Molecular Biology of Bipolar Disorder

Bipolar Disorder: Clinical and Neurobiological Foundations

Volumn , Issue , 2010, Pages 228-243

  Andreazza, Ana ^a   Wang, Jun Feng ^a   Young, Trevor ^a  

^a UNIVERSITY OF BRITISH COLUMBIA   (Canada)

Author keywords

Abnormalities in pathways leading to a functional imbalance in multiple neurotransmitter pathways; BD pathophysiology and treatment implications; Bipolar disorder (BD), common, chronic, recurrent mental illness prevalence of about 1 3 of worldwide population; G protein coupled dopaminergic receptors, D1 and D2 associated with BD; G proteins, integral part of intracellular signaling pathway; Molecular biology of bipolar disorder; Regulation of second messenger GSK 3 by protein kinase B (AKT) and WNT system; Signal protein binding in receptor a second messenger activated; Signal transduction pathways responsible for coordinating cellular response to information impinging on cell from multiple sources and time frames; Signalling pathway modulation central to understanding neuroplasticity mechanism, mechanisms of action of mood stabilizers

Indexed keywords

EID: 84885983148     PISSN: None     EISSN: None     Source Type: Book    
DOI: 10.1002/9780470661277.ch17     Document Type: Chapter

References (182)

1. Kupfer, D.J. (2005) The increasing medical burden in bipolar disorder. JAMA, 293 (20), 2528-2530.
2. Belmaker, R.H. (2004) Bipolar disorder. N. Engl. J. Med., 351 (5), 476-486.
3. Merikangas, K.R., Akiskal, H.S., Angst, J. et al. (2007) Lifetime and 12-month prevalence of bipolar spectrum disorder in the National Comorbidity Survey replication. Arch. Gen. Psychiatry, 64 (5), 543-552.
4. Martinez-Aran, A., Torrent, C., Tabares-Seisdedos, R. et al. (2008) Neurocognitive impairment in bipolar patients with and without history of psychosis. J. Clin. Psychiat., 69 (2), 233-239.
5. Martinez-Aran, A., Vieta, E., Reinares, M. et al. (2004) Cognitive function across manic or hypomanic, depressed, and euthymic states in bipolar disorder. Am. J. Psychiatry, 161 (2), 262-270.
6. Torres, I.J., Boudreau, V.G. and Yatham, L.N. (2007) Neuropsychological functioning in euthymic bipolar disorder: a meta-analysis. Acta Psychiatr. Scand. Suppl. (434), 17-26.
7. Berk, M., Malhi, G.S., Hallam, K. et al. (2009) Early intervention in bipolar disorders: clinical, biochemical and neuroimaging imperatives. J. Affect. Disord., 114 (1-3), 1-13.
8. Goodwin, G.M., Martinez-Aran, A., Glahn, D.C. and Vieta, E. (2008) Cognitive impairment in bipolar disorder: neurodevelopment or neurodegeneration? An ECNP expert meeting report. Eur. Neuropsychopharmacol., 18 (11), 787-793.
9. Goodwin, F.K. (1989) The biology of recurrence: new directions for the pharmacologic bridge. J. Clin. Psychiat., 50 (Suppl.), 40-44, discussion 45-47.
10. Ongur, D., Drevets, W.C. and Price, J.L. (1998) Glial reduction in the subgenual prefrontal cortex in mood disorders. Proc. Natl. Acad. Sci. USA, 95 (22), 13290-13295.
11. Rajkowska, G., Halaris, A. and Selemon, L.D. (2001) Reductions in neuronal and glial density characterize the dorsolateral prefrontal cortex in bipolar disorder. Biol. Psychiatry, 49 (9), 741-752.
12. Benes, F.M., Vincent, S.L. and Todtenkopf, M. (2001) The density of pyramidal and nonpyramidal neurons in anterior cingulate cortex of schizophrenic and bipolar subjects. Biol. Psychiatry, 50 (6), 395-406.
13. Benes, F.M., Kwok, E.W., Vincent, S.L. and Todtenkopf, M.S. (1998) A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives. Biol. Psychiatry, 44 (2), 88-97.
14. Manaye, K.F., Lei, D.L., Tizabi, Y. et al. (2005) Selective neuron loss in the paraventricular nucleus of hypothalamus in patients suffering from major depression and bipolar disorder. J. Neuropathol. Exp. Neurol., 64 (3), 224-229.
15. Bezchlibnyk, Y.B., Sun, X., Wang, J.F. et al. (2007) Neuron somal size is decreased in the lateral amygdalar nucleus of subjects with bipolar disorder. J. Psychiatr. Neurosci., 32 (3), 203-210.
16. Rajkowska, G. (2000) Postmortem studies in mood disorders indicate altered numbers of neurons and glial cells. Biol. Psychiatry, 48 (8), 766-777.
17. Ross, E.M. (1989) Signal sorting and amplification through G protein-coupled receptors. Neuron, 3 (2), 141-152.
18. Bauer, M., Alda, M., Priller, J. et al. (2003) Implications of the neuroprotective effects of lithium for the treatment of bipolar and neurodegenerative disorders. Pharmacopsychiatry, 36 (Suppl. 3), S250-S254.
19. Schloesser, R.J., Huang, J., Klein, P.S. and Manji, H.K. (2008) Cellular plasticity cascades in the pathophysiology and treatment of bipolar disorder. Neuropsychopharmacology, 33 (1), 110-133.
20. Birnbaumer, L. (1992) Receptor-to-effector signaling through G proteins: roles for beta gamma dimers as well as alpha subunits. Cell, 71 (7), 1069-1072.
21. Manji, H.K. and Lenox, R.H. (2000) The nature of bipolar disorder. J. Clin. Psychiat., 61 (Supp. 13), 42-57.
22. Schloesser, M., Schnitzer, A., Ying, H. et al. (2008) iSANLA: intelligent sensor and actuator network for life science applications. Conference proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society.IEEE Engineering in Medicine and Biology Society. Conference, vol. 2008, pp. 2369-2372.
23. Beaulieu, J.M., Gainetdinov, R.R. and Caron, M.G. (2009) Akt/GSK3 signaling in the action of psychotropic drugs. Annu. Rev. Pharmacol. Toxicol., 49, 327-347.
24. Young, L.T., Li, P.P., Kish, S.J. et al. (1991) Postmortem cerebral cortex Gs alpha-subunit levels are elevated in bipolar affective disorder. Brain Res., 553 (2), 323-326.
25. Young, L.T., Li, P.P., Kish, S.J. et al. (1993) Cerebral cortex Gs alpha protein levels and forskolin-stimulated cyclic AMP formation are increased in bipolar affective disorder. J. Neurochem., 61 (3), 890-898.
26. Friedman, E. and Wang, H.Y. (1996) Receptor-mediated activation of G proteins is increased in postmortem brains of bipolar affective disorder subjects. J. Neurochem., 67 (3), 1145-1152.
27. Dowlatshahi, D., MacQueen, G., Wang, J.F. et al. (2000) Increased hippocampal supragranular Timm staining in subjects with bipolar disorder. Neuroreport, 11 (17), 3775-3778.
28. Young, L.T., Asghari, V., Li, P.P. et al. (1996) Stimulatory G-protein alpha-subunit mRNA levels are not increased in autopsied cerebral cortex from patients with bipolar disorder. Brain Res. Mol. Brain Res., 42 (1), 45-50.
29. Rao, J.S., Rapoport, S.I. and Kim, H.W. (2009) Decreased GRK3 but not GRK2 expression in frontal cortex from bipolar disorder patients. Int. J. Neuropsychopharmacol., 12 (6), 851-860.
30. Spleiss, O., van Calker, D., Schärer, L., Adamovic, K., Berger, M. and Gebicke-Haerter, P.J. (1998) Abnormal G protein alpha(s) - and alpha(i2)-subunit mRNA expression in bipolar affective disorder. Mol. Psychiatry, 3 (6), 512-520.
31. Young, L.T., Li, P.P., Kamble, A., Siu, K.P. and Warsh, J.J. (1994) Mononuclear leukocyte levels of G proteins in depressed patients with bipolar disorder or major depressive disorder. Am. J. Psychiatry, 151 (4), 594-596.
32. Schreiber, G. and Avissar, S. (1991) Lithium sensitive G protein hyperfunction: a dynamic model for the pathogenesis of bipolar affective disorder. Med. Hypotheses, 35 (3), 237-243.
33. Avissar, S., Nechamkin, Y., Barki-Harrington, L., Roitman, G. and Schreiber, G.(1997) Differential G protein measures in mononuclear leukocytes of patients with bipolar mood disorder are state dependent. J. Affect. Disord., 43 (2), 85-93.
34. Hahn, C.G., Gomez, G., Restrepo, D. et al. (2005) Aberrant intracellular calcium signaling in olfactory neurons from patients with bipolar disorder. Am. J. Psychiatry, 162 (3), 616-618.
35. Mitchell, P.B., Manji, H.K., Chen, G. et al. (1997) High levels of Gs alpha in platelets of euthymic patients with bipolar affective disorder. Am. J. Psychiatry, 154 (2), 218-223.
36. Alda, M., Grof, P., Rouleau, G.A. et al. (2005) Investigating responders to lithium prophylaxis as a strategy for mapping susceptibility genes for bipolar disorder. Prog. Neuropsychopharmacol. Biol. Psychiatry, 29 (6), 1038-1045.
37. Sklar, P., Smoller, J.W., Fan, J. et al. (2008) Whole-genome association study of bipolar disorder. Mol. Psychiatry, 136), 558-569.
38. Ferreira, M.A., O'Donovan, M.C., Meng, Y.A. et al. (2008) Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder. Nat. Genet., 40 (9), 1056-1058.
39. Fan, J. and Sklar, P. (2008) Genetics of bipolar disorder: focus on BDNF Val66Met polymorphism. Novartis Found. Symp., 289, 60-72, discussion 72-73, 87-93.
40. Fan, J., Ionita-Laza, I., McQueen, M.B. et al. (2009) Linkage disequilibrium mapping of the chromosome 6q21-22.31 bipolar I disorder susceptibility locus. Am. J. Med. Genet., 153, 29-37.
41. Dean, O., Bush, A.I., Berk, M. et al. (2009) Glutathione depletion in the brain disrupts short-term spatial memory in the Y-maze in rats and mice. Behav. Brain Res., 198 (1), 258-262.
42. Catapano, L.A. and Manji, H.K. (2007) G protein-coupled receptors in major psychiatric disorders. Biochim Biophys. Acta, 1768 (4), 976-993.
43. Pearlson, G.D., Wong, D.F., Tune, L.E. et al. (1995) In vivo D2 dopamine receptor density in psychotic and nonpsychotic patients with bipolar disorder. Arch. Gen. Psychiatry, 52 (6), 471-477.
44. Wong, D.F., Pearlson, G.D., Tune, L.E. et al. (1997) Quantification of neuroreceptors in the living human brain: IV. Effect of aging and elevations of D2-like receptors in schizophrenia and bipolar illness. J. Cereb. Blood Flow Metab., 17 (3), 331-342.
45. McInnis, M.G., Lan, T.H., Willour, V.L. et al. (2003) Genomewide scan of bipolar disorder in 65 pedigrees: supportive evidence for linkage at 8q24, 18q22, 4q32, 2p12, and 13q12. Mol. Psychiatry, 8 (3), 288-298.
46. Ranade, S.S., Mansour, H., Wood, J. et al. (2003) Linkage and association between serotonin 2A receptor gene polymorphisms and bipolar I disorder. Am. J. Med. Genet., 121B (1), 28-34.
47. Chee, I.S., Lee, S.W., Kim, J.L. et al. (2001) 5-HT2A receptor gene promoter polymorphism -1438A/G and bipolar disorder. Psychiatr. Genet., 11 (3), 111-114.
48. Rybakowski, J.K., Dmitrzak-Weglarz, M., Suwalska, A. et al. (2009) Dopamine D1 receptor gene polymorphism is associated with prophylactic lithium response in bipolar disorder. Pharmacopsychiatry, 42 (1), 20-22.
49. Massat, I., Souery, D., Del-Favero, J., et al. (2002) Positive association of dopamine D2 receptor polymorphism with bipolar affective disorder in a European Multicenter Association Study of affective disorders. Am. J. Med. Genet., 114 (2), 177-185.
50. Shaltiel, G., Shamir, A., Levi, I. et al. (2006) Lymphocyte G-protein receptor kinase (GRK)3 mRNA levels in bipolar disorder. Int. J. Neuropsychopharmacol., 9 (6), 761-766.
51. Chao, M.V., Rajagopal, R. and Lee, F.S. (2006) Neurotrophin signalling in health and disease. Clin. Sci. (Lond.), 110 (2), 167-173.
52. Arevalo, J.C. and Chao, M.V. (2005) Axonal growth: where neurotrophins meet Wnts. Curr. Opin. Cell Biol., 17 (2), 112-115.
53. Chao, M.V. (2003) Neurotrophins and their receptors: a convergence point for many signalling pathways. Nat. Rev. Neurosci., 4 (4), 299-309.
54. Kapczinski, F., Dias, V.V., Frey, B.N. and Kauer-Sant'Anna, M. (2009) Brain-derived neurotrophic factor in bipolar disorder: beyond trait and state: comment on 'Decreased levels of serum brain-derived neurotrophic factor in both depressed and euthymic patients with unipolar depression and in euthymic patients with bipolar I and II disorders'. Bipolar Disord., 11 (2), 221-222.
55. Post, R.M. (2007) Kindling and sensitization as models for affective episode recurrence, cyclicity, and tolerance phenomena. Neurosci. Biobehav. Rev., 31 (6), 858-873.
56. Cunha, A.B., Frey, B.N., Andreazza, A.C. et al. (2006) Serum brain-derived neurotrophic factor is decreased in bipolar disorder during depressive and manic episodes. Neurosci. Lett., 398 (3), 215-219.
57. Machado-Vieira, R., Dietrich, M.O., Leke, R. et al. (2007) Decreased plasma brain derived neurotrophic factor levels in unmedicated bipolar patients during manic episode. Biol. Psychiatry, 61 (2), 142-144.
58. Monteleone, P., Serritella, C., Martiadis, V. and Maj, M. (2008) Decreased levels of serum brain-derived neurotrophic factor in both depressed and euthymic patients with unipolar depression and in euthymic patients with bipolar I and II disorders. Bipolar Disord., 10 (1), 95-100.
59. de Oliveira, G.S., Ceresér, K.M., Fernandes, B.S., et al. (2009) Decreased brain-derived neurotrophic factor in medicated and drug-free bipolar patients. J. Psychiatr. Res., 43 (14), 1171-1174.
60. Dunham, J.H., Meyer, R.C., Garcia, E.L. and Hall, R.A. (2009) GPR37 surface expression enhancement via N-terminal truncation or protein-protein interactions. Biochemistry, 48 (43), 10286-10297.
61. Hattiangady, B., Rao, M.S., Zaman, V. and Shetty, A.K. (2006) Incorporation of embryonic CA3 cell grafts into the adult hippocampus at 4-months after injury: effects of combined neurotrophic supplementation and caspase inhibition. Neuroscience, 139 (4), 1369-1383.
62. Gooney, M., Messaoudi, E., Maher, F.O. et al. (2004) BDNFinduced LTP in dentate gyrus is impaired with age: analysis of changes in cell signaling events. Neurobiol. Aging, 25 (10), 1323-1331.
63. Yatham, L.N., Kapczinski, F., Andreazza, A.C. et al. (2009) Accelerated age-related decrease in brain-derived neurotrophic factor levels in bipolar disorder. Int. J. Neuropsychopharmacol., 12 (1), 137-139.
64. Kauer-Sant'Anna, M., Kapczinski, F., Andreazza, A.C., et al. (2009) Brain-derived neurotrophic factor and inflammatory markers in patients with early- vs. late-stage bipolar disorder. Int. J. Neuropsychopharmacol. 12 (4), 447-458.
65. Andreazza, A.C., Cassini, C., Rosa, A.R. et al. (2007) Serum S100B and antioxidant enzymes in bipolar patients. J. Psychiatr. Res., 41 (6), 523-529.
66. Machado-Vieira, R., Andreazza, A.C., Viale, C.I. et al. (2007) Oxidative stress parameters in unmedicated and treated bipolar subjects during initial manic episode: a possible role for lithium antioxidant effects. Neurosci. Lett., 421 (1), 33-36.
67. Selek, S., Savas, H.A., Gergerlioglu, H.S. et al. (2007) The course of nitric oxide and superoxide dismutase during treatment of bipolar depressive episode. J. Affect. Disord., 107, 89-94.
68. Selek, S., Savas, H.A., Gergerlioglu, H.S. et al. (2008) The course of nitric oxide and superoxide dismutase during treatment of bipolar depressive episode. J. Affect. Disord., 107 (1-3), 89-94.
69. Savas, H.A., Gergerlioglu, H.S., Armutcu, F. et al. (2006) Elevated serum nitric oxide and superoxide dismutase in euthymic bipolar patients: impact of past episodes. World J. BiolPsychiatry, 7 (1), 51-55.
70. Ranjekar, P.K., Hinge, A., Hegde, M.V. et al. (2003) Decreased antioxidant enzymes and membrane essential polyunsaturated fatty acids in schizophrenic and bipolar mood disorder patients. Psychiatry Res., 121 (2), 109-122.
71. Abdalla, D.S., Monteiro, H.P., Oliveira, J.A. and Bechara, E.J. (1986) Activities of superoxide dismutase and glutathione peroxidase in schizophrenic and manic-depressive patients. Clin. Chem., 32 (5), 805-807.
72. Zohar, J., Lerer, B., Ebstein, R.P. and Belmaker, R.H. (1982) Lithium does not prevent agonist-induced subsensitivity of human adenylate cyclase. Biol. Psychiatry, 17 (3), 343-350.
73. Spaulding, G.F., Jessup, J.M. and Goodwin , T.J. (1993) Advances in cellular construction. J. Cell Biochem., 51 (3), 249-251.
74. Rahman, S., Li, P.P., Young, L.T. et al. (1997) Reduced [3H] cyclic AMP binding in postmortem brain from subjects with bipolar affective disorder. J. Neurochem., 68 (1), 297-304.
75. Fields, A., Li, P.P., Kish, S.J. and Warsh, J.J. (1999) Increased cyclic AMP-dependent protein kinase activity in postmortem brain from patients with bipolar affective disorder. J. Neurochem., 73 (4), 1704-1710.
76. Perez, J., Tardito, D., Mori, S. et al. (2000) Altered Rap1 endogenous phosphorylation and levels in platelets from patients with bipolar disorder. J. Psychiatr. Res., 34 (2), 99-104.
77. Tardito, D., Mori, S., Racagni, G. et al. (2003) Protein kinase A activity in platelets from patients with bipolar disorder. J. Affect. Disord., 76 (1-3), 249-253.
78. Karege, F., Schwald, M., Papadimitriou, P. et al. (2004) The cAMP-dependent protein kinase A and brain-derived neurotrophic factor expression in lymphoblast cells of bipolar affective disorder. J. Affect. Disord., 79 (1-3), 187-192.
79. Taylor, S.J. and Exton, J.H. (1991) Two alpha subunits of the Gq class of G proteins stimulate phosphoinositide phospholipase C-beta 1 activity. FEBS Lett., 286 (1-2), 214-216.
80. Wang, H.Y. and Friedman, E. (1996) Enhanced protein kinase C activity and translocation in bipolar affective disorder brains. Biol. Psychiatry, 40 (7), 568-575.
81. Shimon, H., Agam, G., Belmaker, R.H. et al. (1997) Reduced frontal cortex inositol levels in postmortem brain of suicide victims and patients with bipolar disorder. Am. J. Psychiatry, 154 (8), 1148-1150.
82. Mathews, R., Li, P.P., Young, L.T. et al. (1997) Increased G alpha q/11 immunoreactivity in postmortem occipital cortex from patients with bipolar affective disorder. Biol. Psychiatry, 41 (6), 649-656.
83. Brown, A.S., Mallinger, A.G. and Renbaum, L.C. (1993) Elevated platelet membrane phosphatidylinositol-4,5- bisphosphate in bipolar mania. Am. J. Psychiatry, 150 (8), 1252-1254.
84. Friedman, E., Wang, H.-Y., Levinson, D. et al. (1993) Altered platelet protein kinase C activity in bipolar affective disorder, manic episode. Biol. Psychiatry, 33 (7), 520-525.
85. Soares, J.C. and Mallinger, A.G. (1996) Abnormal phosphatidylinositol (PI)-signalling in bipolar disorder. Biol. Psychiatry, 39 (6), 461-464.
86. Soares, J.C., Dippold, C.S. and Mallinger, A.G. (1997) Platelet membrane phosphatidylinositol-4,5-bisphosphate alterations in bipolar disorder--evidence from a single case study. Psychiatry Res., 69 (2-3), 197-202.
87. Soares, J.C., Chen, G., Dippold, C.S. et al. (2000) Concurrent measures of protein kinase C and phosphoinositides in lithium-treated bipolar patients and healthy individuals: a preliminary study. Psychiatry Res., 95 (2), 109-118.
88. Soares, J.C., Mallinger, A.G., Dippold, C.S. et al. (1999) Platelet membrane phospholipids in euthymic bipolar disorder patients: are they affected by lithium treatment? Biol. Psychiatry, 45 (4), 453-457.
89. Pandey, G.N., Rizavi, H.S., Dwivedi, Y. and Pavuluri, M.N. (2008) Brain-derived neurotrophic factor gene expression in pediatric bipolar disorder: effects of treatment and clinical response. J. Am. Acad. Child Psy., 47 (9), 1077-1085.
90. Dubovsky, S.L., Franks, R.D., Allen, S. and Murphy, J. (1986) Calcium antagonists in mania: a double-blind study of verapamil. Psychiatry Res., 18 (4), 309-320.
91. Dubovsky, S.L., Thomas, M., Hijazi, A. and Murphy, J. (1994) Intracellular calcium signalling in peripheral cells of patients with bipolar affective disorder. Eur. Arch. Psychiatry Clin. Neurosci., 243 (5), 229-234.
92. Hough, C., Lu, S.J., Davis, C.L., Chuang, D.M. and Post, R.M. (1999) Elevated basal and thapsigargin-stimulated intracellular calcium of platelets and lymphocytes from bipolar affective disorder patients measured by a fluorometric microassa . Biol. Psychiatry, 46 (2), 247-255.
93. Kato, T., Ishiwata, M., Mori, K. et al. (2003) Mechanisms of altered Ca2+ signalling in transformed lymphoblastoid cells from patients with bipolar disorder. Int. J. Neuropsychopharmacol., 6 (4), 379-389.
94. Perova, T., Kwan, M., Li, P.P. and Warsh, J.J. (2009) Differential modulation of intracellular Ca2+ responses in B lymphoblasts by mood stabilizers. Int. J. Neuropsychopharmacol., 29, 1-10.
95. El Khoury, A., Petterson, U., Kallner, G. et al. (2002) Calcium homeostasis in long-term lithium-treated women with bipolar affective disorder. Prog. Neuropsychopharmacol. Biol. Psychiatry, 26 (6), 1063-1069.
96. Emamghoreishi, M., Li, P.P., Schlichter, L. et al. (2000) Associated disturbances in calcium homeostasis and G protein-mediated cAMP signaling in bipolar I disorder. Biol. Psychiatry, 48 (7), 665-673.
97. Perova, T., Wasserman, M.J., Li, P.P. and Warsh, J.J. (2008) Hyperactive intracellular calcium dynamics in B lymphoblasts from patients with bipolar I disorder. Int. J. Neuropsychopharmacol., 11 (2), 185-196.
98. Wasserman, M.J., Corson, T.W., Sibony, D. et al. (2004) Chronic lithium treatment attenuates intracellular calcium mobilization. Neuropsychopharmacol., 29 (4), 759-769.
99. Beaulieu, J.M., Tirotta, E., Sotnikova, T.D. et al. (2007) Regulation of Akt signaling by D2 and D3 dopamine receptors in vivo. J. Neurosci., 27 (4), 881-885.
100. Beavo, J.A., Bechtel, P.J. and Krebs, E.G. (1974) Activation of protein kinase by physiological concentrations of cyclic AMP. Proc. Natl. Acad. Sci. USA, 71 (9), 3580-3583.
101. Bezchlibnyk, Y. and Young, L.T. (2002) The neurobiology of bipolar disorder: focus on signal transduction pathways and the regulation of gene expression. Can. J. Psychiat., 47 (2), 135-148.
102. Zanardi, R., Racagni, G., Smeraldi, E. and Perez, J. (1997) Differential effects of lithium on platelet protein phosphorylation in bipolar patients and healthy subjects. Psychopharmacology (Berl.), 129 (1), 44-47.
103. Perez, J., Tardito, D., Mori, S. et al. (1999) Abnormalities of cyclic adenosine monophosphate signaling in platelets from untreated patients with bipolar disorder. Arch. Gen. Psychiatry, 56 (3), 248-253.
104. Karege, F., Schwald, M. and El Kouaissi, R. (2004) Druginduced decrease of protein kinase a activity reveals alteration in BDNF expression of bipolar affective disorder. Neuropsychopharmacology, 29 (4), 805-812.
105. Gould, T.D. and Manji, H.K. (2002) Signaling networks in the pathophysiology and treatment of mood disorders. J. Psychosom. Res., 53 (2), 687-697.
106. Berridge, M.J., Dawson, R.M., Downes, C.P. et al. (1983) Changes in the levels of inositol phosphates after agonistdependent hydrolysis of membrane phosphoinositides. Biochem. J., 212 (2), 473-482.
107. Perez-Gordones, M.C., Lugo, M.R., Winkler, M. et al. (2009) Diacylglycerol regulates the plasma membrane calcium pump from human erythrocytes by direct interaction. Arch. Biochem. Biophys., 489, 55-61.
108. Kato, T. (2008) Molecular neurobiology of bipolar disorder: a disease of 'mood-stabilizing neurons'? Trends Neurosci., 31 (10), 495-503.
109. Belmaker, R.H., Shapiro, J., Vainer, E. et al. (2002) Reduced inositol content in lymphocyte-derived cell lines from bipolar patients. Bipolar Disord., 4 (1), 67-69.
110. Nemanov, L., Ebstein, R.P., Belmaker, R.H. et al. (1999) Effect of bipolar disorder on lymphocyte inositol monophosphatase mRNA levels. Int. J. Neuropsychopharmacol., 2 (1), 25-29.
111. Yoon, I.S., Li, P.P., Siu, K.P. et al. (2001) Altered IMPA2 gene expression and calcium homeostasis in bipolar disorder. Mol. Psychiatry, 6 (6), 678-683.
112. Shamir, A., Ebstein, R.P., Nemanov, L. et al. (1998) Inositol monophosphatase in immortalized lymphoblastoid cell lines indicates susceptibility to bipolar disorder and response to lithium therapy. Mol. Psychiatry, 3 (6), 481-482.
113. Newton, P.M. and Ron, D. (2007) Protein kinase C and alcohol addiction. Pharmacol. Res., 55 (6), 570-577.
114. Crotty, T., Cai, J., Sakane, F. et al. (2006) Diacylglycerol kinase delta regulates protein kinase C and epidermal growth factor receptor signaling. Proc. Natl. Acad. Sci. USA, 103 (42), 15485-15490.
115. Baum, A.E., Akula, N., Cabanero, M. et al. (2008) A genomewide association study implicates diacylglycerol kinase eta (DGKH) and several other genes in the etiology of bipolar disorder. Mol. Psychiatry, 13 (2), 197-207.
116. Zarate, C.A. Jrand Manji, H.K. (2008) Bipolar disorder: candidate drug targets. Mt. Sinai J. Med., 75 (3), 226-247.
117. Kato, T. (2008) Role of mitochondrial DNA in calcium signaling abnormality in bipolar disorder. Cell Calcium, 44 (1), 92-102.
118. Kato, T., Kakiuchi, C. and Iwamoto, K. (2007) Comprehensive gene expression analysis in bipolar disorder. Can. J. Psychiat., 52 (12), 763-771.
119. Gould, T.D., Picchini, A.M., Einat, H. and Manji, H.K. (2006) Targeting glycogen synthase kinase-3 in the CNS: implications for the development of new treatments for mood disorders. Curr. Drug Targets, 7 (11), 1399-1409.
120. Rowe, M.K. and Chuang, D.M. (2004) Lithium neuroprotection: molecular mechanisms and clinical implications. Expert Rev. Mol. Med., 6 (21), 1-18.
121. Salinas, P.C. and Hall, A.C. (1999) Lithium and synaptic plasticity. Bipolar Disord., 1 (2), 87-90.
122. Lucas, F.R., Goold, R.G., Gordon-Weeks, P.R. and Salinas, P. C. (1998) Inhibition of GSK-3beta leading to the loss of phosphorylated MAP-1B is an early event in axonal remodelling induced byWNT-7aor lithium. J. Cell Sci., 111 (Pt 10), 1351-1361.
123. Beurel, E. and Jope, R.S. (2006) The paradoxical pro- and anti-apoptotic actions of GSK3 in the intrinsic and extrinsic apoptosis signaling pathways. Prog. Neurobiol., 79 (4), 173-189.
124. Wodarz, A. and Nusse, R. (1998) Mechanisms of Wnt signaling in development. Annu. Rev. Cell Dev. Biol., 14, 59-88.
125. Gould, T.D. and Manji, H.K. (2002) The Wnt signaling pathway in bipolar disorder. Neuroscientist, 8 (5), 497-511.
126. Rowe, M.K., Wiest, C. and Chuang, D.M. (2007) GSK-3 is a viable potential target for therapeutic intervention in bipolar disorder. Neurosci. Biobehav. Rev., 31 (6), 920-931.
127. Hashimoto, R., Takei, N., Shimazu, K., Christ, L., Lu, B. and Chuang, D.M. (2002) Lithium induces brain-derived neurotrophic factor and activates TrkB in rodent cortical neurons: an essential step for neuroprotection against glutamate excitotoxicity. Neuropharmacol., 43 (7), 1173-1179.
128. Frey, B.N., Andreazza, A.C., Cereser, K.M. et al. (2006) Effects of mood stabilizers on hippocampus BDNF levels in an animal model of mania. Life Sci., 79 (3), 281-286.
129. Chalecka-Franaszek, E. and Chuang, D.M. (1999) Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons. Proc. Natl. Acad. Sci. USA, 96 (15), 8745-8750.
130. Einat, H., Yuan, P., Gould, T.D. et al. (2003) The role of the extracellular signal-regulated kinase signaling pathway in mood modulation. J. Neurosci., 23 (19), 7311-7316.
131. Liang, Z.Q., Wang, X., Li, L.Y. et al. (2007) Nuclear factorkappaB- dependent cyclin D1 induction and DNA replication associated with N-methyl-D-aspartate receptor-mediated apoptosis in rat striatum. J. Neurosci. Res., 85 (6), 1295-1309.
132. Chen, G., Huang, L.D., Jiang, Y.M. and Manji, H.K. (1999) The mood-stabilizing agent valproate inhibits the activity of glycogen synthase kinase-3. J. Neurochem., 72 (3), 1327-1330.
133. Phiel, C.J. and Klein, P.S. (2001) Molecular targets of lithium action. Annu. Rev. Pharmacol. Toxicol., 41, 789-813.
134. Lee, K.Y., Ahn, Y.M., Joo, E.J. et al. (2006) No association of two common SNPs at position 1727 A/T, 50 C/T of GSK- 3 beta polymorphisms with schizophrenia and bipolar disorder of Korean population. Neurosci. Lett., 395 (2), 175-178.
135. Benedetti, F., Serretti, A., Colombo, C. et al. (2004) A glycogen synthase kinase 3-beta promoter gene single nucleotide polymorphism is associated with age at onset and response to total sleep deprivation in bipolar depression. Neurosci. Lett., 368 (2), 123-126.
136. Szczepankiewicz, A., Rybakowski, J.K., Suwalska, A. et al. (2006) Association study of the glycogen synthase kinase- 3beta gene polymorphism with prophylactic lithium response in bipolar patients. World J. Biological Psychiatry, 7 (3), 158-161.
137. Nishiguchi, N., Breen, G., Russ, C. et al. (2006) Association analysis of the glycogen synthase kinase-3beta gene in bipolar disorder. Neurosci. Lett., 394 (3), 243-245.
138. Beasley, C., Cotter, D., Khan, N. et al. (2001) Glycogen synthase kinase-3beta immunoreactivity is reduced in the prefrontal cortex in schizophrenia. Neurosci. Lett., 302 (2-3), 117-120.
139. Benedetti, F., Serretti, A., Pontiggia, A. et al. (2005) Longterm response to lithium salts in bipolar illness is influenced by the glycogen synthase kinase 3-beta -50 T/C SNP. Neurosci. Lett., 376 (1), 51-55.
140. Michelon, L., Meira-Lima, I., Cordeiro, Q. et al. (2006) Association study of the INPP1, 5HTT, BDNF, AP-2beta and GSK-3beta GENE variants and restrospectively scored response to lithium prophylaxis in bipolar disorder. Neurosci. Lett., 403 (3), 288-293.
141. Mamdani, F., Alda, M., Grof, P. et al. (2008) Lithium response and genetic variation in the CREB family of genes. Am. J. Med. Genet., 147B (4), 500-504.
142. McCarty, J.H. (2009) Cell adhesion and signaling networks in brain neurovascular units. Curr. Opin. Hematol., 16 (3), 209-214.
143. Hedgepeth, C.M., Conrad, L.J., Zhang, J. et al. (1997) Activation of the Wnt signaling pathway: a molecular mechanism for lithium action. Dev. Biol., 185 (1), 82-91.
144. Barker, N. (2008) The canonical Wnt/beta-catenin signalling pathway. Methods Mol. Biol., 468, 5-15.
145. Eastman, Q. and Grosschedl, R. (1999) Regulation of LEF-1/ TCF transcription factors by Wnt and other signals. Curr. Opin. Cell Biol., 11 (2), 233-240.
146. Leng, Y., Liang, M.H., Ren, M. et al. (2008) Synergistic neuroprotective effects of lithium and valproic acid or other histone deacetylase inhibitors in neurons: roles of glycogen synthase kinase-3 inhibition. J. Neurosci., 28 (10), 2576-2588.
147. Takayama, S., Xie, Z. and Reed, J.C. (1999)Anevolutionarily conserved family of Hsp70/Hsc70 molecular chaperone regulators. J. Biol. Chem., 274 (2), 781-786.
148. Beere, H.M. and Green, D.R. (2001) Stress management - heat shock protein-70 and the regulation of apoptosis. Trends Cell Biol., 11 (1), 6-10.
149. Beere, H.M., Wolf, B.B., Cain, K. et al. (2000) Heat-shock protein 70 inhibits apoptosis by preventing recruitment of procaspase-9 to the Apaf-1 apoptosome. Nat. Cell Biol., 2 (8), 469-475.
150. Hwang, S.O., Boswell, S.A., Seo, J.S. and Lee, S.W. (2008) Novel oxidative stress-responsive gene ERS25 functions as a regulator of the heat-shock and cell death response. J. Biol. Chem., 283 (19), 13063-13069.
151. Chu, B., Soncin, F., Price, B.D. et al. (1996) Sequential phosphorylation by mitogen-activated protein kinase and glycogen synthase kinase 3 represses transcriptional activation by heat shock factor-1. J. Biol. Chem., 271 (48), 30847-30857.
152. Bijur, G.N. and Jope, R.S. (2003) Glycogen synthase kinase-3 beta is highly activated in nuclei and mitochondria. Neuroreport, 14 (18), 2415-2419.
153. Xavier, I.J., Mercier, P.A., McLoughlin, C.M. et al. (2000) Glycogen synthase kinase 3beta negatively regulates both DNA-binding and transcriptional activities of heat shock factor 1. J. Biol. Chem., 275 (37), 29147-29152.
154. Ren, M., Senatorov, V.V., Chen, R.W. and Chuang, D.M. (2003) Postinsult treatment with lithium reduces brain damage and facilitates neurological recovery in a rat ischemia/ reperfusion model. Proc. Natl. Acad. Sci. USA, 100 (10), 6210-6215.
155. Boyle, W.J., Smeal, T., Defize, L.H. et al. (1991) Activation of protein kinase C decreases phosphorylation of c-Jun at sites that negatively regulate its DNA-binding activity. Cell, 64 (3), 573-584.
156. Wisdom, R. (1999) AP-1: one switch for many signals. Exp. Cell Res., 253 (1), 180-185.
157. Asghari, V., Wang, J.F., Reiach, J.S. and Young, L.T. (1998) Differential effects of mood stabilizers on Fos/Jun proteins and AP-1 DNA binding activity in human neuroblastoma SH-SY5Y cells. Brain Res. Mol. Brain Res., 58 (1-2), 95-102.
158. Chen, G., Yuan, P., Hawver, D.B. et al. (1997) Increase in AP-1 transcription factor DNA binding activity by valproic acid. Neuropsychopharmacology, 16 (3), 238-245.
159. Chen, B., Wang, J.F., Hill, B.C. and Young, L.T. (1999) Lithium and valproate differentially regulate brain regional expression of phosphorylated CREB and c-Fos. Brain Res. Mol. Brain Res., 70 (1), 45-53.
160. Spiliotaki, M., Salpeas, V., Malitas, P. et al. (2006) Altered glucocorticoid receptor signaling cascade in lymphocytes of bipolar disorder patients. Psychoneuroendocrin., 31 (6), 748-760.
161. Meyer, T.E. and Habener, J.F. (1993) Cyclic adenosine 3',5'- monophosphate response element binding protein (CREB) and related transcription-activating deoxyribonucleic acidbinding proteins. Endocr. Rev., 14 (3), 269-290.
162. Shaywitz, A.J. and Greenberg, M.E. (1999) CREB: a stimulus- induced transcription factor activated by a diverse array of extracellular signals. Annu. Rev. Biochem., 68, 821-861.
163. Kinney, J.W., Sanchez-Alavez, M., Barr, A.M. et al. (2009) Impairment of memory consolidation by galanin correlates with in vivo inhibition of both LTP and CREB phosphorylation. Neurobiol. Learn Mem., 92, 429-438.
164. Finkbeiner, S. (2000) CREB couples neurotrophin signals to survival messages. Neuron, 25 (1), 11-14.
165. Freeland, K., Liu, Y.Z. and Latchman, D.S. (2000) Distinct signalling pathways mediate the cAMP response element (CRE)-dependent activation of the calcitonin gene-related peptide gene promoter by cAMP and nerve growth factor. Biochem. J., 345 (Pt 2), 233-238.
166. Kopnisky, K.L., Chalecka-Franaszek, E., Gonzalez-Zulueta, M. and Chuang, D.M. (2003) Chronic lithium treatment antagonizes glutamate-induced decrease of phosphorylated CREB in neurons via reducing protein phosphatase 1 and increasing MEK activities. Neuroscience, 116 (2), 425-435.
167. Nibuya, M., Nestler, E.J. and Duman, R.S. (1996) Chronic antidepressant administration increases the expression of cAMP response element binding protein (CREB) in rat hippocampus. J. Neurosci., 16 (7), 2365-2372.
168. Dowlatshahi, D., MacQueen, G.M., Wang, J.F. and Young, L. T. (1998) Increased temporal cortex CREB concentrations and antidepressant treatment in major depression. Lancet, 352 (9142), 1754-1755.
169. Zubenko, G.S., Hughes, H.B. III, Maher, B.S. et al. (2002) Genetic linkage of region containing the CREB1 gene to depressive disorders in women from families with recurrent, early-onset, major depression. Am. J. Med. Genet., 114 (8), 980-987.
170. Boer, U., Cierny, I., Krause, D. et al. (2008) Chronic lithium salt treatment reduces CRE/CREB-directed gene transcription and reverses its upregulation by chronic psychosocial stress in transgenic reporter gene mice. Neuropsychopharm., 33 (10), 2407-2415.
171. Divish, M.M., Sheftel, G., Boyle, A. et al. (1991) Differential effect of lithium on fos protooncogene expression mediated by receptor and postreceptor activators of protein kinase C and cyclic adenosine monophosphate: model for its antimanic action. J. Neurosci. Res., 28 (1), 40-48.
172. Manji, H.K., Potter, W.Z. and Lenox, R.H. (1995) Signal transduction pathways. Molecular targets for lithium's actions. Arch. Gen. Psychiatry, 52 (7), 531-543.
173. Boer, U., Eglins, J., Krause, D. et al. (2007) Enhancement by lithium of cAMP-induced CRE/CREB-directed gene transcription conferred by TORC on the CREB basic leucine zipper domain. Biochem. J., 408 (1), 69-77.
174. Heinrich, A., Boer, U., Tzvetkov, M. et al. (2009) Stimulation by lithium of the interaction between the transcription factor CREB and its co-activator TORC. Biosci. Rep., 29 (2), 77-87.
175. Daniel, P.B. and Habener, J.F. (1998) Cyclical alternative exon splicing of transcription factor cyclic adenosine monophosphate response element-binding protein (CREB) messenger ribonucleic acid during rat spermatogenesis. Endocrinology, 139 (9), 3721-3729.
176. Karpinski, B.A., Morle, G.D., Huggenvik, J. et al. (1992) Molecular cloning of human CREB-2: an ATF/CREB transcription factor that can negatively regulate transcription from the cAMP response element. Proc. Natl. Acad. Sci. USA, 89 (11), 4820-4824.
177. Mamdani, F., Sequeira, A., Alda, M., Grof, P., Rouleau, G. and Turecki, G.(2007) No association between the PREP gene and lithium responsive bipolar disorder. BMC Psychiatry, 7, 9.
178. Coyle, J.T. and Duman, R.S. (2003) Finding the intracellular signaling pathways affected by mood disorder treatments. Neuron, 38 (2), 157-160.
179. Berridge, M.J. and Irvine, R.F. (1989) Inositol phosphates and cell signalling. Nature, 341 (6239), 197-205.
180. Manji, H.K. and Lenox, R.H. (1999) Ziskind-Somerfeld Research Award. Protein kinase C signaling in the brain: molecular transduction of mood stabilization in the treatment of manic-depressive illness. Biol. Psychiatry, 46 (10), 1328-1351.
181. Frey, B.N., Walss-Bass, C., Stanley, J.A. et al. (2007) Brainderived neurotrophic factor val66met polymorphism affects prefrontal energy metabolism in bipolar disorder. Neuroreport., 18 (15), 1567-1570.
182. Rowe, M.K., Wiest, C. and Chuang, D.M. (2007) GSK-3 is a viable potential target for therapeutic intervention in bipolar disorder. Neurosci. Biobehav. Rev., 31 (6), 920-931.