Journal of Applied Physiology
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J Appl Physiol (April 27, 2006). doi:10.1152/japplphysiol.00167.2006
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Submitted on February 8, 2006
Accepted on April 26, 2006

Advancing age alters the expression of the ryanodine receptor 3 isoform in adult rat superior cervical ganglia

Conwin K Vanterpool1, Elaine A Vanterpool2, William J Pearce1, and John N Buchholz1*

1 Department of Physiology and Pharmacology, Loma Linda University, School of Medicine, Loma Linda, California, United States
2 Department of Microbiology and Molecular Genetics, Loma Linda University, School of Medicine, Loma Linda, California, United States

* To whom correspondence should be addressed. E-mail: jbuchholz{at}llu.edu.

Sympathetic nerves arising from the superior cervical ganglion (SCG) protect the cerebrovasculature during periods of acute hypertension. The function of these nerves depend on calcium release triggered by activation of ryanodine receptor (RyR) channels. RyR channel function is in part dependent on genetic expression and regulation by modulators such as neuronal nitric oxide synthase (nNOS) neurons also found in the SCG. We have shown that release of calcium in SCG cells is altered with advancing age while molecular mechanisms in part accounting for these data are elusive. We tested the hypothesis that advancing age alters the pattern of genetic expression and/or protein levels of RyRs and their modulation by nNOS in the SCG in F-344 rats aged 6, 12 and 24 months. ryr1 expression was undetectable in all age groups. mRNA and protein levels for the RyR2 isoform did not change with advancing age while they increased from 6 to 12 months and declined from 12 to 24 months for RyR3. Phosphorylation levels of the RyRs were similar in all age groups and nNOS protein levels increased from 6 months to 12 months followed by a decline from 12 months to 24 months. These data suggest that advancing age selectively impacts the genetic expression and protein levels of RyR3 as well as modulatory nNOS protein levels. These data may provide some insight into the possible changes in the function of RyRs that may occur with the normal aging process.




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