Neurotransmitters and how to tamper with them

This week’s lecture went through different neurotransmitters as well as their receptors and receptor cascades. A lasting theme throughout the lecture was m-opioid receptors, which was started by discussing with how to block them using naloxone. Naloxone is a m-opioid receptors blocker (i.e. antagonist) that was originally developed as a remedy against opioid abuse, but has also been found effective against alcohol abuse. Alcohol activates many neurotransmitter systems, among them being GABA and endorphin systems which release dopamine into the reward pathway bringing about pleasurable feeling. Of these two, Naloxone targets the endorphin (i.e. endogenous morphine) system by binding to the m-opioid receptors. A note to myself: Remember to look closer into how naloxone affects craving. It appears it does so not directly but gradually extinguishing the pleasure felt while drinking.

We also went through the serotonine hypothesis, which is the basis for treating patients suffering from depression with selective serotonine re-uptake inhibitors (SSRI), a multibillion business. The serotonine hypothesis has been hotly contested, yet it still is the dogma by which millions of people worldwide are being treated.  Finland ranks in top ten with regard to how many antidepressant users we have per capita (70 / 1000), the number one being US (110 / 1000) [].

I raised a point whether GABA levels can be increased via ingesting GABA enriched tea (fermenting tealeaves under nitrogen seems to produce GABA into the fermented leaves, see eg. for explanation in lay terms). I tried to do a literature survey but did not find too veritable evidence of the health benefits.

Posted by Tapio Saarinen

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