Neuroprotection
Bluelighter
- Joined
- Apr 18, 2015
- Messages
- 1,083
I have read a study that claimed to identify the link between Kappa opioid receptor activation and suppression of normal Dopamine release, something that can result in dysphoria from Kappa agonists. Apparently Kappa Activation induces P38Mitogen-Activated Protein Kinases as a down stream pathway, and it is this which signals Dopaminergic cells to dramatically reduce their Dopamine output. The Same study also states that inhibition of this Kinase with small molecules can abolish the Dopaminergic suppression caused by Kappa signalling while maintaining all the other affects.
This rases some interesting questions.
1 How could this affect the Salvia experience?
2 Could inhibiting the P38mitogen-activated protein Kinases reduce the psychotic aspects of Kappa agonists?
3 If this works to make the affects of Kappa opioid Agonists more pleasant, or removes dysphoria, could drugs like Salvia/Salvinorin A become addictive.
4 Could such a breakthrough remove some of the supposed benefits of Kappa agonists, that is, is temporary reduction of Dopamine release important for positive long turm effects e.g. anti-addiction or afterglow.
Just for your information, P38MAPK inhibitors have been studied as anti-inflammatory drugs, but I’m not sure if they are still available.
This rases some interesting questions.
1 How could this affect the Salvia experience?
2 Could inhibiting the P38mitogen-activated protein Kinases reduce the psychotic aspects of Kappa agonists?
3 If this works to make the affects of Kappa opioid Agonists more pleasant, or removes dysphoria, could drugs like Salvia/Salvinorin A become addictive.
4 Could such a breakthrough remove some of the supposed benefits of Kappa agonists, that is, is temporary reduction of Dopamine release important for positive long turm effects e.g. anti-addiction or afterglow.
Just for your information, P38MAPK inhibitors have been studied as anti-inflammatory drugs, but I’m not sure if they are still available.