AI Article Synopsis
- Repeated cocaine and morphine injections in rats lead to molecular changes in the cAMP signaling pathway in specific brain regions.
- Research shows that similar changes occur in human smokers and former smokers, with increased activity of key cAMP signaling components like PKA and adenylate cyclase.
- These findings indicate that smoking causes lasting neuroadaptations in the brain, even in those who have quit, enhancing our understanding of addiction mechanisms related to tobacco use.
Article Abstract
Repeated injections of cocaine and morphine in laboratory rats cause a variety of molecular neuroadaptations in the cAMP signaling pathway in nucleus accumbens and ventral tegmental area. Here we report similar neuroadaptations in postmortem tissue from the brains of human smokers and former smokers. Activity levels of two major components of cAMP signaling, cAMP-dependent protein kinase A (PKA) and adenylate cyclase, were abnormally elevated in nucleus accumbens of smokers and in ventral midbrain dopaminergic region of both smokers and former smokers. Protein levels of the catalytic subunit of PKA were correspondingly higher in the ventral midbrain dopaminergic region of both smokers and former smokers. Protein levels of other candidate neuroadaptations, including glutamate receptor subunits, tyrosine hydroxylase, and other protein kinases, were within normal range. These findings extend our understanding of addiction-related neuroadaptations of cAMP signaling to tobacco smoking in human subjects and suggest that smoking-induced brain neuroadaptations can persist for significant periods in former smokers.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575739 | PMC |
| http://dx.doi.org/10.1523/JNEUROSCI.3661-06.2007 | DOI Listing |
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