What are the effects of lithium at the neurotransmission level?

Lithium inhibits excitatory neurotransmitters such as glutamate and dopamine, and increases GABA-mediated neurotransmission. The chronic absorption of lithium may change the characteristics of GPCR molecules, postsynaptic activation of dopamine receptors is regulated by GPCRs, and as a result the neurotransmission of dopamine is inhibited. Lithium may also induce downregulation of NMDA receptors, which are a subtype of glutamate receptors. Once NMDA receptors become stimulated, glutamate is increased in the postsynaptic neuron. Chronic absorption of lithium leads to the inhibition of glutamate neurotransmission. Lithium increases GABA-mediated neurotransmission through several mechanisms. It increases the amount of GABA in the cerebrospinal fluid, and at the presynaptic level, it mediates GABA release. At the postsynaptic level, it increases GABA-B receptors. Lithium is effective for treating patients with bipolar disorder as studies show they have reduced activity of GABAergic neurotransmission. 

Lithium has also been shown to have neuroprotective effects in various brain regions. Specifically, it is shown that lithium assists in the preservation of gray matter, although the mechanisms of this are still unclear.