The specific biochemical mechanism of<unk> action in stabilizing mood is unknown. Upon ingestion,<unk> becomes widely distributed in the central nervous system and interacts with a number of neurotransmitters and receptors, decreasing norepinephrine release and increasing serotonin synthesis. Unlike many other psychoactive drugs, typically produces no obvious psychotropic effects (such as euphoria) in normal individuals at therapeutic concentrations.<unk> may also increase the release of serotonin by neurons in the brain. In vitro studies performed on serotonergic neurons from rat raphe nuclei have shown that when these neurons are treated with<unk>  serotonin release is enhanced during a depolarization compared to no<unk> treatment and the same depolarization.<unk> both directly and indirectly inhibits GSK-3β which results in the activation of mTOR. This leads to an increase in neuroprotective mechanisms by facilitating the Akt signaling pathway. Importantly, GSK-3β is a downstream target of monoamine systems. As such, it is directly implicated in cognition and mood regulation. During mania, GSK-3β is activated via dopamine overactivity. GSK-3β inhibits the transcription factors β-catenin and cyclic AMP (cAMP) response element binding protein (CREB), by phosphorylation. This results in a decrease in the transcription of important genes encoding for neurotrophins. In addition, several authors proposed that pAp-phosphatase could be one of the therapeutic targets of<unk>  This hypothesis was supported by the low Ki of<unk> for human pAp-phosphatase compatible within the range of therapeutic concentrations of<unk> in the plasma of people (0.8–1 mM). Importantly, the Ki of human pAp-phosphatase is ten times lower than that of GSK3β (glycogen synthase kinase 3β). Inhibition of pAp-phosphatase by<unk> leads to increased levels of pAp (3′-5′ phosphoadenosine phosphate), which was shown to inhibit PARP-1. Another mechanism proposed in 2007 is that<unk> may interact with nitric oxide (NO) signalling pathway in the central nervous system, which plays a crucial role in neural plasticity. The NO system could be involved in the antidepressant effect of<unk> in the Porsolt forced swimming test in mice. It was also reported that NMDA receptor blockage augments antidepressant-like effects of<unk> in the mouse forced swimming test, indicating the possible involvement of NMDA receptor/NO signaling in the action of<unk> in this animal model of learned helplessness.<unk> possesses neuroprotective properties by preventing apoptosis and increasing cell longevity. Although the search for a novel<unk> specific receptor is ongoing, the high concentration of<unk> compounds required to elicit a significant pharmacological effect leads mainstream researchers to believe that the existence of such a receptor is unlikely. Oxidative metabolism Evidence suggests that mitochondrial dysfunction is present in patients with bipolar disorder. Oxidative stress and reduced levels of anti-oxidants (such as glutathione) lead to cell death.<unk> may protect against oxidative stress by up-regulating complex I and II of the mitochondrial electron transport chain. Dopamine and G-protein coupling During mania, there is an increase in neurotransmission of dopamine that causes a secondary homeostatic down-regulation, resulting in decreased neurotransmission of dopamine, which can cause depression. Additionally, the post-synaptic actions of dopamine are mediated through G-protein coupled receptors. Once dopamine is coupled to the G-protein receptors, it stimulates other secondary messenger systems that modulate neurotransmission. Studies found that in autopsies (which do not necessarily reflect living people), people with bipolar disorder had increased G-protein coupling compared to people without bipolar disorder.<unk> treatment alters the function of certain subunits of the dopamine associated G-protein, which may be part of its mechanism of action. Glutamate and NMDA receptors Glutamate levels are observed to be elevated during mania.<unk> is thought to provide long-term mood stabilization and have anti-manic properties by modulating glutamate levels. It is proposed that<unk> competes with magnesium for binding to NMDA glutamate receptor, increasing the availability of glutamate in post-synaptic neurons. The NMDA receptor is also affected by other neurotransmitters such as serotonin and dopamine. Effects observed appear exclusive to<unk> and have not been observed by other monovalent ions such as rubidium and caesium. GABA receptors GABA is an inhibitory neurotransmitter that plays an important role in regulating dopamine and glutamate neurotransmission. It was found that patients with bipolar disorder had lower GABA levels, which results in excitotoxicity and can cause apoptosis (cell loss).<unk> has been shown to increase the level of GABA in plasma and cerebral spinal fluid.<unk> counteracts these degrading processes by decreasing pro-apoptotic proteins and stimulating release of neuroprotective proteins.<unk> s regulation of both excitatory dopaminergic and glutamatergic systems through GABA may play a role in its mood stabilizing effects. Cyclic AMP secondary messengers<unk> s therapeutic effects are thought to be partially attributable to its interactions with several signal transduction mechanisms. The cyclic AMP secondary messenger system is shown to be modulated by<unk> <unk> was found to increase the basal levels of cyclic AMP but impair receptor coupled stimulation of cyclic AMP production. It is hypothesized that the dual effects of<unk> are due to the inhibition of G-proteins that mediate cyclic AMP production. Over a long period of<unk> treatment, cyclic AMP and adenylate cyclase levels are further changed by gene transcription factors. Inositol depletion hypothesis<unk> treatment has been found to inhibit the enzyme inositol monophosphatase, involved in degrading inositol monophosphate to inositol required in PIP2 synthesis. This leads to lower levels of inositol triphosphate, created by decomposition of PIP2. This effect has been suggested to be further enhanced with an inositol triphosphate reuptake inhibitor. Inositol disruptions have been linked to memory impairment and depression. It is known with good certainty that signals from the receptors coupled to the phosphoinositide signal transduction are affected by<unk>  myo-inositol is also regulated by the high affinity sodium mI transport system (SMIT).<unk> is hypothesized to inhibit mI entering the cells and mitigating the function of SMIT. Reductions of cellular levels of myo-inositol results in the inhibition of the phosphoinositide cycle. Neurotrophic Factors Various neurotrophic factors such as BDNF and mesencephalic astrocyte-derived neurotrophic factor have been shown to be modulated by various mood stabilizers.
Lithium 
Chlortalidone
Methylphenidate
Sertraline
Citalopram
Paliperidone
Loprazolam
Dexmethylphenidate