anandamide and arachidonylcyclopropylamide
anandamide has been researched along with arachidonylcyclopropylamide* in 2 studies
Other Studies
2 other study(ies) available for anandamide and arachidonylcyclopropylamide
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Endocannabinoids in the brainstem modulate dural trigeminovascular nociceptive traffic via CB1 and "triptan" receptors: implications in migraine.
Activation and sensitization of trigeminovascular nociceptive pathways is believed to contribute to the neural substrate of the severe and throbbing nature of pain in migraine. Endocannabinoids, as well as being physiologically analgesic, are known to inhibit dural trigeminovascular nociceptive responses. They are also involved in the descending modulation of cutaneous-evoked C-fiber spinal nociceptive responses from the brainstem. The purpose of this study was to determine whether endocannabinoids are involved in the descending modulation of dural and/or cutaneous facial trigeminovascular nociceptive responses, from the brainstem ventrolateral periaqueductal gray (vlPAG). CB1 receptor activation in the vlPAG attenuated dural-evoked Aδ-fiber neurons (maximally by 19%) and basal spontaneous activity (maximally by 33%) in the rat trigeminocervical complex, but there was no effect on cutaneous facial receptive field responses. This inhibitory vlPAG-mediated modulation was inhibited by specific CB1 receptor antagonism, given via the vlPAG, and with a 5-HT1B/1D receptor antagonist, given either locally in the vlPAG or systemically. These findings demonstrate for the first time that brainstem endocannabinoids provide descending modulation of both basal trigeminovascular neuronal tone and Aδ-fiber dural-nociceptive responses, which differs from the way the brainstem modulates spinal nociceptive transmission. Furthermore, our data demonstrate a novel interaction between serotonergic and endocannabinoid systems in the processing of somatosensory nociceptive information, suggesting that some of the therapeutic action of triptans may be via endocannabinoid containing neurons in the vlPAG. Topics: Animals; Arachidonic Acids; Bicuculline; Cannabinoid Receptor Agonists; Disease Models, Animal; Endocannabinoids; GABA-A Receptor Antagonists; Male; Microinjections; Nerve Fibers, Myelinated; Pain; Periaqueductal Gray; Polyunsaturated Alkamides; Rats; Rats, Sprague-Dawley; Reaction Time; Receptor, Cannabinoid, CB1; Receptors, Serotonin; Serotonin Agents; Serotonin Antagonists; Skin; Trigeminal Nuclei | 2013 |
The preventive effect of cannabinoids on reperfusion-induced ischemia of mouse kidney.
Artery occlusion of an organ results in ischemia. When the occlusion is opened and blood flow reinstated there will be tissue injuries identified as reperfusion-induced ischemia (RII). It has been suggested that cannabinoids (CBs) may be involved in the RII. In this study, we assessed the effect of different doses of anandamide analogs and CB receptor agonists: arachidonylcyclopropylamide (ACPA, a CB1 agonist) and JWH133 (a CB2 agonist) in the RII of the mouse kidney. Three doses (0.2, 1 and 5mg/kg, i.p.) of ACPA or JWH133 were used 30min prior initiation of RII. Kidneys were removed 2 and 24h following RII and checked histologically for the grading of ischemic injury. Appropriate control groups were used as well. RII produced lesion comparable with that of ischemia. Different doses of ACPA or JWH133 prevented RII-induced lesions. It is suggestive of the CB system involvement in the kidney RII in mice. Topics: Animals; Arachidonic Acids; Cannabinoid Receptor Agonists; Cannabinoids; Endocannabinoids; Female; Kidney; Mice; Polyunsaturated Alkamides; Reperfusion Injury | 2008 |