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

Regulatory effects of anandamide on intracellular Ca^(2+) concentration increase in trigeminal ganglion neurons
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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.
出处 《Neural Regeneration Research》 SCIE CAS CSCD 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
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 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
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