Inhibition and Depression: GABA a hidden player?

Initially I was pleased to see this news release because it appeared concordant with my earlier post wherein I explored the angle of depression and arousal. Upon further reflection I realise there are some serious problems with the conclusions put forward in the news item.

Nonetheless this study represents a novel approach to the issue of depression. What they did was create a mouse with a defect in GABA A receptors. GABA A receptors are key receptors in inhibition. GABA is the major inhibitory neurotransmitter in nervous function and is strongly implicated in the etiology of epilepsy. Many drugs for epilepsy aim to increase GABA levels, though there is some recent research which suggest astrocyte release of glutamate may also be implicated in the condition. In relation to depression and arousal though the loss of GABA suggests the potential for excessive arousal. Most anxiety drugs also target GABA. Interestingly, depression and anxiety are often co-morbidities so perhaps GABA does play a role.

The problem I have with this study though is that knock out gene studies are very crude instruments. There is value in such studies but we need to be very careful in drawing too many conclusions from such studies. Why? Because we know next to zilch about how nervous systems function as a whole, so when we introduce such a gross morphological deficit there are potentially any number of possible reasons for the observed effects. So we must rely on the old scientific demand: more research is required.