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Core Topics => Drugs => GABAergics => Topic started by: Chip on December 31, 2018, 11:04:09 AM

Title: GHB, GBL and 1,4-Butanediol revisited / Metabolics and Neurotransmission
Post by: Chip on December 31, 2018, 11:04:09 AM

It became obvious to me a while ago that what makes METH such an ugly drug is mainly about the lack of REM sleep and, as discussed earlier, it's inherent triggering of GABA cell death.

I am constantly drawn back to these neurotransmitters. here is some background, courtesy of Wiki:

• acetylcholine. A neurotransmitter used by neurons in the PNS (Peripheral nervous system^Wiki) and CNS (Central nervous system^Wiki) in the control of functions ranging from muscle contraction and heart rate to digestion and memory.
  
  
• norepinephrine. A neurotransmitter involved in arousal, as well as in learning and mood regulation.
  
  
• glutamate
  
  
• endorphin Opiophiles, see, I caught ya !  ;) move on ...
  
  
• serotonin.
  
  
• dopamine
  
  
• GABA
  
  

The most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain.

The next most prevalent is Gamma-Aminobutyric Acid, or GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate.

What I am researching is how to induce, improve, synthesise REM sleep as I have a hunch that the "G" receptors hold the key to not only restoring sanity to the METH user but to perhaps the general population.

I personally have serious sleep issues caused by long term concurrent opiate and GABA drug usage.

I have attached an excellent GHB user, receptor, metabolic etc. reference but please do not reproduce.

(a bit out of date) here is an abstract:

Quote

A growing body of evidence shows that gamma-hydroxybutyric acid (GHB) is an addictive substance.

Its precursors gammabutyrolactone (GBL) and 1,4-butanediol (1,4-BD) show the same properties and may pose even more risks due to different pharmacokinetics.

There are indications that problematic GHB use is increasing in the European Union. This review investigates the existing literature on the neurochemistry of GHB and its precursors, their acute toxicity, addiction potential and withdrawal, the proposed molecular mechanism underlying addiction and the treatment of withdrawal and addiction.

Current evidence shows that GHB and its precursors are highly addictive, both in humans and animals, probably through a GABAB receptor related mechanism. Severity of withdrawal symptoms can be considered as a medical emergency.

Recent studies suggest that benzodiazepines are not very effective, showing a high treatment resistance, whereas detoxification with pharmaceutical GHB proved to be successful.

However, relapse in GHB use is frequent and more research is warranted on relapse prevention. This might aid medical practitioners in the field and improve general understanding of the severity of addiction to GHB, GBL and 1,4-BD.