by Aden D. » Tue Dec 11, 2012 9:40 am
Gamma-amino butyric acid (GABA) acts as a primary inhibitory neurotransmitter in the brain. To put it another way, GABA is the transmitter that modulates the other transmitters (serotonin, norepinephrine, etc.) to prevent them from over activity. Most benzodiazepine anti-anxiety drugs perform their therapeutic role by modulating GABA receptors to produce a calming effect. In a similar fashion, most mood stabilizing medications (generally the mainstay in bipolar psychopharmalogical treatment) also affect GABA by preventing neurons from over-firing.
Glutamate, the chemical precursor to GABA is the most abundant excitatory neurotransmitter. It is hypothesized that misfiring of glutamate receptors in the brain (and therefore causing erratic fluctuations in GABA, and by association, the other neurotransmitters that it inhibits) is the cause of manic and mixed episodes, while the invariable reuptake of serotonin and dopamine leads to the depressive episodes of bipolar disorder (which could also explain why depressive episodes almost always follow manic episodes).