Second messenger systems and mood disorders

Current Opinion in Psychiatry

Volumn 9, Issue 1, 1996, Pages 23-29

  Warsh, Jerry J ^a,b   Li, Peter P ^a,b  

^a UNIVERSITY OF TORONTO   (Canada)

^b UNIVERSITY OF TORONTO   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM ION; GUANINE NUCLEOTIDE BINDING PROTEIN; LITHIUM; PHOSPHATIDYLINOSITIDE;

AFFECTIVE NEUROSIS; AUTOPSY; CALCIUM CELL LEVEL; HUMAN; MANIC DEPRESSIVE PSYCHOSIS; MOOD; REVIEW; SECOND MESSENGER; SIGNAL TRANSDUCTION;

EID: 0030025356     PISSN: 09517367     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001504-199601000-00005     Document Type: Review

References (53)

1. Hudson CJ, Young LT, Li PP, Warsh JJ: CNS signal transaction in the pathophysiology and pharmacotherapy of affective disorders and schizophrenia. Synapse 1993, 13:278-293.
2. Nestler EJ: Molecular neurobiology of drug addiction. Neuropsychopharmacol 1994, 11:77-87. Although directed at the molecular mechanisms of drug addiction, this review highlights the importance of transmembrane and intracellular signal transduction and signal transcription-coupling processes in mediating physiological and drug effects, and in this context is relevant to understanding the pathophysiology of neuropsychiatric disorders in general. The review is highly informative and presents molecular and cellular signaling concepts in a clear and understandable fashion for the nonexpert reader.
3. a protein levels and forskolin-stimulated cyclic AMP formation are increased in bipolar affective disorder. J Neurochem 1993, 61:890-898. The authors show the application of the postmortem research strategy to evaluate directly signal-transduction processes in brains of patients with bipolar affective disorder. The authors provide the first direct demonstration of increased immunolabeling of stimulatory G protein α-subunits in cortical regions of post-mortem bipolar affective disorder brain compared with control individuals and preliminary evidence that these G protein changes are functionally relevant. The specificity of these changes to bipolar affective disorder are also supported.
4. Offermanns S, Schultz G: Complex information processing by the transmembrane signaling system involving G proteins. Naunyn Schmiedebergs Arch Pharmacol 1994, 350:329-338.
5. Young LT, Li PP, Kish SJ, Warsh JJ: Cerebral cortex β-adrenoceptor binding in bipolar affective disorder. J Affective Disord 1994, 30:89-92.
6. Port JD, Malbon CC: Integration of transmembrane signaling: cross-talk among G-protein-linked receptors and other signal transduction pathways. Trends Cardiovasc Med 1993, 3:85-92.
7. Schreiber G, Avissar S, Danon A, Belmaker RH: Hyperfunctional G proteins in mononuclear leukocytes of patients with mania. Biol Psychiatry 1991, 29:273-280.
8. Ozawa H, Gsell W, Frolich L, Zochling R, Pantucek F, Beckmann H, Riederer P: Imbalance of the Gs and Gl/o function in post-mortem human brain of depressed patients. J Neural Transm 1993, 94:63-69.
9. Cowburn RF, Marcusson JO, Eriksson A, Wiehager B, O'Neill C: Adenylyl cyclase activity and G-protein subunit levels in postmortem frontal cortex of suicide victims. Brain Res 1994, 633:297-304. A well designed postmortem-brain signal transduction study showing reduced G-protein coupled adenylyl cyclase signaling occurs in patients who died of suicide with a history of violent means or depression.
10. Ozawa H, Katamura Y, Hatta S, Saito T, Katada T, Gsell W, Froelich L, Takahata N, Riederer P: Alterations of guanine nucleotide-binding proteins in post-mortem human brain in alcoholics. Brain Res 1993, 620:174-179.
11. Escriba PV, Sastre M, Garcia-Sevilla JA: Increased density of guanine nucleotide-binding proteins in the postmortem brains of heroin addicts. Arch Gen Psychiatry 1994, 51:494-501.
12. a may be trait-dependent.
13. i is a potential target of lithium's action.
14. Odagaki Y. Koyama T, Yamashita I: Platelet pertussis toxin-sensitive G proteins in affective disorders. J Affective Disord 1994, 31:173-177.
15. Maes M: Evidence for an immune response in major depression: a review and hypothesis. Prog Neuropsychopharmacol Biol Psychiatry 1995, 19:11-38
16. Perez J, Zanardi R, Mori S, Gasperini M, Smeraldi E, Racagni G: Abnormalities of cAMP-dependent endogenous phosphorylation in platelets from patient with bipolar disorder. Am J Psychiatry 1995, 152:1204-1206. An intriguing study showing cAMP-stimulated phosphorylation of a specific platelet protein (-22 kDa) is significantly higher in euthymic bipolar patients compared with matched control individuals. The abnormality in cAMP-dependent endogenous phosphorylation may be associated with compensatory mechanisms related to reported changes in G proteins and second messengers (e.g. calcium) in bipolar affective disorder.
17. Le F, Mitchell P, Vivero C, Waters B, Donald J, Selbie LA, Shine J, Schofield P: Exclusion of close linkage of bipolar disorder to the G(s)-α subunit gene in nine Australian pedigrees J Affective Disord 1994, 32: 187-195.
18. Gejman PV, Martinez M, Cao Q, Friedman E, Berettini WH, Goldin LR, Koroulakis P, Ames C, Lerman MA, Gershon ES: Linkage analysis of fifty-seven microsatellite loci to bipolar disorder. Neuropsychopharmacol 1993, 9:31-40.
19. olf may be involved in the pathogenesis of bipolar affective disorder. Another important candidate gene encoded in this region and implicated in affective disorders, however, is that for encoding the corticotropin receptor.
20. Nestler EJ, Terwilliger RZ, Duman RS: Regulation of endogenous ADP-ribosylation by acute and chronic lithium in rat brain. J Neurochem 1995, 64:2319-2324.
21. Donnelly LE, Boyd RS, Williams RJ, Kelly E, MacDermot J: Inhibition of ADP-ribosyltransferase increases synthesis of Gsα in neuroblastoma x glioma hybrid cells and reverses iloprost-dependent heterologous loss of fluoride-sensitive adenylate cyclase. Biochem Pharmacol 1995, 49:767-776.
22. Jope RS, Williams MB Lithium and brain signal transduction systems. Biochem Pharmacol 1994, 47:429-441. A thorough review of the effects of lithium on brain signal transduction systems with an emphasis on the phosphoinositide system. Some of the problems with the 'inositol depletion hypothesis' of lithium are concisely and critically addressed, with consideration of G protein function, protein phosphorylation and gene expression as other potential targets for the action of the lithium.
23. Manji HK, Potter WZ, Lenox RH: Signal transduction pathways: molecular targets for lithium's actions. Arch Gen Psychiatry 1995, 52:531-543. This extensive review attempts to integrate the exciting recent progress in the identification of second-messenger generating systems as targets for the action of the lithium, thus regulating multiple neurotransmitter systems in critical regions of the brain. This thought provoking review provides impetus for further research in signal transduction processes in understanding the mechanism of the moodstabilizing drug's actions.
24. Manji HK, Lenox RH: Long-term action of lithium - a role for transcriptional and posttranscriptional factors regulated by protein kinase C. Synapse 1994, 16:11-28. A comprehensive review of the literature relating to the effects of lithium on gene expression, highlighting the potential role of PKC in regulating nuclear transcriptional regulatory factors as the underlying mechanism for the lithium's action.
25. Li PP, Sibony D, Green, MA, Wash JJ: Lithium modulation of phosphoinositide signaling system in rat cortex: selective effect on phorbol ester binding. J Neurochem 1993, 61:1722-1730.
26. Manji HK, Etcheberrigaray R, Chen G, Olds JL: Lithium decreases membrane-associated protein kinase-C in hippocampus - selectivity for the a isozyme. J Neurochem 1993, 61:2303-2310.
27. Chen CC: Alterations of protein kinase C isozyme and substrate proteins in mouse brain after electroconvulsive seizures. Brain Res 1994, 648:65-72.
28. Casebolt TL, Jope RS: Effects of chronic lithium treatment on protein kinase C and cyclic AMP-dependent protein phosphorylation. Biol Psychiatry 1991, 29:233-243.
29. Lenox RH, Watson DG: Lithium and the brain: a psychopharmacological strategy to a molecular basis for manic depressive illness. Clin Chem 1994, 40:309-314.
30. Friedman E, Wang HY, Levinson D, Connell TA, Singh H: Altered platelet protein kinase C activity in bipolar affective disorder, manic episode. Biol Psychiatry 1993, 33:520-525.
31. Brown AS, Mallinger AG, Renbaum LC: Elevated platelet membrane phosphatidylinositol-4,5-biphosphate in bipolar mania. Am J Psychiatry 1993, 150:1252-1254.
32. 31P Nuclear magnetic resonance spectroscopy: neurodevelopment and schizophrenia. Schizophrenia Bull 1993, 19:35-53.
33. 31P and Li magnetic resonance spectroscopy. J Affective Disord 1993, 27:53-60.
34. Kato T, Shiori T, Murashita J, Hamakawa H, Inubushi T, Takahashi S: Phosphorus-31 magnetic resonance spectroscopy and ventricular enlargement in bipolar disorder. Psychiatry Res: Neuroimaging 1994, 55:41-50.
35. Deicken RF, Weiner MW, Fein G: Decreased temporal lobe phophomonoesters in bipolar disorder. J Affective Disord 1995, 33:195-199.
36. Deicken RF, Fein G, Weiner MW: Abnormal frontal lobe phosphorus metabolism in bipolar disorder. Am J. Psychiatry 1995, 152:915-918. The authors provide a very recent example of the application of in-vivo measurement of brain membrane phospholipid metabolism. The study examined 12 medication-free (1 week) euthymic male bipolar disorder patients, demonstrating increased phosphodiester and decreased phosphomonoester in frontal lobe. The findings extend to bipolar disorder the notion that membrane phospholipid disturbances contribute to its pathophysiology, but at the same time highlight that these changes may not be specific, as they are similar to those observed in schizophrenic brain.
37. + in the treatment of bipolar disorder. Trends Neurosci 1995, 18:343-349.
38. Vadnal R, Parlhasarathy R: Myo-inositol monophosphatase: diverse effects of lithium, carbamazepine, and valproate. Neuropsychopharmacol 1995, 12:277-285. This paper provides evidence that inhibition of myoinositol monophosphatase is not a common neurochemical mechanism for mood stabilizing medications.
39. Barkai AI, Dunner DL, Gross HA, Mayo P, Fieve RR: Reduced myo-inositol levels in cerebrospinal fluid from patients with affective disorder. Biol Psychiatry 1978, 13:65-72.
40. Kofman O. Belmaker RH: Biochemical, behavioral, and clinical studies of the role of inositol in lithium treatment and depression. Biol Psychiatry 1993, 34:839-852.
41. Agam G, Shapiro Y, Bersudsky Y, Kofman O, Belmaker RH: High-dose peripheral inositol raises brain inositol levels and reverses behavioral effects of inositol depletion by lithium. Pharmacol Biochem. Behav 1994, 49:341-343.
42. Levine J, Gonsalves M, Babur I, Stier S, Elizur A, Kofman O, Belmaker RH: Inositol 6 g daily may be effective in depression but not in schizophrenia. Human Psychopharmacol 1993, 8:49-53.
43. Levine J, Rapaport A, Lev L., Bersudsky Y, Kofman O, Belmaker RH, Shapiro J, Agam G: Inositol treatment raises CSF inositol levels. Brain Res 1993, 627:168-170.
44. Levine J, Goldberger I, Rapaport A, Schwartz M, Schield C, Elizur C, Elizur A, Belmaker RH, Shapiro J, Agam G: CSF inositol in schizophrenia and high-dose inositol treatment of schizophrenia. Eur Neuropsychopharmacol 1994, 4:487-490.
45. Levine J, Barak Y, Gonzalves M, Szor H, Elizur A, Kofman O, Belmaker RH: Double-blind, controlled trial of inositol treatment of depression. Am J Psychiatry 1995, 152:792-794. Among one of the more important scientific contributions in the area of mood disorder research in the past 12 months. A controlled, double-blind trial demonstrating the therapeutic effiacacy of inositol in treating depression. This is the first use of the precursor strategy for a second messenger (ie myoinositol) rather than a neurotransmitter in the treatment of depression.
46. 1 in lymphocytes from bipolar but not control patients.
47. 1 responses in affective disorders. Furthermore, it provides preliminary evidence suggesting this altered response may be a trait-marker of depression.
48. Okamoto Y, Kagaya A, Shinno H, Motohashi N, Yamawaki S: Serotonin-induced platelet calcium mobilization in enhanced is mania. Life Sci 1994, 56:327-332.
49. Mikuni M, Kagaya A, Takahashi K, Meltzier HY: Serotonin but not norepinephrine-induced calcium mobilization of platelets is enhanced in affective disorders. Psychopharmacol 1992, 106:311-314.
50. Eckert A, Gann H, Riemann D, Aldenhoff J, Muller WE: Platelet and lymphocyte free intracellular calcium in affective disorders. Eur Arch Psychiatry Clin Neurosci 1994, 243:235-239.
51. Bothwell RA, Eccleston D, Marshall E: Platelet intracellular calcium in patients with recurrent affective disorders. Psychopharmacol 1994, 114:375-381.
52. 2+-response in neutrophils of manic-depressive patients: effect of lithium therapy. Neuropsychobiol 1993, 27:180-183.
53. 2+] in single T-lymphocytes from depressed patients and healthy controls. Eur Arch Psychiatry Clin Neurosci 1994, 243:214-217.