Regulatory effects of anandamide on intracellular Ca^(2+) concentration increase in trigeminal ganglion neurons  

作　　者：Yi Zhang Hong Xie Gang Lei Fen Li Jianping Pan Changjin Liu Zhiguo Liu Lieju Liu Xuehong Cao 

机构地区：[1]Department of Anesthesiology,Tongji Hospital Affiliated to Tongji Medical College,Huazhong University of Science and Technology [2]Jingzhou Central Hospital [3]Department of Physiology,Tongji Medical College,Huazhong University of Science and Technology [4]Department of Bioengineering,Wuhan Institute of Engineering

出　　处：《Neural Regeneration Research》2014年第8期878-887,共10页中国神经再生研究（英文版）

基　　金：supported by NIH,grant No.GM-63577;NNSF,grant No.30571537,No.30271500;the National Natural Science Foundation of China,No.30271500,30571537 and 81370246;2010 National Clinical Key Disciplines Construction Grant from the Ministry of Health of the People’s Republic of China

摘　　要：Activation of cannabinoid receptor type 1 on presynaptic neurons is postulated to suppress neu- ~ ~ ~ 2＋ ~ ~ 2＋ rotransmlsslon by decreasing Ca reflux through high voltage-gated Ca channels. However, recent studies suggest that cannabinoids which activate cannabinoid receptor type 1 can increase neurotransmitter release by enhancing Ca2＋ influx in vitro. The aim of the present study was to investigate the modulation of intracellular Ca2＋ concentration by the cannabinoid receptor type 1 agonist anandamide, and its underlying mechanisms. Using whole cell voltage-damp and calcium imaging in cultured trigeminal ganglion neurons, we found that anandamide directly caused Ca2＋ influx in a dose-dependent manner, which then triggered an increase of intracellular Ca2＋ concentration. The cyclic adenosine and guanosine monophosphate-dependent protein kinase systems, but not the protein kinase C system, were involved in the increased intracellular Ca2＋concentration by anandamide. This result showed that anandamide increased intracellu- lar Ca2＋ concentration and inhibited high voltage-gated Ca2＋ channels through different signal transduction pathways.Activation of cannabinoid receptor type 1 on presynaptic neurons is postulated to suppress neu- ~ ~ ~ 2＋ ~ ~ 2＋ rotransmlsslon by decreasing Ca reflux through high voltage-gated Ca channels. However, recent studies suggest that cannabinoids which activate cannabinoid receptor type 1 can increase neurotransmitter release by enhancing Ca2＋ influx in vitro. The aim of the present study was to investigate the modulation of intracellular Ca2＋ concentration by the cannabinoid receptor type 1 agonist anandamide, and its underlying mechanisms. Using whole cell voltage-damp and calcium imaging in cultured trigeminal ganglion neurons, we found that anandamide directly caused Ca2＋ influx in a dose-dependent manner, which then triggered an increase of intracellular Ca2＋ concentration. The cyclic adenosine and guanosine monophosphate-dependent protein kinase systems, but not the protein kinase C system, were involved in the increased intracellular Ca2＋concentration by anandamide. This result showed that anandamide increased intracellu- lar Ca2＋ concentration and inhibited high voltage-gated Ca2＋ channels through different signal transduction pathways.

关 键 词：nerve regeneration trigeminal ganglion NEURONS ENDOCANNABINOIDS ANANDAMIDE can-nabinoid receptor type 1 voltage-dependent calcium channels vanilloid receptor patch-damp tech-nique calcium cyclic adenosine monophosphate protein kinase protein kinase C NIH grant neuralregeneration 

分 类 号：R741[医药卫生—神经病学与精神病学]