Inverse Anxiety? Excessive GABA?

[xbandit07x]

Why do I and have always felt like i had excessive GABA. Like I never had anxiety and it caused anxiety to not have enough Dopamine.

In college Freshman year I took 3 MG xanax one of the weeks none of the weed dealers were on campus and the campus was empty (Night back after winter break) and had a legit inner panic attack in the shower because i thought my brain was locked up and id never be Satisfied.

Then I found stimulants acted as a sedative. Etc. and find they calm me down so much.

They say Benzos do not have Euphoria which i understand, but Alone whenever a benzo is eaten it always makes me Filled with FEAR.

 

[AlphaMethylPhenyl]

They've been cited for possible paradoxical effects

 

[Cotcha Yankinov]

Well there are parts of the amygdala that are largely GABAergic, see the dorsolateral amygdala - 95% GABAergic.

I'm not quite sure how those cells actually signal fear related stuff (if they turn off to signal fear or turn on to signal fear)

Dopamine can act to inhibit GABA cells (and vice versa)

 

[sekio]

It's impossible to judge neurotransmitter levels based upon how you feel, unfortunately.

BZDs are known for having paradoxical effects where they can make people more likely to have stupid worries and ungrounded fears through disinhibition of behaviour. And stimulants increasing focus is also pretty typical, they don't neccesarily make everyone bounce off the walls.

 

[xbandit07x]

Its actually really easy to feel and classify the neurotransmitters if you know what drug you had taken, and what the drug acts on.

Its 90% accurate to say a 2 mg Xanax has to do with a brain, if it had extra gaba than normal. and from there Vala

 

[Cotcha Yankinov]

Except for drugs aren't acting the same way as endogenous neurotransmitter mediated transmission in multiple ways.

Endogenous neurotransmitter release is timed in a particular way and cells target specific areas with their neurotransmitters.

Taking agonists/PAMs that fill the entirety of your brain without regard for endogenous spatial/temporal release means that it's different from e.g. spatially targeted/time coordinated, phasic or tonic, endogenous dopamine release

PAMs are a bit better because they essentially just enhance endogenous transmission but I still don't think there is a 1 to 1 representation of GABA there (if you increased GABA levels by another method you may get a different effect - GABA-B receptors aside)


Releasing agents are most certainly different from endogenous transmission.

 

[AlphaMethylPhenyl]

In most cases, no. For example, anecdotes upon anecdotes of people trying some herb and claiming it to be cannabamimetic, though no experiment validates it.

There are cases such as with Kava, that one of its chemicals was found to interact with CB1 by a very questionable, small study. Now Kava is one of the aforementioned substances, which along with said nebulous study has people certain that "Kave acts like weed"--4th grade logic. Most have never heard of a PAM, NAM, competitive antagonist, nor the meaning of "affinity" and "efficacy" when it relates to neural chemicals.

Exogenous substances are present in such large concentrations, generally speaking, than their endogenous counterparts, that new thresholds of activity, and with that, effects, are reached.

That last sentence seems pretty random. How did you come up with 90%? Xanax does not add GABA to the brain. Did you know that? Case in point.