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This Article Full Text Full Text (PDF) All Versions of this Article: 584/2/373    most recent jphysiol.2007.137497v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hashimotodani, Y. Articles by Kano, M. Search for Related Content PubMed PubMed Citation Articles by Hashimotodani, Y. Articles by Kano, M. Related Collections Review articles

¹ Department of Neurophysiology
² Department of Cellular Neuroscience, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
³ Department of Impairment Study, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-0942, Japan
⁴ Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060-8638, Japan

Endocannabinoids are released from postsynaptic neurons, activate presynaptic cannabinoid receptors and cause various forms of short-term and long-term synaptic plasticity throughout the brain. Using hippocampal and cerebellar neurons, we have revealed that endocannabinoid release can be induced through two different pathways. One is independent of phospholipase C (PLC) and driven by Ca²⁺ elevation alone (Ca²⁺-driven endocannabinoid release, CaER), and the other is PLC-dependent and driven by activation of G_q/11-coupled receptors (receptor-driven endocannabinoid release, RER). CaER is induced by activation of either voltage-gated Ca²⁺ channels or NMDA receptors. RER is functional even at resting Ca²⁺ levels (basal RER), but markedly enhanced by a small Ca²⁺ elevation (Ca²⁺-assisted RER). In Ca²⁺-assisted RER, PLC serves as a coincidence detector of receptor activation and Ca²⁺ elevation. We have also demonstrated that Ca²⁺-assisted RER is essential for the endocannabinoid release triggered by synaptic activity. Our anatomical data show that a set of receptors and enzymes required for RER are well organized so that the excitatory input can trigger RER effectively. Certain forms of spike-timing-dependent plasticity (STDP) are reported to depend on endocannabinoid signalling. The NMDA receptor and PLC might play key roles in the endocannabinoid-dependent forms of STDP as coincidence detectors with different timing dependences.

(Received 28 May 2007; accepted after revision 3 July 2007; first published online 5 July 2007)
Corresponding author M. Kano: Department of Cellular Neuroscience, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan. Email: mkano{at}cns.med.osaka-u.ac.jp

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