One of ginsenosides in question was found to be a D2 agonist, so:
In hypodopaminergic people, chronic use is likely to worsen the problem.
In healthy people, I don't think it will be too much of a problem, unless used in large doses every day.
In cases of mental illness, reduced dopamine activity/receptor density could be desirable ([1], [2]).
The study in my above post did find it prevented an induced dopamine release, but that's not a model that occurs in a healthy/normal person.
The results of the present study suggest that GTS acts not only on dopaminergic neurons directly or indirectly to prevent nicotine-induced DA release but also postsynaptically by binding to DA D2 receptors
It is like a double-edged sword, useful in the unhealthy: known to restore receptor supersensitivity to baseline ...
Modulatory effect of ginseng total saponin on dopamine release and tyrosine hydroxylase gene expression induced by nicotine in the rat
no effect on resting levels of extracelluar DA ... increase in accumbens DA release produced by systemic nicotine was completely blocked by systemic pre-treatment with GTS ... did not affect the basal TH mRNA expression, attenuated nicotine-induced TH mRNA expression
Inhibition by ginseng total saponin of the development of morphine reverse tolerance and dopamine receptor supersensitivity in mice
prevented the development of dopamine receptor supersensitivity induced by the chronic administration of morphine
Blockade by ginseng total saponin of the development of cocaine induced reverse tolerance and dopamine receptor supersensitivity in mice
reverse tolerance to the ambulation-accelerating effect of cocaine may be associated with the enhanced dopamine receptor sensitivity because both phenomena were blocked by GTS
Things are rarely simple. For example cannabis reduces receptors in the striatum [1], but increases them in the nigrostriatal bundle and mesoaccumbens [2]. These areas are adjacent to the striatum, and probably try to compensate for the striatum's reduced input by increasing their own receptor expression, in other words the receptors in these two regions become supersensitized, which is not at all good. It's forcing your body to adapt to a hyperexcited state, to find a new equilibrium/homeostasis.
The nigrostriatal bundle is involved in locomotion, and so receptor hypersensitivity in that region makes one particularly sensitive to the locomotion-enhancing effects of stimulants.
Chronic (−)-Δ9-tetrahydrocannabinol treatment induces sensitization to the psychomotor effects of amphetamine in rats
Edited by gamesguru, 14 August 2015 - 06:00 PM.
