Gabriel Schreiber

TL;DR: G proteins (Gs and Gj or G0) are suggested as the molecular site of action for both the antimanic and antidepressant effects of lithium.

TL;DR: The coupling of both muscarinic-cholinergic receptors and beta-adrenergic receptors to pertussis toxin-sensitive G proteins or cholera toxin- sensitive G proteins was compared among untreated manic patients, lithium-treated euthymic bipolar patients, and healthy volunteers using mononuclear leukocyte (MNL) membrane preparations to suggest an altered G protein function is of pathophysiological importance in bipolar affective disorder.

TL;DR: The results suggest that attenuation of beta-adrenergic receptor-coupled Gs protein function, which is common to both antidepressant and antibipolar treatments, may be the mechanism underlying their antidepressant therapeutic efficacy.

TL;DR: Pertussis toxin-blockable, carbamylcholine-induced increases in GTP binding capacity were found to be mediated through M1 muscarinic receptors, as M1-selective antagonists were 100-fold more effective than M2 selective antagonists in blocking carbamelcholine effects.

TL;DR: The findings in the rat study suggest beta-arrestin-1 elevation as a biochemical mechanism for antidepressant-induced receptor down-regulation for depression, and the findings in human subjects support the implication of beta- Arrestins in the pathophysiology of mood disorders.