Lithium normalizes elevated intracellular sodium

Bipolar Disorders

Volumn 9, Issue 3, 2007, Pages 298-300

  Huang, Xian ^a   Lei, Zhenmin ^a   El mallakh, Rif S ^a  

^a University of Louisville School of Medicine   (United States)

Author keywords

Bipolar disorder; Glial cells; Intracellular; Ionic displacement; Lithium; LN292; Mechanism; Sodium

Indexed keywords

LITHIUM CHLORIDE; MOOD STABILIZER; OUABAIN; SODIUM;

ARTICLE; ATOMIC ABSORPTION SPECTROMETRY; BIPOLAR DEPRESSION; BIPOLAR MANIA; CONCENTRATION (PARAMETERS); CONTROLLED STUDY; DRUG MECHANISM; GLIOMA CELL; HUMAN; HUMAN CELL; PATHOPHYSIOLOGY; PRIORITY JOURNAL; SODIUM CELL LEVEL; SODIUM TRANSPORT; TREATMENT OUTCOME;

ANTIPSYCHOTIC AGENTS; BIPOLAR DISORDER; CELL LINE, TUMOR; GLIOMA; HUMANS; ION TRANSPORT; LITHIUM CARBONATE; NEURONS; OUABAIN; SODIUM; SODIUM CHANNELS; SPECTRUM ANALYSIS;

EID: 34047273052     PISSN: 13985647     EISSN: 13995618     Source Type: Journal    
DOI: 10.1111/j.1399-5618.2007.00429.x     Document Type: Article

References (16)

1. El-Mallakh RS, Wyatt RJ. The Na,K-ATPase hypothesis for bipolar illness. Biol Psychiatry 1995; 37: 235-244.
2. El-Mallakh RS, Jaziri WA. Calcium channel blockers in affective illness: role of sodium-calcium exchange. J Clin Psychopharmacol 1990; 10: 203-206.
3. El-Mallakh RS, Li R. Is the Na,K-ATPase the link between phosphoinositide metabolism and bipolar disorder? J Neuropsychiatry Clin Neurosci 1993; 5: 361-368.
4. Looney SW, El-Mallakh RS. Meta-analysis of erythrocyte Na,K-ATPase activity in bipolar illness. Depress Anxiety 1997; 5: 53-65.
5. El-Mallakh RS, El-Masri MA, Huff MO, Li X-P, Decker S, Levy RS. Intracerebroventricular administration of ouabain as a model of mania in rats. Bipolar Disord 2003; 5: 362-365.
6. El-Mallakh RS, Huff MO. Mood stabilizers and ion regulation. Harv Rev Psychiatry 2001; 9: 23-32.
7. El-Mallakh RS. Ion homeostatis and the mechanism of action of lithium. Clin Neurosci Res 2004; 4: 227-231.
8. Schurr A, Payne R, Miller J, Rigor B. Glia are the main source of lactate utilized by neurons for recovery of function posthypoxia. Brain Res 1997; 774: 221-224.
9. Ongur P, Drevets WC, Price JL. Glial reduction in the subgenual prefrontal cortex in mood disorders. Proc Natl Acad Sci USA 1998; 95: 13290-13295.
10. Rajkowska G, Halaris A, Selemon LD. Reductions in neuronal and glial density characterize the dorsolateral prefrontal cortex in bipolar disorder. Biol Psychiatry 2001; 49: 741-752.
11. Yuan P, Gould TD, Gray NA et al. Neurotrophic signaling cascades are major long-term targets for lithium: Clinical implications. Clin Neurosci Res 2004; 4: 137-153.
12. Jope RS. Inhibition of glycogen synthase kinase-3: A potential therapeutic target of lithium. Clin Neurosci Res 2004; 4: 171-179.
13. Li R, El-Mallakh RS. A novel evidence of different mechanisms of lithium and valproate neuroprotective action on human SY5Y neuroblastoma cells: Caspase-3 dependency. Neurosci Lett 2000; 294: 147-150.
14. Eickholt BJ, Williams RSB, Harwood AJ. Mood stabilizers and the cell biology of neuronal growth cones. Clin Neurosci Res 2004; 4: 189-199.
15. McNamara RK, Lenox RH. The myristoylated alanine-rich C kinase substrate: A lithium-regulated protein linking cellular signaling and cytoskeletal plasticity. Clin Neurosci Res 2004; 4: 155-169.
16. Wasserman MJ, Corson TW, Sibony D et al. Chronic lithium treatment attenuates intracellular calcium mobilization. Neuropsychopharmacology 2004; 29: 759-769.