If anxiety is caused by overactive noradrenergic neurons, then why are SNRIs effective at mitigating and controlling the attacks? Shouldn't the extra norepinepherine, now sitting around in the synaptic cleft due to the inhibitor, exacerbate the symptoms?
I found this article on PubMed, which addresses the paradox, though from what I read, it fails to explain the why behind the phenomenon. ( I do have to admit that I didn't make it through the entire article.) The article analyzed several published studies and comes to the conclusion that there is no significant evidence to prove that SNRIs are anxiogenic. The studies actually show otherwise—that SNRIs effectively treat anxiety.
My question still remains though, as to why SNRIs effectively reduce anxiety symptoms and fail to replicate those attacks when it is seemingly mimicking the biological mechanism behind anxiety.