Endocannabinoid signaling in the brain.
Rachel I Wilson, Roger A Nicoll
Science April 26, 2002 DOI: 10.1126/science.1063545 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Review Peer reviewed |
|---|---|
| Key findings | Argues that endogenous cannabinoids function as retrograde synaptic messengers, released from postsynaptic neurons to activate CB1 receptors on presynaptic axons and suppress neurotransmitter release, and that this mechanism may mediate cannabinoid effects on memory, cognition, and pain perception. |
Abstract
The primary psychoactive ingredient in cannabis, Delta9-tetrahydrocannabinol (Delta9-THC), affects the brain mainly by activating a specific receptor (CB1). CB1 is expressed at high levels in many brain regions, and several endogenous brain lipids have been identified as CB1 ligands. In contrast to classical neurotransmitters, endogenous cannabinoids can function as retrograde synaptic messengers: They are released from postsynaptic neurons and travel backward across synapses, activating CB1 on presynaptic axons and suppressing neurotransmitter release. Cannabinoids may affect memory, cognition, and pain perception by means of this cellular mechanism.
Citations in the library
Cited by 50
- Gone to Pot – A Review of the Association between Cannabis and Psychosis Frontiers in Psychiatry May 22, 2014
- Human Laboratory Studies on Cannabinoids and Psychosis. Biological Psychiatry April 1, 2016
- Mitigation of post‐traumatic stress symptoms by Cannabis resin: A review of the clinical and neurobiological evidence Drug Testing and Analysis June 26, 2012
- The cannabinoid CB 1 receptor and the endocannabinoid anandamide: possible antidepressant targets Expert Opinion on Therapeutic Targets October 14, 2008
- Cannabinoid ‘model’ psychosis, dopamine–cannabinoid interactions and implications for schizophrenia Cambridge University Press eBooks May 27, 2004
and 45 more in the library
Cites 2
- Supersensitivity to anandamide and enhanced endogenous cannabinoid signaling in mice lacking fatty acid amide hydrolase. Proceedings of the National Academy of Sciences of the United States of America July 31, 2001
- Unresponsiveness to cannabinoids and reduced addictive effects of opiates in CB1 receptor knockout mice. Science January 15, 1999