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Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants.
Proc Natl Acad Sci U S A. 1998 Jul 07; 95(14):8268-73.PN

Abstract

The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana, and the psychotropic cannabinoid (-)Delta9-tetrahydrocannabinol (THC). Cannabinoids protected equally well against neurotoxicity mediated by N-methyl-D-aspartate receptors, 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid receptors, or kainate receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown to be calcium dependent; this study demonstrates that 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid/kainate receptor-type neurotoxicity is also calcium-dependent, partly mediated by voltage sensitive calcium channels. The neuroprotection observed with cannabidiol and THC was unaffected by cannabinoid receptor antagonist, indicating it to be cannabinoid receptor independent. Previous studies have shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol, THC and several synthetic cannabinoids all were demonstrated to be antioxidants by cyclic voltametry. Cannabidiol and THC also were shown to prevent hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. Cannabidiol was more protective against glutamate neurotoxicity than either ascorbate or alpha-tocopherol, indicating it to be a potent antioxidant. These data also suggest that the naturally occurring, nonpsychotropic cannabinoid, cannabidiol, may be a potentially useful therapeutic agent for the treatment of oxidative neurological disorders such as cerebral ischemia.

Authors+Show Affiliations

Laboratory of Cellular and Molecular Regulation, National Institutes of Mental Health, Bethesda, MD 20892, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

9653176

Citation

Hampson, A J., et al. "Cannabidiol and (-)Delta9-tetrahydrocannabinol Are Neuroprotective Antioxidants." Proceedings of the National Academy of Sciences of the United States of America, vol. 95, no. 14, 1998, pp. 8268-73.
Hampson AJ, Grimaldi M, Axelrod J, et al. Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proc Natl Acad Sci U S A. 1998;95(14):8268-73.
Hampson, A. J., Grimaldi, M., Axelrod, J., & Wink, D. (1998). Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proceedings of the National Academy of Sciences of the United States of America, 95(14), 8268-73.
Hampson AJ, et al. Cannabidiol and (-)Delta9-tetrahydrocannabinol Are Neuroprotective Antioxidants. Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8268-73. PubMed PMID: 9653176.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants. AU - Hampson,A J, AU - Grimaldi,M, AU - Axelrod,J, AU - Wink,D, PY - 1998/7/8/pubmed PY - 1998/7/8/medline PY - 1998/7/8/entrez SP - 8268 EP - 73 JF - Proceedings of the National Academy of Sciences of the United States of America JO - Proc Natl Acad Sci U S A VL - 95 IS - 14 N2 - The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana, and the psychotropic cannabinoid (-)Delta9-tetrahydrocannabinol (THC). Cannabinoids protected equally well against neurotoxicity mediated by N-methyl-D-aspartate receptors, 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid receptors, or kainate receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown to be calcium dependent; this study demonstrates that 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid/kainate receptor-type neurotoxicity is also calcium-dependent, partly mediated by voltage sensitive calcium channels. The neuroprotection observed with cannabidiol and THC was unaffected by cannabinoid receptor antagonist, indicating it to be cannabinoid receptor independent. Previous studies have shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol, THC and several synthetic cannabinoids all were demonstrated to be antioxidants by cyclic voltametry. Cannabidiol and THC also were shown to prevent hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. Cannabidiol was more protective against glutamate neurotoxicity than either ascorbate or alpha-tocopherol, indicating it to be a potent antioxidant. These data also suggest that the naturally occurring, nonpsychotropic cannabinoid, cannabidiol, may be a potentially useful therapeutic agent for the treatment of oxidative neurological disorders such as cerebral ischemia. SN - 0027-8424 UR - https://www.unboundmedicine.com/medline/citation/9653176/Cannabidiol_and____Delta9_tetrahydrocannabinol_are_neuroprotective_antioxidants_ L2 - http://www.pnas.org/cgi/pmidlookup?view=long&pmid=9653176 DB - PRIME DP - Unbound Medicine ER -