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Endocannabinoid signalling triggered by NMDA receptor-mediated calcium entry into rat hippocampal neurons.

Endocannabinoid signalling triggered by NMDA receptor-mediated calcium entry into rat hippocampal neurons. Research Abstract Details 

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  • Endocannabinoid signalling triggered by NMDA receptor-mediated calcium entry into rat hippocampal neurons. Abstract Text:

    takako ohno-shosakuTakako Ohno-Shosaku,yuki hashimotodaniYuki Hashimotodani,masato anoMasato Ano,sachi takedaSachi Takeda,hiroshi tsubokawaHiroshi Tsubokawa,masanobu kanoMasanobu Kano,takako ohno-shosakuTakako Ohno-Shosaku,yuki hashimotodaniYuki Hashimotodani,masato anoMasato Ano,sachi takedaSachi Takeda,hiroshi tsubokawaHiroshi Tsubokawa,masanobu kanoMasanobu Kano,takako ohno-shosakuTakako Ohno-Shosaku,yuki hashimotodaniYuki Hashimotodani,masato anoMasato Ano,sachi takedaSachi Takeda,hiroshi tsubokawaHiroshi Tsubokawa,masanobu kanoMasanobu Kano,

    Endocannabinoids are released from neurons in activity-dependent manners, act retrogradely on presynaptic CB(1) cannabinoid receptors, and induce short-term or long-term suppression of transmitter release. The endocannabinoid release is triggered by postsynaptic activation of voltage-gated Ca(2+) channels and/or G(q)-coupled receptors such as group I metabotropic glutamate receptors (I-mGluRs) and M(1)/M(3) muscarinic receptors. However, the roles of NMDA receptors, which provide another pathway for Ca(2+) entry into neurons, in endocannabinoid signalling have been poorly understood. In the present study, we investigated the possible contribution of NMDA receptors in endocannabinoid production by recording IPSCs in cultured hippocampal neurons. Under the conditions minimizing the activation of voltage-gated Ca(2+) channels, local application of NMDA (200 mum) transiently suppressed cannabinoid-sensitive IPSCs, but not cannabinoid-insensitive IPSCs. This NMDA-induced suppression was abolished by blocking NMDA receptors, CB(1) receptors and diacylglycerol lipase, but not by inhibiting voltage-gated Ca(2+) channels. When the postsynaptic neuron was dialysed with 30 mm BAPTA, the NMDA-induced suppression was reduced significantly. A lower dose of NMDA (20 mum) exerted little effect when applied alone, but markedly enhanced the cannabinoid-dependent suppression driven by muscarinic receptors or I-mGluRs. These data clearly indicate that the activation of NMDA receptors facilitates the endocannabinoid release either alone or in concert with the G(q)-coupled receptors.

    Endocannabinoid signalling triggered by NMDA receptor-mediated calcium entry into rat hippocampal neurons. Publishing Authors By Initials

    t ohno-shosakuT Ohno-Shosaku,y hashimotodaniY Hashimotodani,m anoM Ano,s takedaS Takeda,h tsubokawaH Tsubokawa,m kanoM Kano,t ohno-shosakuT Ohno-Shosaku,y hashimotodaniY Hashimotodani,m anoM Ano,s takedaS Takeda,h tsubokawaH Tsubokawa,m kanoM Kano,t ohno-shosakuT Ohno-Shosaku,y hashimotodaniY Hashimotodani,m anoM Ano,s takedaS Takeda,h tsubokawaH Tsubokawa,m kanoM Kano,

    For similar abstracts research abstracts see: abstracts research

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    Endocannabinoid signalling triggered by NMDA receptor-mediated calcium entry into rat hippocampal neurons. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: The Journal of physiology

    VOLUME: 584

    Page Numbers: 407-18

    Journal Abbreviation: J. Physiol. (Lond.)

    ISSN: 0022-3751

    DAY: 5

    MONTH: 07

    YEAR: 2007

    Endocannabinoid signalling triggered by NMDA receptor-mediated calcium entry into rat hippocampal neurons. Information

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    LANGUAGE: eng

    NlmUniqueID: 266262

    Endocannabinoid signalling triggered by NMDA receptor-mediated calcium entry into rat hippocampal neurons. Keywords Mesh Terms:

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    Grant and Affiliation Information for Endocannabinoid signalling triggered by NMDA receptor-mediated calcium entry into rat hippocampal neurons.

    AFFILIATION: Department of Cellular Neuroscience, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan. mkano@cns.med.osaka-u.ac.jp.

    Country: England

    England Research PublicationEngland Research Publication

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    MEDLINETA: J Physiol

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