aguineapig
Member
- Joined
- May 16, 2019
- Messages
- 159
Exploring the schizophrenic propensity towards cigarette binges led to this very interesting study.
It seems to show that nicotine simply optimizes/removes obstacles of endogenous GABA production rather than acting as a GABA agonist, which is ostensibly much less dicey than direct agonism since there are feedback loops to limit endogenous production, and we all know the potential problems with GABAergic withdrawals when people are too heavy handed with them.
I am very curious if niacinamide acts through a similar mechanism, thus perhaps explaining it's anxiolytic/ GABAergic effect despite only minor observable binding affinity? If the case that would make B3 a very safe upstream GABA option.
Why Schizophrenics Smoke
Full study
From the Cover: Nicotine decreases DNA methyltransferase 1 expression and glutamic acid decarboxylase 67 promoter methylation in GABAergic interneurons
It seems to show that nicotine simply optimizes/removes obstacles of endogenous GABA production rather than acting as a GABA agonist, which is ostensibly much less dicey than direct agonism since there are feedback loops to limit endogenous production, and we all know the potential problems with GABAergic withdrawals when people are too heavy handed with them.
I am very curious if niacinamide acts through a similar mechanism, thus perhaps explaining it's anxiolytic/ GABAergic effect despite only minor observable binding affinity? If the case that would make B3 a very safe upstream GABA option.
Why Schizophrenics Smoke
Full study
From the Cover: Nicotine decreases DNA methyltransferase 1 expression and glutamic acid decarboxylase 67 promoter methylation in GABAergic interneurons