Product Name: Lithium gluconate
Molecular Formula: C6H11LiO7
Molecular Weight: 202.1
CAS Number: 60816-17-8
Lithium is an alkali metal widely used in industry. Lithium salts are used to treat manic episodes of bipolar disorder. The application of lithium in psychiatry can be traced back to the mid-19th century. However, the early work was soon forgotten, and John Cade is regarded as the one who reintroduced lithium salts into psychiatry for the treatment of mania in 1949. In 1954, Mogens Schou conducted a randomized controlled trial on mania. During the research process, he became curious about lithium as a preventive drug for depression.
In 1970, the United States became the 50th country to allow lithium to enter the market. The specific mechanism by which lithium exerts its role in stabilizing emotions remains unclear. Lithium seems to have the function of preserving or increasing the volume of brain structure. At the neuronal level, lithium reduces excitability (dopamine and glutamate), but increases inhibitory effects (GABA) involved in mood regulation, such as in the prefrontal cortex, hippocampus and amygdala, which may reflect its neuroprotective neurotransmission;
However, these extensive effects are supported by complex neurotransmitter systems that strive to achieve homeostasis through compensatory changes. For instance, within cells and at the molecular level, lithium targets further regulate the second messenger system of neural transmission. For instance, the effects of lithium on adenosine cyclase and inosine phosphate pathways as well as protein kinase C may help inhibit excessive excitatory neurotransmission. In addition to these hypothetical mechanisms, it has also been proposed that the neuroprotective effect of lithium is the key to its therapeutic effect. In this regard, lithium has been proven to reduce oxidative stress that occurs during multiple episodes of manic and depressive disorders. Furthermore, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces the apoptotic process by inhibiting glycogen synthase kinase 3 and autophagy.
