DE - Do I have to go into the mechanics of lithium blocking a runaway intracellular phosphoinositol cycle in neurons and subsequently resulting in the stabilization of intracellular calcium ion concentrations by normalizing the ion's influx into the cell, as well as it's release from the the endoplasmic reticulum.

This is just one theory. Other evidence show that lithium decreases Na,K-ATPase activity in neurons (esp. in the hippocampus) and this decreases neuronal membrane excitability in hyperactive nerve cells.

Lithium also interacts with all the major neurotransmitters (dopamine, serotonin, norepinephrine, GABA, acetylcholine, glutamate) in complex ways, resulting in a modulation of electrical signaling in the brain.

Chronic lithium use may alter signal transduction cascades and gene expression, which may result in long term changes neuronal plasticity and cytoskeletal remodeling. I guess the lithium acts like a good city traffic engineer by altering patterns of electrical signaling (in neurons rather than traffic lights) throughout critical regions of the brain.

Or could it be lithium's actions on second messenger systems (eg. adenylyl cyclase, several kinases, and various G-proteins) that result in lithium's mood stabilizing effects?

Who knows how lithium works? The more I read about it, the less I seem to know. Clinically, I have seen lithium decrease both mania and depression in people who were diagnosed with bipolar disorder.

So, what does lithium do? I guess it helps many people, who otherwise would not be able, to lead "normal", productive, and full lives.

- Cam

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