Behavioral effects of cocaine mediated by nitric oxide-GAPDH transcriptional signaling

Risheng Xu; Anthony V. Serritella; Tanusree Sen; Justin M. Farook; Thomas W. Sedlak; Jay Baraban; Solomon H. Snyder; Nilkantha Sen

doi:10.1016/j.neuron.2013.03.021

Behavioral effects of cocaine mediated by nitric oxide-GAPDH transcriptional signaling

Risheng Xu, Anthony V. Serritella, Tanusree Sen, Justin M. Farook, Thomas W. Sedlak, Jay Baraban, Solomon H. Snyder, Nilkantha Sen

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

26 Scopus citations

Abstract

Cocaine@s behavioral-stimulant effects derive from potentiation of synaptic signaling by dopamine and serotonin leading to transcriptional alterations in postsynaptic cells. We report that a signaling cascade involving nitric oxide (NO) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mediates cocaine@s transcriptional and behavioral actions. Lower, behavioral-stimulant doses enhance the cAMP response element-binding (CREB) signaling system, while higher, neurotoxic doses stimulate the p53 cytotoxic system. The drug CGP3466B, which potently and selectively blocks GAPDH nitrosylation and GAPDH-Siah binding, prevents these actions as well as behavioral effects of cocaine providing a strategy for anticocaine therapy

Original language	English (US)
Pages (from-to)	623-630
Number of pages	8
Journal	Neuron
Volume	78
Issue number	4
DOIs	https://doi.org/10.1016/j.neuron.2013.03.021
State	Published - May 22 2013
Externally published	Yes

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/j.neuron.2013.03.021

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title = "Behavioral effects of cocaine mediated by nitric oxide-GAPDH transcriptional signaling",

abstract = "Cocaine@s behavioral-stimulant effects derive from potentiation of synaptic signaling by dopamine and serotonin leading to transcriptional alterations in postsynaptic cells. We report that a signaling cascade involving nitric oxide (NO) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mediates cocaine@s transcriptional and behavioral actions. Lower, behavioral-stimulant doses enhance the cAMP response element-binding (CREB) signaling system, while higher, neurotoxic doses stimulate the p53 cytotoxic system. The drug CGP3466B, which potently and selectively blocks GAPDH nitrosylation and GAPDH-Siah binding, prevents these actions as well as behavioral effects of cocaine providing a strategy for anticocaine therapy",

author = "Risheng Xu and Serritella, {Anthony V.} and Tanusree Sen and Farook, {Justin M.} and Sedlak, {Thomas W.} and Jay Baraban and Snyder, {Solomon H.} and Nilkantha Sen",

note = "Funding Information: We thank Roxanne Barrow, Bindu Paul, Adele Snowman, and other members of the Snyder lab for their help and support throughout this project. This work was supported by USPHS grant DA-000266. ",

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AU - Xu, Risheng

AU - Serritella, Anthony V.

AU - Sen, Tanusree

AU - Farook, Justin M.

AU - Sedlak, Thomas W.

AU - Baraban, Jay

AU - Snyder, Solomon H.

AU - Sen, Nilkantha

N1 - Funding Information: We thank Roxanne Barrow, Bindu Paul, Adele Snowman, and other members of the Snyder lab for their help and support throughout this project. This work was supported by USPHS grant DA-000266.

PY - 2013/5/22

Y1 - 2013/5/22

N2 - Cocaine@s behavioral-stimulant effects derive from potentiation of synaptic signaling by dopamine and serotonin leading to transcriptional alterations in postsynaptic cells. We report that a signaling cascade involving nitric oxide (NO) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mediates cocaine@s transcriptional and behavioral actions. Lower, behavioral-stimulant doses enhance the cAMP response element-binding (CREB) signaling system, while higher, neurotoxic doses stimulate the p53 cytotoxic system. The drug CGP3466B, which potently and selectively blocks GAPDH nitrosylation and GAPDH-Siah binding, prevents these actions as well as behavioral effects of cocaine providing a strategy for anticocaine therapy

AB - Cocaine@s behavioral-stimulant effects derive from potentiation of synaptic signaling by dopamine and serotonin leading to transcriptional alterations in postsynaptic cells. We report that a signaling cascade involving nitric oxide (NO) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mediates cocaine@s transcriptional and behavioral actions. Lower, behavioral-stimulant doses enhance the cAMP response element-binding (CREB) signaling system, while higher, neurotoxic doses stimulate the p53 cytotoxic system. The drug CGP3466B, which potently and selectively blocks GAPDH nitrosylation and GAPDH-Siah binding, prevents these actions as well as behavioral effects of cocaine providing a strategy for anticocaine therapy

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Behavioral effects of cocaine mediated by nitric oxide-GAPDH transcriptional signaling

Abstract

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