Quinpirole for ADHD
There is no description of a sensible use of quinpirole for ADHD.
The presentation is only for the sake of completeness.
Quinpirole is a selective D2 and D3 agonist.1
Quinpirole reduces dopamine levels in the left PFC, but increases them in the striatum and amygdala.2
Hypermotor activity and compulsive behavior are intensified.
Whether this increase in hypermotor activity also occurs in ADHD-HI/ADHD-C sufferers must be questioned. Hyperactivity is located in the striatum. However, symptoms are caused by suboptimal neurotransmitter levels, in this case hyperactivity caused by a lack of dopamine as well as an excess of dopamine.
If quinpirole increases the dopamine level in the striatum, it is plausible that hyperactivity symptoms occur in those not affected.
In ADHD-HI and ADHD-C, however, there is a dopamine deficit in the striatum. It should therefore follow that quinpirole eliminates this deficit and at the same time reduces hyperactivity.
In ADHD, a dopamine deficiency in the PFC is also assumed. A further reduction in dopamine levels would therefore be detrimental.
However, the medial and right PFC is primarily affected in ADHD.
How harmful the reduction in dopamine levels in the left PFC caused by quinpirole is in ADHD remains to be seen.
In addition, quinpirole - as well as aripiprazole (Abilify), a partial D2 receptor agonist - reduces cue-induced craving for cocaine in adult (but not in young) rats and can thus help with addiction problems.3
Another study in rats showed significant THC-like effects of quinpirole when the metabolic degradation of anandamide is inhibited, supporting the hypothesis that these effects of quinpirole are mediated by cannabinoid CB1 receptors.4
In DAT-KD rats, which have a dopamine transporter effect reduced to 10 %, quinpirole reduced hyperactivity, as did the D2 agonist apomorphine and amphetamine as an indirect dopamine receptor agonist.5
Sullivan, Talangbayan, Einat, Szechtman (1998): Effects of quinpirole on central dopamine systems in sensitized and non-sensitized rats. Neuroscience. 1998 Apr;83(3):781-9 ↥
Zbukvic, Ganella, Perry, Madsen, Bye, Lawrence, Kim (2016): Role of Dopamine 2 Receptor in Impaired Drug-Cue Extinction in Adolescent Rats; Cereb. Cortex (2016) 26 (6): 2895-2904. doi: 10.1093/cercor/bhw051 ↥
Solinas, Tanda, Wertheim, Goldberg (2010): Dopaminergic augmentation of delta-9-tetrahydrocannabinol (THC) discrimination: possible involvement of D2-induced formation of anandamide; Psychopharmacology (Berl). 2010 Apr; 209(2): 191–202. doi: 10.1007/s00213-010-1789-8; PMCID: PMC2834964; NIHMSID: NIHMS180022 ↥
Zhuang X, Oosting RS, Jones SR, Gainetdinov RR, Miller GW, Caron MG, Hen R (2001): Hyperactivity and impaired response habituation in hyperdopaminergic mice. Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1982-7. doi: 10.1073/pnas.98.4.1982. PMID: 11172062; PMCID: PMC29368. ↥