A single in-vivo exposure to delta 9THC blocks endocannabinoid-mediated synaptic plasticity.
Susana Mato, Vivien Chevaleyre, David Robbe, Angel Pazos, Pablo E Castillo, Olivier J. J. Manzoni
Nature Neuroscience June 2004 DOI: 10.1038/nn1251 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal study (in vivo THC exposure with in vitro electrophysiology) Peer reviewed |
|---|---|
| Population | Mice |
| Intervention | Delta 9-tetrahydrocannabinol (THC) |
| Duration | Effect reversible within 3 days |
| Topics | Neuroplasticity |
| Key points | A single in-vivo THC exposure abolished endocannabinoid-mediated retrograde signaling underlying synaptic plasticity in the nucleus accumbens and hippocampus in vitro. The effect was reversible within 3 days and associated with a transient modification of cannabinoid receptor functional properties. |
Abstract
Endogenous cannabinoids (eCB) mediate synaptic plasticity in brain regions involved in learning and reward. Here we show that in mice, a single in-vivo exposure to Delta 9-tetrahydrocannabinol (THC) abolishes the retrograde signaling that underlies eCB-mediated synaptic plasticity in both nucleus accumbens (NAc) and hippocampus in vitro. This effect is reversible within 3 days and is associated with a transient modification in the functional properties of cannabinoid receptors.
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Citations in the library
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