Inhibition of cyclooxygenase-2 potentiates retrograde endocannabinoid effects in hippocampus

Jimok Kim; Bradley E. Alger

doi:10.1038/nn1262

Inhibition of cyclooxygenase-2 potentiates retrograde endocannabinoid effects in hippocampus

Jimok Kim, Bradley E. Alger

Research output: Contribution to journal › Article › peer-review

207 Scopus citations

Abstract

In hippocampal pyramidal cells, a rise in Ca²⁺ releases endocannabinoids that activate the presynaptic cannabinoid receptor (CB1R) and transiently reduce GABAergic transmission-a process called depolarization- induced suppression of inhibition (DSI). The mechanism that limits the duration of endocannabinoid action in intact cells is unknown. Here we show that inhibition of cyclooxygenase-2 (COX-2), not fatty acid amide hydrolase (FAAH), prolongs DSI, suggesting that COX-2 limits endocannabinoid action.

Original language	English (US)
Pages (from-to)	697-698
Number of pages	2
Journal	Nature Neuroscience
Volume	7
Issue number	7
DOIs	https://doi.org/10.1038/nn1262
State	Published - Jul 2004
Externally published	Yes

ASJC Scopus subject areas

General Neuroscience

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title = "Inhibition of cyclooxygenase-2 potentiates retrograde endocannabinoid effects in hippocampus",

abstract = "In hippocampal pyramidal cells, a rise in Ca2+ releases endocannabinoids that activate the presynaptic cannabinoid receptor (CB1R) and transiently reduce GABAergic transmission-a process called depolarization- induced suppression of inhibition (DSI). The mechanism that limits the duration of endocannabinoid action in intact cells is unknown. Here we show that inhibition of cyclooxygenase-2 (COX-2), not fatty acid amide hydrolase (FAAH), prolongs DSI, suggesting that COX-2 limits endocannabinoid action.",

author = "Jimok Kim and Alger, {Bradley E.}",

note = "Funding Information: We thank S. Thompson and A. Keller for comments, and D. Piomelli for URB-597. The work was supported by National Institutes of Health grants RO1 DA14 725 and RO1 NS30219 to B.E.A. This work is contained in J.K.{\textquoteright}s Ph.D. thesis.",

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N1 - Funding Information: We thank S. Thompson and A. Keller for comments, and D. Piomelli for URB-597. The work was supported by National Institutes of Health grants RO1 DA14 725 and RO1 NS30219 to B.E.A. This work is contained in J.K.’s Ph.D. thesis.

PY - 2004/7

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N2 - In hippocampal pyramidal cells, a rise in Ca2+ releases endocannabinoids that activate the presynaptic cannabinoid receptor (CB1R) and transiently reduce GABAergic transmission-a process called depolarization- induced suppression of inhibition (DSI). The mechanism that limits the duration of endocannabinoid action in intact cells is unknown. Here we show that inhibition of cyclooxygenase-2 (COX-2), not fatty acid amide hydrolase (FAAH), prolongs DSI, suggesting that COX-2 limits endocannabinoid action.

AB - In hippocampal pyramidal cells, a rise in Ca2+ releases endocannabinoids that activate the presynaptic cannabinoid receptor (CB1R) and transiently reduce GABAergic transmission-a process called depolarization- induced suppression of inhibition (DSI). The mechanism that limits the duration of endocannabinoid action in intact cells is unknown. Here we show that inhibition of cyclooxygenase-2 (COX-2), not fatty acid amide hydrolase (FAAH), prolongs DSI, suggesting that COX-2 limits endocannabinoid action.

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Inhibition of cyclooxygenase-2 potentiates retrograde endocannabinoid effects in hippocampus

Abstract

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