natural Science Research of Higher Learning School of Guangdong Province (Mechanism of non-typical apoptosis of brain neurons following stroke), No. 06Z007 （Mechanism of non-typical apoptosis of brain neurons following stroke）
the Key Project of Science and Technology of Guangzhou City (Key technique research and instrument research and development of rapid remedy in traffic accident-induced craniocerebral and spinal cord injury), No. 2007zl-E0081 （Key technique research and instrument research and development of rapid remedy in traffic accident-induced craniocerebral and spinal cord injury）
the Program for Changjiang Scholars and Innovative Research Team (Cell signal mechanism and new drug selection for inflammation-related diseases), No. IRT0731. （Cell signal mechanism and new drug selection for inflammation-related diseases）
