Acute neuronal injury, excitotoxicity, and the endocannabinoid system

M. Stelt, van der, W.B. Veldhuis, M. Maccarrone, P.R. Bär, K. Nicolaij, G.A. Veldink, M. Di, V., J.F.G. Vliegenthart

    Research output: Contribution to journalArticleAcademicpeer-review

    120 Citations (Scopus)

    Abstract

    The endocannabinoid system is a valuable target for drug discovery, because it is involved in the regulation of many cellular and physiological functions. The endocannabinoid system constitutes the endogenous lipids anandamide, 2-arachidonoylglycerol and noladin ether, and the cannabinoid CB1 and CB2 receptors as well as the proteins for their inactivation. It is thought that (endo)cannabinoid-based drugs may potentially be useful to reduce the effects of neurodegeneration. This paper reviews recent developments in the endocannabinoid system and its involvement in neuroprotection. Exogenous (endo)cannabinoids have been shown to exert neuroprotection in a variety of in vitro and in vivo models of neuronal injury via different mechanisms, such as prevention of excitotoxicity by CB1-mediated inhibition of glutamatergic transmission, reduction of calcium influx, and subsequent inhibition of deleterious cascades, TNF-a formation, and anti-oxidant activity. It has been suggested that the release of endogenous endocannabinoids during neuronal injury might be a protective response. However, several observations indicate that the role of the endocannabinoid system as a general endogenous protection system is questionable. The data are critically reviewed and possible explanations are given
    Original languageEnglish
    Pages (from-to)317-346
    JournalMolecular Neurobiology
    Volume26
    Issue number2-3
    DOIs
    Publication statusPublished - 2002

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