Editing Cannabinol (section)

====Neurotransmitter interactions====
[[File:DSI_DSE_Diagram_-_Mechanism_of_Action_of_eCB_ligands_at_CB1R_in_the_brain.jpg|thumb|400x400px|In the brain, the canonical mechanism of CB1 receptor activation is a form of short-term [[synaptic plasticity]] initiated via [[retrograde signaling]] of [[endogenous]] CB1 agonists such as [[2-Arachidonoylglycerol|2AG]] or [[Anandamide|AEA]] (two primary endocannabinoids).|left]]

In the brain, the canonical mechanism of CB1 receptor activation is a form of short-term [[synaptic plasticity]] initiated via [[retrograde signaling]] of [[endogenous]] CB1 agonists such as [[2-Arachidonoylglycerol|2AG]] or [[Anandamide|AEA]] (two primary endocannabinoids). This mechanism of action is called depolarization-induced suppression of inhibition (DSI) or depolarization-induced suppression of excitation (DSE),<ref name="Diana-2004">{{cite journal | vauthors = Diana MA, Marty A | title = Endocannabinoid-mediated short-term synaptic plasticity: depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE) | journal = British Journal of Pharmacology | volume = 142 | issue = 1 | pages = 9–19 | date = May 2004 | pmid = 15100161 | pmc = 1574919 | doi = 10.1038/sj.bjp.0705726 }}</ref> depending on the classification of the [[Chemical synapse|presynaptic neuron]] acted upon by the retrograde messenger (''see diagram at left''). In the case of CB1R agonism on the presynaptic membrane of a [[Γ-Aminobutyric acid|GABAergic interneuron]], activation leads to a net effect of increased activity, while the same activity on a [[Glutamate (neurotransmitter)|glutamatergic neuron]] leads to the opposite net effect. The release of other neurotransmitters is also modulated in this way, particularly [[dopamine]], [[dynorphin]], [[oxytocin]], and [[vasopressin]].<ref name="Diana-2004" />