Anti-bipolar therapy:
mechanism of action of lithium

Jope RS
Department of Psychiatry and Behavioral Neurobiology,
University of Alabama at Birmingham, 35294-0017, USA.
Mol Psychiatry 1999 Mar; 4(2):117-28


This review introduces the concepts that multiple actions of lithium are critical for its therapeutic effect, and that these complex effects stabilize neuronal activities, support neural plasticity, and provide neuroprotection. Three interacting systems appear most critical. (i) Modulation of neurotransmitters by lithium likely readjusts balances between excitatory and inhibitory activities, and decreased glutamatergic activity may contribute to neuroprotection. (ii) Lithium modulates signals impacting on the cytoskeleton, a dynamic system contributing to neural plasticity, at multiple levels, including glycogen synthase kinase-3beta, cyclic AMP-dependent kinase, and protein kinase C, which may be critical for the neural plasticity involved in mood recovery and stabilization. (iii) Lithium adjusts signaling activities regulating second messengers, transcription factors, and gene expression. The outcome of these effects appears likely to result in limiting the magnitudes of fluctuations in activities, contributing to a stabilizing influence induced by lithium, and neuroprotective effects may be derived from its modulation of gene expression.
Lithium at 50
Beyond lithium?
Bipolar disorders
Drugs for bipolars
Lithium prophylaxis
Lithium augmentation
Lithium and depression
Lithium pharmacokinetics
Lithium: antisuicide effect
Recurrent brief depression
Lithium maintenance: review
Mood stabilisers: common mechanism?
Lithium augmentation in refractory major depression
Lithium prophylaxis in unipolar major depressive disorder
Chronic lithium use, brain- and serum- DHEA and DHEA-sulphate

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