Kaleida
Bluelight Crew
- Joined
- Sep 6, 2015
- Messages
- 2,806
perpetualdawn, I think that's a perfectly rational theory given our current level of understanding about these systems.
Even without going too deep into ideas like increased brain communication and synesthesia and stuff, I think it's clear from the science that psychedelics create their subjective effects at least in part by altering levels of excitatory and inhibitory neurotransmission throughout the brain. Interestingly, considering the way GABAergics do seem to generally reduce the strength of trips, the 5-HT2A receptor has also been shown consistently to increase the release of both glutamate and GABA in cortical areas when activated.
I should also say that I feel that the science has shown sufficient evidence that the 5-HT2A receptor is necessary for truly psychedelic effects, but I also believe that the picture beyond that is likely much more complex. For instance, it's worth considering that because that receptor has multiple functional pathways that can be activated with different relative affinities and efficacies by ligands, even two drugs that bind only to 5-HT2A could still have very different net effects on neurotransmitter release and overall excitability, and then when you add in all the other receptors that most psychedelics do bind to, the interactions should just become remarkably complex, leading to the well-known diversity of different psychedelics.
In relation to how GABAergics can blunt a trip, I think it's probably also worth considering that as the excitability of part of the brain increases, the chemical reactions occurring there through other means can also become more intense, and that should include activities caused by those off-target receptors, further strengthening their modifications to the effects of 5-HT2A. Likewise, in other parts of the brain their impact may be inhibited compared to normal, making the whole system even more complex and altered.
When it comes to the actual hallucinations and intense emotions and thoughts caused by psychedelics, I wouldn't be at all surprised if they're a result of excitatory activity, and so I do think an indirect effect of decreasing excitability that most GABAergics have would be a logical explanation for their impact on a trip. However, I must say that I find certain effects of psychedelics, such as memory loss, to be enhanced by GABAergics instead, so perhaps that and other subjective effects of theirs could still depend on their inhibitory activity.
Even without going too deep into ideas like increased brain communication and synesthesia and stuff, I think it's clear from the science that psychedelics create their subjective effects at least in part by altering levels of excitatory and inhibitory neurotransmission throughout the brain. Interestingly, considering the way GABAergics do seem to generally reduce the strength of trips, the 5-HT2A receptor has also been shown consistently to increase the release of both glutamate and GABA in cortical areas when activated.
I should also say that I feel that the science has shown sufficient evidence that the 5-HT2A receptor is necessary for truly psychedelic effects, but I also believe that the picture beyond that is likely much more complex. For instance, it's worth considering that because that receptor has multiple functional pathways that can be activated with different relative affinities and efficacies by ligands, even two drugs that bind only to 5-HT2A could still have very different net effects on neurotransmitter release and overall excitability, and then when you add in all the other receptors that most psychedelics do bind to, the interactions should just become remarkably complex, leading to the well-known diversity of different psychedelics.
In relation to how GABAergics can blunt a trip, I think it's probably also worth considering that as the excitability of part of the brain increases, the chemical reactions occurring there through other means can also become more intense, and that should include activities caused by those off-target receptors, further strengthening their modifications to the effects of 5-HT2A. Likewise, in other parts of the brain their impact may be inhibited compared to normal, making the whole system even more complex and altered.
When it comes to the actual hallucinations and intense emotions and thoughts caused by psychedelics, I wouldn't be at all surprised if they're a result of excitatory activity, and so I do think an indirect effect of decreasing excitability that most GABAergics have would be a logical explanation for their impact on a trip. However, I must say that I find certain effects of psychedelics, such as memory loss, to be enhanced by GABAergics instead, so perhaps that and other subjective effects of theirs could still depend on their inhibitory activity.