This is a supremely stupid idea.
NOW... if you want something that targets fear-response, and the amygdala, then I suggest you check out Propanolol and 6-hydroxynorketamine.
Propanolol have been proven to inhibit signalling from the amygdala at certain dosages - meaning, that if you hit the right dose, the anxiolytic effect is NOT just one caused by peripheral relaxation - it's actually less fear. There's a reason Propanolol is used by many, many performers in showbiz. It has a decades-long reputation of good effects - now we finally know why.
6-hydroxynorketamine, or HNK is a derivative of Ketamine - they have FINALLY isolated the antidepressant effects of Ketamine, and this is the safest, most effective derivative ever produced. If you're at all familiar with the trials of Ketamine on depression, you will have noticed that the results show that Ketamine is the most effective against ANXIOUS depression - there are two mechanisms possibly contributing to this:
1. NMDA-antagonism - as I've told you before... anxiety can be caused by GLUTAMATE-overload, not just Serotonin. NMDA-antagonists have been proven to be anxiolytic. I will vouch for it, because I've felt it myself.
2. Nicotinic Acetacholinergic Alpha-7-antagonism - 6-hydroxynorketamine effects this sub-receptor, and guess what? What part of the brain has these receptors, working as a gating-mechanism to control the activity in and out of it? The Amygdala. We had a whole thread here about how Alpha-7-antagonism could decrease the enhanced activity out of the brains of Borderline people. (they have diminished amygdalas, with haywire high activity out of them)
6-HNK was synthesized in a recent group buy - with a bit of luck, you can still find it if you contact the original organizers - they have sold several dosages to new patients even after the group buy completed.
http://www.longecity...for-depression/
For god's sake man! Try these things BEFORE you do anything else, ok?
References:
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Dose-sensitive excitation and inhibition of spontaneous amygdala activity by propranolol
http://www.ncbi.nlm....pubmed/11420072
Inhibition of the amygdala central nucleus by stimulation of cerebellar output in rats: a putative mechanism for extinction of the conditioned fear response.
http://www.ncbi.nlm....pubmed/25185877
Evidence that Borderliners have a faulty amygdala, and that the cholinergic system is involved (acetacholine is the body's own substance affecting nicotinic receptors)
Evidence of abnormal amygdala functioning in borderline personality disorder: a functional MRI study.
https://www.ncbi.nlm...pubmed/11522264
Amygdala-prefrontal disconnection in borderline personality disorder.
http://www.ncbi.nlm....pubmed/17203018
Behavioral Inhibition System activity is associated with increased amygdala and hippocampal gray matter volume: A voxel-based morphometry study
http://www.sciencedi...05381190600797X
Evidence that nAch-Alpha-7-receptors could have a key-role in mediating activity out of the amygdala:
α7-Containing nicotinic acetylcholine receptors on interneurons of the basolateral amygdala and their role in the regulation of the network excitability.
http://www.ncbi.nlm....pubmed/24004528
Depressive response to physostigmine challenge in borderline personality disorder patients.
http://www.ncbi.nlm..../pubmed/9326751
Physostigmine is an indirect Alpha-7-agonist, increasing cholinergic signalling in multiple sites in the brain