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Comment · Fri, May 22, 2020

🌿 New Blog | Green Tea: A Natural Plant Extract High In EGCG Content For Our Brain, Mood, and Metabolic Health 🌿

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NootropicsDepotCom · 8 points

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🌿 New Blog | Green Tea: A Natural Plant Extract High In EGCG Content For Our Brain, Mood, and Metabolic Health 🌿

Camellia sinensis, better known to us as tea and the source of many different varieties of tea, is a treasure trove of unique bioactive molecules! What is often somewhat poorly understood, is that oolong tea, black tea, green tea, matcha tea, white tea, pu’erh tea and even kukicha tea are all the same species of tea: Camellia sinensis. The difference between all of these different types of tea is that they are processed and grown differently. For example, the only difference between black and green tea is that black tea has been oxidized whereas green tea has not. This oxidization process has a major impact on the flavor, aroma and appearance of Camellia sinensis leaves. These changes in aroma and appearance also correspond to chemical changes... (click here to read more)

[Read This Green Tea Extract Blog](https://nootropicsdepot.com/articles/green-…

What they were answering

GettinWiggyWiddit · 3 points

Very cool. What GABA receptor is this working on? When you say “reversing negative modulation of GABA” does that mean it’s helping stimulate, or is it helping repair GABA receptors?

I’m curious as a weekly phenibut user if this could mitigate any GABA-B damage I may be doing.

Thanks!

u/MisterYouAreSoDumb

What GABA receptor is this working on?

It acts on the GABA-A receptors.

\(−\)-Epigallocatechin gallate attenuates acute stress responses through GABAergic system in the brain

When you say “reversing negative modulation of GABA” does that mean it’s helping stimulate, or is it helping repair GABA receptors?

Anxiolytic properties of green teapolyphenol \(−\)-epigallocatechin gallate \(EGCG\)

However, we observed that EGCG could reverse significantly in a concentration-dependent manner the inhibition of GABA currents induced by benzodiazepine negative modulator β-carboline (β-CCM) (F(4,42)=42.14;P<0.0001). In the presence ofβ-CCM (10μM), GABA currents were significantly reduced to 75±2% of control GABA currents(n=12;P<0.0001) (Figs. 1C–E). It is interesting to note that this value was close to that obtained for another negative benzodiazepine agonist methyl-6,7-dimethoxy-4-ethyl-β-car-boline-3-carboxylate (DMCM) when tested at 10μM on acutely dissociated CA1 hippocampal neurons (Tietz et al., 1999). In the presence of EGCG (from 0.1 to 10μM) a concentration-dependent reversal of theβ-CCM-induced GABA currents inhibition could be observed.

So the negative GABA-A modulator β-carboline was counteracted by EGCG. It's not talking about repair of anything like that. It's just saying that it counteracts the effects of negative modulators of GABA-A.

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