Abstract
Although lithium’s efficacy in affective illness has been well proven (1), the mechanisms of action responsible for its therapeutic effect remain unknown, especially when one considers its long lasting dual antimanic and antidepressant properties. Several hypotheses have been formulated to explain how lithium exerts its action. Chronic lithium in clinically equivalent concentrations, inhibits differentially adenylate cyclases in animals and humans. Considering that these actions seem to be the most consistent findings of the lithium neurochemica1 studies, Belmaker and coworkers (2, 3) suggested that it might be the mechanism of lithium action. Another hypothesis was raised by Bunney and coworkers. They first speculated that manic depressive illness might be caused, at least partially, by oscillations in catecho1 amine receptor sensitivity, in an attempt to further develop the original catecho1 ami ne hypothesis, thus extending it to the receptor level (4). Their idea was based on clinical observation that dopamine receptor antagonists (neuro1epties) acutely suppress manic symptomatology, while dopamine agonists (such as piribedil and 1-Dopa) can precipitate manic episodes in certain depressed patients. These findings led to the idea that receptor sensitivity changes underlie the behavioral signs in bipolar illness: mania being a consequence of an abnormal increase and depression from an abnormal decrease.
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Calil, H.M., Rodrigues, F.C. (1984). Does lithium prevent the development of dopamine receptor supersensitivity? Behavioural studies. In: Corsini, G.U. (eds) Current Trends in Lithium and Rubidium Therapy. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-7318-6_6
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DOI: https://doi.org/10.1007/978-94-011-7318-6_6
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