Altered CTX-catalyzed and endogenous [32P]ADP-ribosylation of stimulatory G protein αs isoforms in postmortem bipolar affective disorder temporal cortex
✍ Scribed by Stavroula Andreopoulos; Peter P. Li; Kin Po Siu; Stephen J. Kish; Jerry J. Warsh
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 133 KB
- Volume
- 72
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Abstract
Reports of elevated Gs α subunit (α~s~) immunolabeling and cAMP‐mediated hyper‐functionality in autopsied cerebral cortical brain regions from bipolar affective disorder (BD) patients suggest signal transduction abnormalities occur in this disorder. Because covalent modification of α~s~ can affect its turnover and levels, we determined whether CTX‐catalyzed and endogenous [^32^P] adenosine diphosphate (ADP)‐ribosylation of α~s~ isoforms are altered in temporal and occipital cortical regions, which show elevated α~s~ levels in BD as compared to nonpsychiatric subjects. Reduced CTX‐catalyzed [^32^P]ADP‐ribosylated α~s‐S~ and endogenous [^32^P]ADP‐ribosylation of a 39‐kDa α~s~‐like protein were found in BD temporal cortex compared to controls. These findings suggest that clearance of these α~s~ isoforms through ADP‐ribosylation may be decreased in BD temporal cortex. Although no differences were observed in mean levels of endogenous and CTX‐catalyzed [^32^P]ADP‐ribosylation of α~s‐L~ in BD temporal cortex, α~s‐L~ immunolabeling was elevated significantly and correlated inversely with the degree of endogenous [^32^P]ADP‐ribosylation of this subunit. In addition, endogenous [^32^P]ADP‐ribosylation of an exogenous substrate, myelin basic protein, was similar in BD and comparison subject temporal cortex. Taken together, these observations suggest that elevations of α~s~ in BD brain are more likely related to factors affecting the disposition or availability of α~s~ to this posttranslational enzymatic modification. © 2003 Wiley‐Liss, Inc.