Alexis Fernandez-Preiksa

That is GABA that is already produced within the body.

Now, when GABA binds, chloride ions flow into this neuron.

The neuron becomes negatively charged.

Neural firing becomes less likely because it is negatively charged.

And therefore, methoqualone is enhancing that inhibitory effect.

So functionally, your neurons are less active.

Your cortical activity slows down.

Arousal goes down.

Also, your motor coordination gets worse.

But then...

your anxiety reduces, good times, and sedation also increases.

Now, the reason that it works differently to other drugs like benzos, for example, is because it's not binding to the same site as benzos, as one example.

So the research is kind of showing that it's acting at a distinct allosteric site on the GABA-A receptor.

So I'm not going to go into crazy details, but you've got receptor subtypes and they're assembled in like

subunits of like alpha beta gamma delta right so different combinations of where it's binding to is going to have a different effect on the brain so it's really fiddly and I don't want to go into the crazy details because I don't want to like give you unnecessary confusion when we talk about you know the mechanism of action but that's roughly why you might see or hear of a drug that's

that binds to a receptor.

And you think, well, if they're both binding and they're both working, you know, on like modulating GABA, why aren't you getting the exact same effects?

It's because you might be looking at different subunits of where they're binding to, and that might explain why the effects could be different.

But in a nutshell, you're getting all these different brain regions affected, like the cortex, and that's why it impairs your judgment, thinking, inhibition.

Your limbic system, this is your amygdala, emotional response circuits, and that's why you have lowered anxiety.