Endocannabinoid Signaling in the Brain

By Rachel I. Wilson, R. Nicoll. Science, 2002

1,263 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Pharmacology

View Paper: https://www.semanticscholar.org/paper/ff9728733e790c394791321d9b9b079dacb7c01d

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In Cellular and Molecular Neuroscience

In Cognitive Neuroscience

In Pharmacology

Citations in the corpus

Chronic monoacylglycerol lipase blockade causes functional antagonism of the endocannabinoid system (2010, neutral): “, forms of synaptic plasticity that have been shown to require the CB 1 recepto”
Synaptic plasticity and addiction (2007, background): “At many CNS glutamatergic and γ-aminobutyric acid (GABA)-releasing synapses, a brief, strong postsynaptic Ca 2+ influx (and in some cases activation of mGluRs or muscarinic receptors alone) triggers the synthesis of endocannabinoids (eCBs), lipophilic molecules that travel retrogradely across the s”
Cloning of the first sn1-DAG lipases points to the spatial and temporal regulation of endocannabinoid signaling in the brain (2003, background): “However, in the adult brain there is a specific postsynaptic requirement for the synthesis of one or more endocannabinoids that act as retrograde messengers on presynaptic CB1 receptors to suppress further transmitter release at both excitatory and inhibitory synapses (Wilson and Nicoll, 2002).”
The Endocannabinoid System as an Emerging Target of Pharmacotherapy (2006, background): “This finding illustrates that, despite growing interest in endocannabinoids and their roles as retrograde neurotransmitters (Wilson and Nicoll, 2002; Chevaleyre et al., 2006), the mechanism of their release is not well understood.”
The emerging role of the endocannabinoid system in endocrine regulation and energy balance. (2006, background): “They thus mediate a retrograde signal (30, 106, 107).”
Involvement of the endocannabinoid system in drug addiction. (2006, background): “Endocannabinoids are thought to act as retrograde messengers in the CNS [ 11 ] and behave as neuromodulators in many physiological processes.”
The Psychotomimetic Effects of Intravenous Delta-9-Tetrahydrocannabinol in Healthy Individuals: Implications for Psychosis (2004, background): “…GABA release by interneurons (Sullivan, 1999; Katona et al, 1999a), which in turn would disrupt the synchronization of pyramidal cell activity (Wilson and Nicoll, 2002; Hoffman and Lupica, 2000), thereby interfering with associative functions, disrupting normal gating mechanisms, and…”
Cannabinoid physiology and pharmacology: 30 years of progress. (2004, background): “In the hippocampus, DSI is initiated by depolarization-induced opening of N-type voltage-controlled Ca channels (VCCs) (Wilson and Nicoll, 2002), which in turn effects release of endocannabinoids via a Ca dependent process (Piomelli, 2003).”
Anandamide and arachidonic acid use epoxyeicosatrienoic acids to activate TRPV4 channels (2003, background): “Interestingly, TRPV4 is also expressed in parts of the brain such as the hypothalamus, and might therefore contribute to the psychoactive effects of endocannabinoid”
The endocannabinoid system and its therapeutic exploitation (2004, positive): “In particular, endocannabinoids in the CNS intervene in both short-term and long-term forms of synaptic plasticity, including depolarization-induced suppression of both excitatory and inhibitory neurotransmission, long-term potentiation and depression, and long-term depression of inhibitio”
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “A major advance over the last decade has been the demonstration of the existence of endogenous cannabinoids (termed endocannabinoids) and their roles in modulating synaptic function (Chevaleyre et al, 2006; Freund et al, 2003; Kreitzer and Regehr, 2002; Piomelli, 2003; Wilson and Nicoll, 2002).”
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.”
Heterosynaptic LTD of hippocampal GABAergic synapses: a novel role of endocannabinoids in regulating excitability. (2003, neutral): “(C) The long-term depression of IPSCs induced by 50 M DHPG (white circles, n 4) was blocked by 2 M AM251, whereas the transient depression during DHPG application remained unchanged (n 4). gehr, 2002; Wilson and Nicoll, 2002).”