Intravenous self-administration of the cannabinoid CB1 receptor agonist WIN 55,212-2 in rats

2001 ◽  
Vol 156 (4) ◽  
pp. 410-416 ◽  
Author(s):  
Liana Fattore ◽  
Gregorio Cossu ◽  
Cristina Martellotta ◽  
Walter Fratta
Keyword(s):  
Receptor Agonist ◽  
Cb1 Receptor ◽  
Cannabinoid Cb1 Receptor ◽  
Self Administration

Increased motivation for beer in rats following administration of a cannabinoid CB1 receptor agonist

1999 ◽  
Vol 370 (3) ◽  
pp. 233-240 ◽  
Author(s):  
Jason E. Gallate ◽  
Tanya Saharov ◽  
Paul E. Mallet ◽  
Iain S. McGregor
Keyword(s):  
Receptor Agonist ◽  
Cb1 Receptor ◽  
Cannabinoid Cb1 Receptor

scholarly journals Cannabinoid CB1 receptor agonist ACEA alleviates brain ischemia/reperfusion injury via CB1–Drp1 pathway

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Shuai Yang ◽  
Bin Hu ◽  
Zongming Wang ◽  
Changming Zhang ◽  
Haosen Jiao ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Brain Ischemia ◽  
Receptor Agonist ◽  
Ischemia Reperfusion Injury ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
Cb1 Receptor ◽  
Cannabinoid Cb1 Receptor ◽  
Neuroprotective Effects

Abstract Activation of the cannabinoid CB1 receptor induces neuroprotection against brain ischemia/reperfusion injury (IRI); however, the mechanism is still unknown. In this study, we used oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in neuronal cells and middle cerebral artery occlusion (MCAO)-induced brain IRI in rats to mimic ischemic brain injury, and hypothesized that the CB1 receptor agonist arachidonyl-2-chloroethylamide (ACEA) would protect ischemic neurons by inhibiting mitochondrial fission via dynamin-related protein 1 (Drp1). We found that OGD/R injury reduced cell viability and mitochondrial function, increased lactate dehydrogenase (LDH) release, and increased cell apoptosis, and mitochondrial fission. Notably, ACEA significantly abolished the OGD/R-induced neuronal injuries described above. Similarly, ACEA significantly reversed MCAO-induced increases in brain infarct volume, neuronal apoptosis and mitochondrial fission, leading to the recovery of neurological functions. The neuroprotective effects of ACEA were obviously blocked by coadministration of the CB1 receptor antagonist AM251 or by the upregulation of Drp1 expression, indicating that ACEA alleviates brain IRI via the CB1–Drp1 pathway. Our findings suggest that the CB1 receptor links aberrant mitochondrial fission to brain IRI, providing a new therapeutic target for brain IRI treatment.

ACEA (a highly selective cannabinoid CB1 receptor agonist) stimulates hippocampal neurogenesis in mice treated with antiepileptic drugs

2015 ◽  
Vol 1624 ◽  
pp. 86-94 ◽  
Author(s):  
Marta Andres-Mach ◽  
Agnieszka Haratym-Maj ◽  
Miroslaw Zagaja ◽  
Radoslaw Rola ◽  
Maciej Maj ◽  
...  
Keyword(s):  
Antiepileptic Drugs ◽  
Receptor Agonist ◽  
Cb1 Receptor ◽  
Hippocampal Neurogenesis ◽  
Cannabinoid Cb1 Receptor
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