2015
DOI: 10.1016/j.physbeh.2015.01.038
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Acute administration of a cannabinoid CB1 receptor antagonist impairs stress-induced antinociception in fish

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Cited by 13 publications
(9 citation statements)
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“…These results have been extended by reports demonstrating that analgesia occurring after exposure to the context of footshock similarly involves an eCB mechanism in the periaqueductal gray (Olango et al, 2012). More so, these results have been extended by other reports that global disruption of CB1 receptor signaling block stress-induced analgesia (Kurrikoff et al, 2008), as well as a recent report that eCB signaling similarly mediates stress-induced analgesia in fish (Wolkers et al, 2015). As such, there seems to be substantial evidence that stress-induced increases in eCB signaling mediate the acute analgesic effect that occurs after exposure to stress.…”
Section: Functional Role Of Ecb Signaling In the Neurobiological Effesupporting
confidence: 59%
“…These results have been extended by reports demonstrating that analgesia occurring after exposure to the context of footshock similarly involves an eCB mechanism in the periaqueductal gray (Olango et al, 2012). More so, these results have been extended by other reports that global disruption of CB1 receptor signaling block stress-induced analgesia (Kurrikoff et al, 2008), as well as a recent report that eCB signaling similarly mediates stress-induced analgesia in fish (Wolkers et al, 2015). As such, there seems to be substantial evidence that stress-induced increases in eCB signaling mediate the acute analgesic effect that occurs after exposure to stress.…”
Section: Functional Role Of Ecb Signaling In the Neurobiological Effesupporting
confidence: 59%
“…AA-5-HT. This finding is in line with our previous studies, where CB1 blockade with AM-251 barely reduced the anti-allodynic effect caused by another FAAH inhibitor [75], and might be due in part to the previously reported anti-nociceptive and antiinflammatory effects of CB1 antagonists [80,84], although we used a per se inactive dose of AM-251.…”
Section: Discussionsupporting
confidence: 93%
“…Activation of the anandamide/CB 1 / PI3K pathway was recently reported to protect rat brains from cocaine-induced neurotoxicity (Vilela et al, 2015). Some evidence indicates that pharmacological manipulation of the cannabinoid system can alleviate symptoms of several conditions, including addiction, seizures, neurodegenerative disease, and nociception (Adamczyk et al, 2009;Almeida-Santos et al, 2013;Pietropaolo et al, 2015;Vilela et al, 2015;Wolkers et al, 2015). For example, treatment with a CB 1 receptor agonist, WIN 55,212-2 [(R)-(1)-[2,3-dihydro-5methyl-3-4-morpholinylmethyl)pyrrolo[1,2,3,-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate], prevented the appearance of motor deficits, decreased the number of striatal huntingtin inclusions, and rescued striatal medium-sized spiny neurons loss in a Huntington disease mouse model (Pietropaolo et al, 2015).…”
Section: Cb 1 Receptor: Pharmacology and Cell Signaling Pathwaysmentioning
confidence: 99%