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(±)-Salsolinol targets depolarize dopamineric neurons.

Dopaminergic neurons produce dopamine, a neurotransmitter with various roles in neurological functions. Progressive loss of dopaminergic neurons is considered as the cause of many motor symptoms associated with Parkinson’s disease.

In vitro: A previous study found that (±)-salsolinol could activate the μ-opioid receptor by the classical G protein-adenylate cyclase pathway. The agonist action of (±)-salsolinol was blocked by the μ-opioid antagonist. The EC50 for the purified stereoisomers (R)- salsolinol and (S)-salsolinol were 6 × 10-4 M and 9 × 10-6 M, respectively. It was found that (±)-salsolinol did not promote the recruitment of β-arrestin. Molecular docking studies showed that the interaction of (R)- and (S)-salsolinol with the μ-opioid receptor was similar to that predicted for the agonist morphine [1].

In vivo: Male Wistar rats were subjected to continuous i.p. dosing of salsolinol at 200 mg/kg for 2 or 4 weeks with either high-fat or normal diet. Results showed that salsolinol could reduce total body mass significantly with no differences in total food intake. In addition, the epididymal fat pad weight over final body mass ratio was lower in salsolinol treated rats with high fat diet. Moreover, the perimeter, e area, as well as short and long axis of the fad pad adipocytes decreased in salsolinol treated animals significantly [2].

Clinical trial: So far, no clinical study has been conducted.

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