Hypothetical situation. If one wanted to induce panic disorder in a person or an animal (for medical research, state sponsored terrorism against dissidents, etc) how is it done? I know treatments for panic disorder involve increasing GABA, so would lowering GABA levels create it? GABA drugs, SSRIs and SNRIs seem to treat it, would depleting those neurotransmitters cause it?
With depression I assume you could lower serotonin, dopamine, NE and/or increase acetylcholine and GABA to help trigger a depression.
Is the etiology of panic disorder well understood biologically to the point where it can be caused or treated (biologically, not psychologically)?
I’m not sure if you can actually induce a full blown disorder, but there are numerous chemicals which when administered can induce the symptoms of a panic attack. Many of these, as you might suspect, act as direct or indirect antagonists at GABA-A receptors. A fragment of Cholecystekinin, termed CCK-4, is used for this purpose (as a peptide, it is short acting as the body breaks it down pretty quickly after injected, and it is often used to test anxiolytic drugs for efficacy), as can Bicuculline and Picrotoxin (as a non-competitive blocker of the GABA-A ion channel).
Panic disorder, of course, like most other psychiatric disorders, still isn’t well understood. We understand bits and pieces of it like the above antagonism of GABA-A acutely causing panic attacks, and some of the brain “structures” known to be involved in the symptomatology, but I haven’t run across any conclusively proven neurobiology outlining most/all aspects behind it.
Next, acetylcholine is, very generally speaking, excitatory in the CNS, and should probably be lumped in with dopamine, not GABA.
Finally, it’s important to understand that the mechanisms of action of some of the antidepressants we use still aren’t very well understand. We nominally refer to Fluoxetine (Prozac) as a Specific Serotonin Reuptake Inhibitor and Duloxetine (Cymbalta) as a Serotonin-Norepinephrine Reuptake Inhibitor, but in truth, the monoamine deficiency theory behind depression (and anxiety disorders) has largely been viewed as…incomplete, at best, or as dead wrong, at worst, since well before I was a pharmacy student learning this stuff in 2006 (the year we covered these topics, for me), so the current evidence seems to be leaning against their nominal categorical names being all that relevant as to what they actually are doing.
Then it goes through the list of therapies, self-help, etc. Under medication, it gives SSRIs and then
With the caveat that I’m simply someone who has the condition and not an expert on treatment, from what I’ve read and in discussions with other people who also have the disorder, I don’t know how possible it would be to mimic or induce this disorder strictly chemically, even if the mechanics were known a little more. So much of what is unpleasant about the attacks are the triggers, and I wouldn’t know how to go about creating those (chemically).
Give them something that causes a panic attack, but keep them from figuring out when it is, and only give them when they are out of the house. You’ll have to do it multiple times, but it should invoke panic disorder/agoraphobia in anyone.
At least, that would jibe with the current understanding of the subject. People who don’t get panic disorder from panic attacks generally don’t have them often, are educated about what they are and that they are ultimately harmless, and have a clear idea of what caused them, and thus have no reason to fear them happening again.
My understanding is THC and lactate can trigger them, but I think only in people who have had one in the past. THC can trigger one even in people who have smoked for years, and after that each time they smoke another panic attack happens.
So yeah maybe priming someone with lactate and THC, then exposing them to something scary and doing that over and over.
An easy way is to get someone (predisposed most likely) and give them benzodiazepines or other anxiolytics, or certain drugs like MDMA. Then take them off of the drug. The rebound effect can be rough, although there are also other negative effects.
The neurotransmitter is important, but also important is where in the nervous system you are increasing or decreasing release. GABA, glutamate, and acetylcholine are pretty widespread, and you could affect the wrong areas even if targeting the right NT depending on drug. Also, as alluded to above, some may only affect certain subcategories of receptors.