作者: David M. Lovinger
DOI: 10.1007/978-3-540-74805-2_14
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摘要: Modulation of neurotransmitter release by G-protein-coupled receptors (GPCRs) is a prominent presynaptic mechanism for regulation synaptic transmission. Activation GPCRs located at the terminal can decrease probability release. This depression involves activation Gi/o-type G-proteins that mediate different inhibitory mechanisms, including inhibition voltage-gated calcium channels, potassium and direct vesicle fusion process. A variety neurotransmitters modulatory agents activate produce depression. Among these are lipid metabolites serve as agonists GPCRs. The discovery endocannabinoids their cognate receptors, CB 1 receptor, has stimulated intense investigation into neurophysiological roles metabolites. It now clear major physiological role receptor. Endocannabinoids this receptor mainly via retrograde signaling process in which compounds synthesized released from postsynaptic neuronal elements, travel back to act on CB1 endocannabinoid modulation been implicated short-term depression, suppression excitatory or transmission induced depolarization transient during agonist treatment activation. also play key one form long-term (LTD) long-lasting Endocannabinoid-dependent plasticity have brain processes, learning memory. present chapter discusses our current knowledge about cellular molecular mechanisms involved endocannabinoid-mediated endocannabinoid-dependent LTD.