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Anandamide inhibits metabolism and physiological actions of 2-arachidonoylglycerol in the striatum.

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Title: Anandamide inhibits metabolism and physiological actions of 2-arachidonoylglycerol in the striatum.
Authors: Maccarrone, Mauro, Rossi, Silvia, Bari, Monica, De Chiara, Valentina, Fezza, Filomena, Musella, Alessandra, Gasperi, Valeria, Prosperetti, Chiara, Bernardi, Giorgio, Finazzi-Agrò, Alessandro, Cravatt, Benjamin F., Centonze, Diego
Source: Nature Neuroscience. Feb2008, Vol. 11 Issue 2, p152-159. 8p. 7 Graphs.
Subjects: Glutamic acid, Presynaptic receptors, Laboratory mice, Pharmacology, TRP channels, Genetics
Abstract: Of the endocannabinoids (eCBs), anandamide (AEA) and 2-arachidonoylglycerol (2-AG) have received the most study. A functional interaction between these molecules has never been described. Using mouse brain slices, we found that stimulation of metabotropic glutamate 5 receptors by 3,5-dihydroxyphenylglycine (DHPG) depressed inhibitory transmission in the striatum through selective involvement of 2-AG metabolism and stimulation of presynaptic CB1 receptors. Elevation of AEA concentrations by pharmacological or genetic inhibition of AEA degradation reduced the levels, metabolism and physiological effects of 2-AG. Exogenous AEA and the stable AEA analog methanandamide inhibited basal and DHPG-stimulated 2-AG production, confirming that AEA is responsible for the downregulation of the other eCB. AEA is an endovanilloid substance, and the stimulation of transient receptor potential vanilloid 1 (TRPV1) channels mimicked the effects of endogenous AEA on 2-AG metabolism through a previously unknown glutathione-dependent pathway. Consistently, the interaction between AEA and 2-AG was lost after pharmacological and genetic inactivation of TRPV1 channels. [ABSTRACT FROM AUTHOR]
Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Anandamide inhibits metabolism and physiological actions of 2-arachidonoylglycerol in the striatum.
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  Data: <searchLink fieldCode="AR" term="%22Maccarrone%2C+Mauro%22">Maccarrone, Mauro</searchLink><br /><searchLink fieldCode="AR" term="%22Rossi%2C+Silvia%22">Rossi, Silvia</searchLink><br /><searchLink fieldCode="AR" term="%22Bari%2C+Monica%22">Bari, Monica</searchLink><br /><searchLink fieldCode="AR" term="%22De+Chiara%2C+Valentina%22">De Chiara, Valentina</searchLink><br /><searchLink fieldCode="AR" term="%22Fezza%2C+Filomena%22">Fezza, Filomena</searchLink><br /><searchLink fieldCode="AR" term="%22Musella%2C+Alessandra%22">Musella, Alessandra</searchLink><br /><searchLink fieldCode="AR" term="%22Gasperi%2C+Valeria%22">Gasperi, Valeria</searchLink><br /><searchLink fieldCode="AR" term="%22Prosperetti%2C+Chiara%22">Prosperetti, Chiara</searchLink><br /><searchLink fieldCode="AR" term="%22Bernardi%2C+Giorgio%22">Bernardi, Giorgio</searchLink><br /><searchLink fieldCode="AR" term="%22Finazzi-Agrò%2C+Alessandro%22">Finazzi-Agrò, Alessandro</searchLink><br /><searchLink fieldCode="AR" term="%22Cravatt%2C+Benjamin+F%2E%22">Cravatt, Benjamin F.</searchLink><br /><searchLink fieldCode="AR" term="%22Centonze%2C+Diego%22">Centonze, Diego</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Nature+Neuroscience%22">Nature Neuroscience</searchLink>. Feb2008, Vol. 11 Issue 2, p152-159. 8p. 7 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22Glutamic+acid%22">Glutamic acid</searchLink><br /><searchLink fieldCode="DE" term="%22Presynaptic+receptors%22">Presynaptic receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Laboratory+mice%22">Laboratory mice</searchLink><br /><searchLink fieldCode="DE" term="%22Pharmacology%22">Pharmacology</searchLink><br /><searchLink fieldCode="DE" term="%22TRP+channels%22">TRP channels</searchLink><br /><searchLink fieldCode="DE" term="%22Genetics%22">Genetics</searchLink>
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  Data: Of the endocannabinoids (eCBs), anandamide (AEA) and 2-arachidonoylglycerol (2-AG) have received the most study. A functional interaction between these molecules has never been described. Using mouse brain slices, we found that stimulation of metabotropic glutamate 5 receptors by 3,5-dihydroxyphenylglycine (DHPG) depressed inhibitory transmission in the striatum through selective involvement of 2-AG metabolism and stimulation of presynaptic CB1 receptors. Elevation of AEA concentrations by pharmacological or genetic inhibition of AEA degradation reduced the levels, metabolism and physiological effects of 2-AG. Exogenous AEA and the stable AEA analog methanandamide inhibited basal and DHPG-stimulated 2-AG production, confirming that AEA is responsible for the downregulation of the other eCB. AEA is an endovanilloid substance, and the stimulation of transient receptor potential vanilloid 1 (TRPV1) channels mimicked the effects of endogenous AEA on 2-AG metabolism through a previously unknown glutathione-dependent pathway. Consistently, the interaction between AEA and 2-AG was lost after pharmacological and genetic inactivation of TRPV1 channels. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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