Mood stabilizers are psychotropic medications that promote euthymia in bipolar disorder. They generally treat and prevent the recurrence of manic or depressed moods. The term mood stabilizers traditionally refers to lithium, valproate, carbamazepine, and lamotrigine. More recently, it has been proven that some atypical antipsychotics have mood-stabilizing properties, meaning that they are able to treat and prevent the recurrence of manic or depressed phases of bipolar disorder.
LITHIUM
Lithium's mechanism of action in the treatment of mania is not well determined. Lithium alters at least two intracellular second messenger systems-the adenyl cyclase, cyclic adenosine monophosphate system, and the G protein-coupled phosphoinositide systems-and, as an ion, can directly alter ion channel function. Because norepinephrine and serotonin in the central nervous system (CNS) use G protein-coupled receptors as one of their mechanisms of action, their function is altered by lithium. Lithium also alters γ-aminobutyric acid (GABA) metabolism.
VALPROATE
Valproate's mechanism of action is thought to be due in part to augmentation of GABA function in the CNS. Valproate increases GABA synthesis, decreases GABA breakdown, and enhances its postsynaptic efficacy.
LAMOTRIGINE
The mechanism of action of lamotrigine in bipolar disorder is unknown. Lamotrigine is approved by the FDA for use in the maintenance and depressed phases of bipolar I disorder (lamotrigine is not approved for the acute treatment of mania because it appears to be less effective in this phase). Lamotrigine in vitro has been shown to inhibit voltage-sensitive sodium channels. This effect is believed to stabilize neuronal membranes and modulate presynaptic excitatory neurotransmitter release.
CARBAMAZEPINE
The mechanism of action of carbamazepine in bipolar illness is unknown. Carbamazepine blocks sodium channels in neurons that have just produced an action potential, blocking the neuron from repetitive firing. In addition, carbamazepine decreases the amount of transmitter release at presynaptic terminals. Carbamazepine also appears to indirectly alter central GABA receptors.
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