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
- Johns Hopkins University,
- Medical College of Georgia,
Scholary Output:
Contribution to journal
Article
Peer-review
Open access
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
Publication Information
Output type
Scholary Output:
Contribution to journal
Article
Peer-reviewOriginal language
English (US)Pages from-to (Number of pages)
Pages 623-630 (8 pages)Journal (Volume, Issue Number)
Neuron (Volume 78, Issue 4)Publication milestones
- Published - 05/22/2013
Publication status
Published - 05/22/2013
ISSN
0896-6273Publication IDs
- Scopus: 84878448265
- PubMed: 23719162
Publication metrics
Metrics
SciVal
citations
23
SciVal
FWCI
0.78
SciVal
Author count
8
SciVal
Paper percentile
82
Fractional count
1
Fractional count
0.13
Fractional count
7
Fractional count
0.88
Fractional count
1
Fractional count
1
PlumX, opens in new tab
Captures
50
Citation count
32
Funding Details
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.
FundersFunding numbers
NINDS
K08NS057824
USPHS
DA-000266