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Journal of Affective Disorders
Volume 65, Issue 2
, Pages 117-122
, July 2001
Is lithium response related to Gsα levels in transformed lymphoblasts from subjects with bipolar disorder?
References
- . Use of cyclosporin H in establishing Epstein–Barr virus-transformed human lymphoblastoid cell lines. In Vitro. 1984;20:856–858
- . Lithium inhibits adrenergic and cholinergic increases in GTP binding in rat cortex. Nature. 1988;331:440–442
- . Reduced β-adrenergic receptor-coupled Gs protein function and Gs immunoreactivity in mononuclear leukocytes of patients with depression. Biol. Psychiatry. 1996;39:755–760
- . Differential G protein measures in mononuclear leukocytes of patients with bipolar mood disorder are state dependent. J. Affect. Disord. 1997;43:85–93
- . A rapid and sensitive method for the quantification of microgram quantities of protein utilizing the principle of protein-dye binding. Anal. Biochem. 1976;72:248–252
-
Chronic lithium regulates the expression of adenylyl cyclase Gi-protein a subunit in rat cerebral cortex.
Proc. Natl. Acad. Sci. USA. 1991;88:10634–10637
- . G-protein coupled cAMP signalling in mood disorders: effects of diagnosis, treatment at the time of death and suicide. J. Neurochem. 1999;73:1121–1126
- . A diagnostic interview: the schedule for affective disorders and schizophrenia. Arch. Gen. Psychiatry. 1978;35:773–782
- . Receptor mediated activation of G proteins is increased in postmortem brains of bipolar affective disorder subjects. J. Neurochem. 1996;67:1145–1152
- . Linkage analysis of fifty-seven microsatellite loci to bipolar disorder. Neuropsychopharmacology. 1993;9:31–40
- . Lithium response and genetics of affective disorders. J. Affect. Disord. 1994;32:85–95
- . Anti-bipolar therapy: mechanism of action of lithium. Mol. Psychiatry. 1999;4:117–128
- . Exclusion of close linkage of bipolar disorder to the Gs-α subunit gene in nine Australian pedigrees. J. Affect. Disord. 1994;32:187–195
- . Selective inhibition of the expression of signal transduction proteins by lithium in nerve growth factor-differentiated PC12 cells. J. Neurochem. 1995;65(6):2500–2508
- . Lithium decreases Gs, Gi-1 and Gi-2 α-subunit mRNA levels in rat cortex. Eur. J. Pharmacol. 1991;206:165–166
-
.
Effects of chronic lithium and carbamazepine treatment on G protein subunit expression in rat cortex.
Biol. Psychiatry. 1993;34:167–170
- . Guanine nucleotide-binding proteins in bipolar affective disorder: effects of long-term lithium treatment. Arch. Gen. Psychiatry. 1995;52:135–144
- . High levels of Gs alpha in platelets of euthymic patients with bipolar affective disorder. Am. J. Psychiatry. 1997;154(2):218–223
- . Effects of lithium ex vivo on the GTP-mediated inhibition of calcium-stimulated adenylyl cyclase activity in rat brain. Eur. J. Pharmacol. 1989;168:347–354
- . Effects of GTP on hormone-stimulated adenylyl cyclase activity in cerebral cortex, striatum and hippocampus from rats treated chronically with lithium. Biol. Psychiatry. 1989;26:279–288
- . Abnormalities of cAMP-dependent endogenous phosphorylation in platelets from patients with bipolar disorder. Am. J. Psychiatry. 1995;152(8):1204–1206
- . Reduced 3H cAMP binding in postmortem brain from subjects with bipolar affective disorder. J. Neurochem. 1997;68(1):297–304
- The mechanisms of action of lithium. II. Effects on adenylate cyclase activity and beta-adrenergic receptor binding in normal subjects. Arch. Gen. Psychiatry. 1991;48(6):513–524
- . Hyperfunctional G proteins in mononuclear leukocytes of patients with mania. Biol. Psychiatry. 1991;29:273–280
- . Research diagnostic criteria: rationale and reliability. Arch. Gen. Psychiatry. 1978;35:773–782
- . Evidence for a role of phospholipase C-gamma 1 in the pathogenesis of bipolar disorder. Mol. Psychiatry. 1998;3:534–538
- . Cyclic AMP responsive element binding protein phosphorylation and DNA binding is decreased by chronic lithium but not valproate treatment of SH-SY5Y neuroblastoma cells. Neuroscience. 1999;91(2):771–776
-
.
Postmortem cerebral cortex Gs alpha-subunit levels are elevated in bipolar affective disorder.
Brain Res. 1991;551:323–326
- . Cerebral cortex Gsα protein levels and forskolin-stimulated cyclic AMP formation are increased in bipolar affective disorder. J. Neurochem. 1993;61:890–898
- . Mononuclear leukocyte levels of G-proteins in depressed patients with bipolar disorder or major depressive disorder. Am. J. Psychiatry. 1994;151:594–596
-
.
Stimulatory G-protein alpha-subunit mRNA levels are not increased in autopsied cerebral cortex from patients with bipolar disorder.
Brain Res. 1996;42(1):45–50
PII: S0165-0327(00)00166-X
© 2001 Elsevier Science B.V. All rights reserved.
« Previous
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Journal of Affective Disorders
Volume 65, Issue 2
, Pages 117-122
, July 2001
