Endocannabinoid-mediated synaptic plasticity in the CNS.

By Vivien Chevaleyre, Kanji A. Takahashi, P. Castillo. Annual Review of Neuroscience, 2006

798 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Pharmacology

View Paper: https://www.semanticscholar.org/paper/0e634cdf1479bdda8bdf2962559303a2ea39639a

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Citations in the corpus

Burst timing-dependent plasticity of NMDA receptor-mediated transmission in midbrain dopamine neurons: A putative cellular substrate for reward learning (2009, neutral): “mediated processes (Chevaleyre et al., 2006), activity-dependent changes in ion channels (Catterall and Few, 2008; Wang, 2008), and even activation of presynaptic conductances by decreases in cleft Ca accompanying sustained pre- and postsynaptic spiking (Phillips et al.”
Synaptic plasticity and addiction (2007, background): “At some synapses, however, prolonged eCB release instead causes LTD, which is mediated by a long-lasting depression of transmitter release (eCB-LTD”
Synaptic Mechanisms for Plasticity in Neocortex (2009, background): “A third form of LTD involves cannabinoid type 1 (CB1) receptors (Chevaleyre et al. 2006).”
Striatal plasticity and basal ganglia circuit function (2008, positive): “Yet this alone would not induce sufficient endocannabinoid release to elicit LTD (Chevaleyre et al., 2006; Ronesi et al., 2004).”
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “The mechanisms of endocannabinoid release are unclear and may involve a transporter, which facilitates diffusion across the plasma membrane (Chevaleyre et al, 2006) Such retrograde signaling by postsynaptic release of endocannabinoids can be initiated by strong depolarization or activation of…”
Endocannabinoid signaling and synaptic function (2012, background): “Their role as retrograde messengers suppressing transmitter release in a transient or long-lasting manner, at both excitatory and inhibitory synapses, is now well established (Alger, 2012; Chevaleyre et al., 2006; Freund et al., 2003; Kano et al., 2009; Katona and Freund, 2012).”
The spike timing dependence of plasticity (2012, background): “…LTD, which is linked most strongly to STDP, postsynaptic calcium and mGluR activation trigger dendritic synthesis of endocannabinoids, which diffuse retrogradely to activate CB1Rs on the presynaptic terminal and drive a long-lasting decrease in release probability (Chevaleyre et al., 2006).”
Dysconnection in Schizophrenia: From Abnormal Synaptic Plasticity to Failures of Self-monitoring (2009, background): “several forms of transient and persistent synaptic plasticity.(199,200) ‘‘Given the widespread role of CB1 receptors and endocannabinoids in eliciting or shaping neuronal plasticity, it is reasonable to speculate that THC and other cannabinoids produce their psychoactive effects by perturbing endoca”
Pyramidal Neuron Conductance State Gates Spike-Timing-Dependent Plasticity (2010, background): “…that t-LTP and t-LTD involve separate calcium sources and coincidence detection mechanisms (Sjöström et al., 2003, 2004; Bender et al., 2006; Chevaleyre et al., 2006; Duguid and Sjöström, 2006; Nevian and Sakmann, 2006; Rodríguez-Moreno and Paulsen, 2008; Sjöström et al., 2008;…”
Distinct coincidence detectors govern the corticostriatal spike timing‐dependent plasticity (2010, background): “Since such a calcium entry occurs when NMDARs are activated in t-LTP, we tested the putative effects of endocannabinoids on t-LTP, especially in light of the fact that endocannabinoids can modulate a CB1R-independent LTP (Chevaleyre et al. 2006; Kano et al. 2009).”
Endocannabinoid signaling as a synaptic circuit breaker in neurological disease (2008, background): “Although the general outcome of retrograde endocannabinoid signaling is always a decrease in synaptic transmission, the time course of expression of this phenomenon divides endocannabinoid-mediated synaptic plasticity into two types with potentially distinct physiological and pathophysiological impl”
Dendritic excitability and synaptic plasticity. (2008, positive): “Dendritic spikes have also been implicated in a relatively short-lasting form of synaptic plasticity, such as DSE, which is mediated by retrograde endocannabinoid signaling from the postsynaptic cell (128, 225, 394, 601, 842) (sect.”
The endocannabinoid system controls key epileptogenic circuits in the hippocampus. (2006, neutral): “…system exerts important functions in the central nervous system, such as retrograde inhibition of neurotransmitter release (Alger, 2002; Chevaleyre et al., 2006; Marsicano and Lutz, 2006), control of neuronal excitability (Marsicano et al., 2003), and regulation of various forms of…”