Can you believe that your brain is intrinsically unreliable? I can't, I implicitly trust it. I have no choice. In this news release they address one of the great mysteries of nervous function: is "noise" a byproduct of nervous function or does it serve some fundamental purpose?
I used to become very annoyed at people who likened brains to complicated computers. The analogy is so stupid it is hardly worthy of serious consideration yet Artificial Intelligence bods adopted it as a working assumption. They should stick to designing computer games because I'm bored with ones I've got.
As an "information processing" device, and I have great difficulty with that phrase but I won't go there, the brain represents a formidable challenge in understanding its function. This is because......
Saturday, July 3, 2010
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.
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.
Friday, July 2, 2010
Oils Aint Oils: EPA for Depression
One of the more remarkable features about depression is the number of therapies that have proved beneficial. I explored that issue in this post. This latest study highlights the importance of prostaglandin regulation in depression. This latest study, the largest ever trial on omega 3 fats in treating depression, demonstrates a careful delineation that helps clarify the role of omega 3's in treating depression. The nutshell is this: they focused on EPA, typically at 120mg in your fish oil tablets, and boosted that intake to a big 1000mg per day. That's a lot but given the role of EPA in regulating prostaglandin pathways makes good sense.
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