jaspersilence
Bluelighter
If you are taking Gabapentin for WDs or recreational...I must stress this...Do not expect to feel the same taking Gaba 2 days in a row...You must separate high doses by days to feel any effect.
Quote taken from wikipedia:
Some of its activity may involve interaction with voltage-gated calcium channels. Gabapentin binds to the α2δ subunit
I think it basically GABA?Gabapentin (Neurontin) is a pharmaceutical drug, specifically a GABA analog.
it's a gaba analogue that doesn't mean it works on GABA. Iirc orally active GABA is Phenibut, they just add a phenyl ring to get GABA to cross the BBB. Like I said Gabapentin's activity isn't fully understood but it is definitely believed to work on calcium channels,
Have anyone taken both phenbute and either lyrica and gabapentin and if so how do their effects differ?
Thanks for pointing this out and everything I looked into confirms what you are saying. Since we do not know how it works and since GABA doesn't pass through the blood brain barrier so we dont know what direct effects increasing its levels directly have then how do we know that the the analogs aren't similar enough to be somewhat interchangeable with the GABA and that the idea that they cause an increase of GABA through a calcium channel interaction. Not doubting I just wonder how we know this as this is getting into areas I haven't yet studied and am looking for an explanation rather than trying to argue.
The mechanism of action of the antiepileptic and antinociceptive drugs of the gabapentinoid family has remained poorly understood. Gabapentin (GBP) binds to an exofacial epitope of the α 2 δ-1 and α 2 δ-2 auxiliary subunits of voltage-gated calcium channels, but acute inhibition of calcium currents by GBP is either very minor or absent. We formulated the hypothesis that GBP impairs the ability of α 2 δ subunits to enhance voltage-gated Ca 2+ channel plasma membrane density by means of an effect on trafficking.
Gabapentin (GBP) itself was originally developed as an analog of γ-amino-butyric acid (GABA), but is now believed to have no effect on GABA receptors or transporters (for review see ref. 6 ). The first key to understanding the mechanism of action of GBP came from purification of the GBP-binding protein from porcine brain ( 7 ), which was identified as the α 2 δ-1 auxiliary subunit of VGCCs. It is now known that GBP binds to an exofacial epitope present in both the α 2 δ-1 and α 2 δ-2 subunits