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Pregabalin: Difference between revisions
>Alpyne m then -> than |
>Nutmeg enjoyer 11 m I added to the pharmacology section that reduction in glutamate and acetylcholine release caused by Ca channel blockage might be the cause behind why pregabalin can induce dissocative and derlaint like effects. I have talked to lots of pregabalin users and have used it for years, high doses are known for ketamine and delirious like hallucinations. This would make sense because less glutamate available means less of it activates nmda, and same with aCh receptors. |
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Although pregabalin is a chemical derivative of [[GABA]], it displays no activity at any GABA receptors, including GABA<sub>A</sub>, GABA<sub>B</sub> and the [[benzodiazepine]] site. Pregabalin, despite its GABA backbone, does not appear to alter GABA levels in the brain, so its pharmacological activity is presumed to be unrelated to GABA.<ref>Taylor, C. P., Angelotti, T., & Fauman, E. (2007). Pharmacology and mechanism of action of pregabalin: The calcium channel α2–δ (alpha2-delta) subunit as a target for antiepileptic drug discovery. Epilepsy Research, 73(2), 137–150. https://doi.org/10.1016/j.eplepsyres.2006.09.008</ref> Instead, it is its binding to the α2δ-1 site of voltage-gated calcium channels which appears to be the source of its subjective effects. By binding to this site, pregabalin reduces the release of several excitatory neurotransmitters, including [[glutamate]], [[substance P]], [[acetylcholine]] and [[norepinephrine]]. | Although pregabalin is a chemical derivative of [[GABA]], it displays no activity at any GABA receptors, including GABA<sub>A</sub>, GABA<sub>B</sub> and the [[benzodiazepine]] site. Pregabalin, despite its GABA backbone, does not appear to alter GABA levels in the brain, so its pharmacological activity is presumed to be unrelated to GABA.<ref>Taylor, C. P., Angelotti, T., & Fauman, E. (2007). Pharmacology and mechanism of action of pregabalin: The calcium channel α2–δ (alpha2-delta) subunit as a target for antiepileptic drug discovery. Epilepsy Research, 73(2), 137–150. https://doi.org/10.1016/j.eplepsyres.2006.09.008</ref> Instead, it is its binding to the α2δ-1 site of voltage-gated calcium channels which appears to be the source of its subjective effects. By binding to this site, pregabalin reduces the release of several excitatory neurotransmitters, including [[glutamate]], [[substance P]], [[acetylcholine]] and [[norepinephrine]]. | ||
Reduction in the release of glutamate and acetylcholine might be the cause of dissociative / deliriant like effects in high doses. | |||
One study has also shown that pregabalin promotes deep sleep, thus enhancing sleep quality. This may be substantial because reductions in slow-wave sleep have been associated with anxiety and fibromyalgia.<ref>Hindmarch, I., Dawson, J., & Stanley, N. (2005). A double-blind study in healthy volunteers to assess the effects on sleep of pregabalin compared with alprazolam and placebo. Sleep, 28(2), 187–93. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/16171242</ref> | One study has also shown that pregabalin promotes deep sleep, thus enhancing sleep quality. This may be substantial because reductions in slow-wave sleep have been associated with anxiety and fibromyalgia.<ref>Hindmarch, I., Dawson, J., & Stanley, N. (2005). A double-blind study in healthy volunteers to assess the effects on sleep of pregabalin compared with alprazolam and placebo. Sleep, 28(2), 187–93. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/16171242</ref> | ||