Cannabidiol anormal

El Cannabidiol anormal (abn-cbd) es un regioisómero sintético del cannabidiol. A diferencia de los demás cannabinoides produce vasodilatación, baja presión sanguínea, además de inducir al crecimiento celular y la activación en la microglía de la proteína quinasa activada por mitógenos. No produce efectos psicoactivos.^[1]^[2] Es agonista de los receptores cannabinoides huérfanos GPR55 y GPR18. Investigación adicional sugiere la existencia de receptores cannabinoides adicionales.^[3]^[4]^[5]^[6]

Véase también

GPR55
GPR18

Referencias

↑ Adams MD, Earnhardt JT, Martin BR, Harris LS, Dewey WL, Razdan RK. (1977). «A cannabinoid with cardiovascular activity but no overt behavioral effects». Experientia 33 (9): 1204-1205. PMID 891878. doi:10.1007/BF01922330.
↑ McHugh D, Hu SS, Rimmerman N, Juknat A, Vogil Z, Walker JM, Bradshaw HB. (marzo de 2010). «N-arachidonoyl glycine, an abundant endogenous lipid, potently drives directed cellular migration through GPR18, the putative abnormal cannabidiol receptor». BMC Neuroscience 11: 44. PMC 2865488. PMID 20346144. doi:10.1186/1471-2202-11-44.
↑ Brown AJ. (noviembre de 2007). «Novel cannabinoid receptors». British Journal of Pharmacology 152 (5): 567-575. PMC 2190013. PMID 17906678. doi:10.1038/sj.bjp.0707481.
↑ Johns DG, Behm DJ, Walker DJ, Ao Z, Shapland EM, Daniels DA, Riddick M, Dowell S, Staton PC. (2007). «The novel endocannabinoid receptor GPR55 is activated by atypical cannabinoids but does not mediate their vasodilator effects». British Journal of Pharmacology 152 (5): 825-831. PMC 2190033. PMID 17704827. doi:10.1038/sj.bjp.0707419.
↑ McHugh D, Tanner C. (2008). «Inhibition of human neutrophil chemotaxis by endogenous cannabinoids and phytocannabinoids: evidence for a site distinct from CB1 and CB2». Molecular Pharmacology 73 (2): 441-450. PMID 17965195. doi:10.1124/mol.107.041863.
↑ Kreutz S, Koch M, Böttger C, Ghadban C, Korf HW, Dehghani F. (2009). «2-Arachidonoylglycerol elicits neuroprotective effects on excitotoxically lesioned dentate gyrus granule cells via abnormal-cannabidiol-sensitive receptors on microglial cells». Glia 57 (3): 286-294. PMID 18837048. doi:10.1002/glia.20756.

Datos: Q27074295

[1] Adams MD, Earnhardt JT, Martin BR, Harris LS, Dewey WL, Razdan RK. (1977). «A cannabinoid with cardiovascular activity but no overt behavioral effects». Experientia 33 (9): 1204-1205. PMID 891878. doi:10.1007/BF01922330.

[pmid20346144-2] McHugh D, Hu SS, Rimmerman N, Juknat A, Vogil Z, Walker JM, Bradshaw HB. (marzo de 2010). «N-arachidonoyl glycine, an abundant endogenous lipid, potently drives directed cellular migration through GPR18, the putative abnormal cannabidiol receptor». BMC Neuroscience 11: 44. PMC 2865488. PMID 20346144. doi:10.1186/1471-2202-11-44.

[pmid17906678-3] Brown AJ. (noviembre de 2007). «Novel cannabinoid receptors». British Journal of Pharmacology 152 (5): 567-575. PMC 2190013. PMID 17906678. doi:10.1038/sj.bjp.0707481.

[4] Johns DG, Behm DJ, Walker DJ, Ao Z, Shapland EM, Daniels DA, Riddick M, Dowell S, Staton PC. (2007). «The novel endocannabinoid receptor GPR55 is activated by atypical cannabinoids but does not mediate their vasodilator effects». British Journal of Pharmacology 152 (5): 825-831. PMC 2190033. PMID 17704827. doi:10.1038/sj.bjp.0707419.

[5] McHugh D, Tanner C. (2008). «Inhibition of human neutrophil chemotaxis by endogenous cannabinoids and phytocannabinoids: evidence for a site distinct from CB1 and CB2». Molecular Pharmacology 73 (2): 441-450. PMID 17965195. doi:10.1124/mol.107.041863.

[6] Kreutz S, Koch M, Böttger C, Ghadban C, Korf HW, Dehghani F. (2009). «2-Arachidonoylglycerol elicits neuroprotective effects on excitotoxically lesioned dentate gyrus granule cells via abnormal-cannabidiol-sensitive receptors on microglial cells». Glia 57 (3): 286-294. PMID 18837048. doi:10.1002/glia.20756.

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