Endocannabinoid signaling in the brain.
Rachel I Wilson, Roger A Nicoll
Science (New York, N.Y.) 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.