GABAB receptor

For cataplexy specifically, sodium oxybate is an established treatment, also improving daytime sleepiness.

Sodium oxybate acts on GABA-B receptors, and it's the medical form of a compound called GHB.

That's part of why it's so tightly controlled, and in the UK, it's provided only through specialist NHS commissioning arrangements.

More recently, NICE has recommended an option for excessive daytime sleepiness.

Okay, let's talk about muscle relaxants.

GABA, GABA-B agonist at the spinal cord for upper motor neuron spasticity causes sedation, weakness, dangerous withdrawal if it's intrathecal especially.

Tizanidine, central alpha-2 agonist, there's sedation, hypotension, bradycardia, dry mouth, hepatotoxicity, CYP1A2 interaction.

cyclobenzaprine, tricyclic-like agent, acute musculoskeletal spasm, anticholinergic effects, sedation, serotoninergic reactions, methylcarbinol, central CNS depressant, acute spasm, sedation, and dizziness, and metilaxone, CNS depression.

of NMDA receptor encephalitis at the moment.

And NMDA receptor encephalitis is often an example for all the other forms of, such as LGA1 or Casper2 or GABA-B.

We know a lot more of these diseases, of course, but that would be really helpful for the future to improve treatment strategies for these patients.

Yeah, I would fully agree here and can maybe add that, as you said, what we learned from NMDA receptor encephalitis, we may be able to transform or translate into other encephalitides.

It is a central nervous system depressant developed in Russia, so you know it's legit.

As an anti-anxiety agent, it acts on GABA-B receptors, so similar to GHB, or GHB is essentially like roofies, right? Or baclofen, which is a muscle relaxant.

So some dangers with Phenibut are that it can have a rapid tolerance buildup.

So you start it and before you know it, you're having to do a lot more to get the same fix, the same high, and withdrawal can trigger some severe anxiety, hallucinations, psychosis, and seizures.