Role of different types of potassium channels and peroxisome proliferator-activated receptors γ in the antidepressant-like activity of bis selenide in the mouse tail suspension test

In the present study we investigated the role of potassium (K+) channels and peroxisome proliferator-activated receptor gamma (PPARγ) in the antidepressant-like effect of bis selenide in the mouse tail suspension test (TST). Intracerebroventricular (i.c.v.) pretreatment with tetraethyl ammonium (TEA, a non-specific inhibitor of K+ channels, 25 pg/site), glibenclamide (an ATP-sensitive K+ channel inhibitor, 0.5 pg/site), charybdotoxin (a large and intermediate conductance calcium-activated K+ channel inhibitor, 25 pg/site) or apamin (a small-conductance calcium-activated K+ channel inhibitor, 10 pg/site) produced a synergistic action with a sub effective dose of bis selenide (0.1 mg/kg, per oral - p.o.). Picrotoxin (1 mg/kg, intraperitoneally - i.p.) pretreatment did not prevent the reduction in immobility time elicited by bis selenide (1 mg/kg, p.o.) in the TST. The reduction in the immobility time elicited by an effective dose of bis selenide (1 mg/kg, p.o.) was prevented by the pretreatment of mice with cromakalim, minoxidil (K+ channel openers, 10 μg/site, i.c.v.) and GW 9662 (a PPARγ antagonist, 10 μg/site, i.c.v.). The findings clearly suggest that an acute oral dose of bis selenide produced an antidepressant-like effect in the mouse TST by a mechanism that involves the K+ channels and PPARγ receptors.

Research highlights▶ K+ channels are involved in bis selenide antidepressant-like action. ▶ PPARγ receptors are involved in bis selenide antidepressant-like effect. ▶ Cromakalim, minoxidil and GW 9662 prevented antidepressant-like effect of bis selenide.