Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 40, Issue 1-2, Pages 185-195Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-009-9233-4
Keywords
Nicotinic receptor; Schizophrenia; Smoking; Gene expression; alpha 7; CHRNA7
Categories
Funding
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH081177, P50MH068582] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA009457] Funding Source: NIH RePORTER
- NIDA NIH HHS [R01 DA009457, R01 DA009457-09, DA09457, R01 DA009457-11, R01 DA009457-10A2] Funding Source: Medline
- NIMH NIH HHS [R01 MH081177-03, MH081177, R01 MH081177, P50 MH068582, R01 MH081177-02, MH068582] Funding Source: Medline
Ask authors/readers for more resources
The alpha 7 neuronal nicotinic receptor gene (CHRNA7) has been implicated in the pathophysiology of schizophrenia by genetic and pharmacological studies. Expression of the alpha 7* receptor, as measured by [I-125]alpha-bungarotoxin autoradiography, is decreased in postmortem brain of schizophrenic subjects compared to non-mentally ill controls. Most schizophrenic patients are heavy smokers, with high levels of serum cotinine. Smoking changes the expression of multiple genes and differentially regulates gene expression in schizophrenic hippocampus. We examined the effects of smoking on CHRNA7 expression in the same tissue and find that smoking differentially regulates expression of both mRNA and protein for this gene. CHRNA7 mRNA and protein levels are significantly lower in schizophrenic nonsmokers compared to control nonsmokers and are brought to control levels in schizophrenic smokers. Sufficient protein but low surface expression of the alpha 7* receptor, seen in the autoradiographic studies, suggests aberrant assembly or trafficking of the receptor.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available