PMID- 12749029
OWN - NLM
STAT- MEDLINE
DCOM- 20030716
LR  - 20151119
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 72
IP  - 5
DP  - 2003 Jun 1
TI  - Altered CTX-catalyzed and endogenous [32P]ADP-ribosylation of stimulatory G 
      protein alphas isoforms in postmortem bipolar affective disorder temporal cortex.
PG  - 638-45
AB  - Reports of elevated Gs alpha subunit (alpha(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 alpha(s) can affect its 
      turnover and levels, we determined whether CTX-catalyzed and endogenous [(32)P] 
      adenosine diphosphate (ADP)-ribosylation of alpha(s) isoforms are altered in 
      temporal and occipital cortical regions, which show elevated alpha(s) levels in 
      BD as compared to nonpsychiatric subjects. Reduced CTX-catalyzed 
      [(32)P]ADP-ribosylated alpha(s-S) and endogenous [(32)P]ADP-ribosylation of a 
      39-kDa alpha(s)-like protein were found in BD temporal cortex compared to 
      controls. These findings suggest that clearance of these alpha(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 alpha(s-L) in BD temporal cortex, alpha(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 alpha(s) in BD brain are 
      more likely related to factors affecting the disposition or availability of 
      alpha(s) to this posttranslational enzymatic modification.
CI  - Copyright 2003 Wiley-Liss, Inc.
FAU - Andreopoulos, Stavroula
AU  - Andreopoulos S
AD  - Laboratory of Cellular and Molecular Pathophysiology, Center for Addiction and 
      Mental Health, Clarke Site, Toronto, Canada.
FAU - Li, Peter P
AU  - Li PP
FAU - Siu, Kin Po
AU  - Siu KP
FAU - Kish, Stephen J
AU  - Kish SJ
FAU - Warsh, Jerry J
AU  - Warsh JJ
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Myelin Basic Protein)
RN  - 0 (Phosphorus Isotopes)
RN  - 61D2G4IYVH (Adenosine Diphosphate)
RN  - 9012-63-9 (Cholera Toxin)
RN  - 9FN79X2M3F (Lithium)
RN  - EC 3.6.5.1 (Heterotrimeric GTP-Binding Proteins)
SB  - IM
MH  - Adenosine Diphosphate/*metabolism
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Bipolar Disorder/*metabolism/physiopathology
MH  - Cholera Toxin/pharmacology
MH  - Female
MH  - Heterotrimeric GTP-Binding Proteins/*metabolism
MH  - Humans
MH  - Immunohistochemistry
MH  - Lithium/metabolism/pharmacology
MH  - Male
MH  - Middle Aged
MH  - Myelin Basic Protein/drug effects/metabolism
MH  - Neurons/*metabolism
MH  - Occipital Lobe/metabolism/physiopathology
MH  - Phosphorus Isotopes
MH  - Temporal Lobe/*metabolism/physiopathology
EDAT- 2003/05/16 05:00
MHDA- 2003/07/17 05:00
CRDT- 2003/05/16 05:00
PHST- 2003/05/16 05:00 [pubmed]
PHST- 2003/07/17 05:00 [medline]
PHST- 2003/05/16 05:00 [entrez]
AID - 10.1002/jnr.10620 [doi]
PST - ppublish
SO  - J Neurosci Res. 2003 Jun 1;72(5):638-45. doi: 10.1002/jnr.10620.