Neurotransmitter GABA important for major depression

This paper just published in the journal Biological Psychiatry reports on valuable finding that is important for anyone suffering from or treating major depression needs to know: the neurotransmitter GABA can play a significant role in the biological component of major depression. GABA is the most abundant inhibitory neurotransmitter in our bodies. The authors note that

"Several lines of evidence suggest that major depressive disorder is associated with deficits in γ-aminobutyric acid (GABA) inhibitory neurotransmission."

In their study they used transcranial magnetic stimulation to measure the integrity of GABA function in

"medicated patients with treatment resistant major depressive disorder (TRD), unmedicated patients with major depressive disorder, and medicated euthymic [normal mood] patients with a history of major depressive disorder and compare them with healthy subjects."

Their compelling findings were that

"All major depressive disorder patient groups demonstrated significant cortical silent period deficits [GABA(B) receptor-mediated inhibitory neurotransmission] compared with healthy subjects." Interestingly, "only TRD [treatment resistant depression] patients demonstrated significant deficits in short-interval cortical inhibition [GABA(A) receptor-mediated inhibitory neurotransmission] compared with healthy subjects, medicated euthymic major depressive disorder patients, and unmedicated major depressive disorder patients."

I'm sure readers know that there is much more to the story of major depression than one neurotransmitter. But this is a welcome study for functional medicine practitioners who have seen empirically positive results since we have excellent resources for physiologically supporting improved GABA function. They also noted another finding important for functional medicine doctors and neurotherapists who treat additional biological causes of depression (metabolic, inflammatory, electrical, etc):

"TRD patients also demonstrated a significantly greater resting motor threshold compared with all other clinical subgroups and healthy subjects, suggesting that TRD was also associated with hypoexcitability of the frontal cortex."

The authors state in conclusion:

"Our findings suggest that GABA(B) neurophysiological deficits are closely related to pathophysiology of major depressive disorder. Our findings also suggest that more severe illness is selectively associated with GABA(A) receptor-mediated inhibitory deficits."

By the way, four years earlier to the day there was a paper published in the same journal that concluded:

"This study provides evidence of reduced GABAergic [GABA function] tone and motor threshold asymmetry in patients with major depression."

For an easy reading description on how this investigative approach can help personalize the treatment of depression and more on why GABA is important see this article.