Combination with the selective serotonin (5-HT) reuptake inhibitor (SSRI) fluoxetine (CAS 56296-78-7) significantly improved the situation. However, the potential 5-HT1A receptor- and 5-HT1B receptor-signals involved in the antidepressant effects are still unclear. The effects click here of 5-HT1A receptor- and 5-HT1B receptor signals were analyzed by using the mouse forced swimming test (FST), a predictive test of antidepressant-like action. The present results indicated that (1) fluoxetine (administrated intragastrically, 30 mg/kg; not subactive dose: 15 mg/kg) significantly reduced IFN-alpha-induced increase of the immobility time in the forced swimming test; (2) 5-HT1A receptor- and 5-HT1B

receptor ligands alone or in combination had no effects on IFN-alpha-induced increase of the immobility time in the FST; (3) surprisingly, WAY 100635 (5-HT1A receptor antagonist, 634908-75-1) and 8-OH-DPAT(5-HT1A receptor agonist, CAS 78950-78-4) markedly enhanced the antidepressant effect of fluoxetine at the subactive dose (15 mg/kg, i.g.) on the IFN-alpha-treated mice in the FST. Further investigations showed that fluoxetine combined LDN-193189 in vivo with WAY 100635 and 8-OH-DPAT failed to produce antidepressant effects in the FST. (4) Co-application of CGS 12066A (5-HT1B receptor agonist, CAS 109028-09-3) or GR 127935 (5-HT1B/1D receptor antagonist, CAS 148642-42-6) with fluoxetine

had no synergistic effects on the IFN-alpha-induced increase of immobility time in FST. (5) Interestingly, co-administration of GR 127935, WAY 100635 and fluoxetine significantly reduced the IFN-alpha-induced increase in immobility SN-38 cost time of FST, being more effective than co-administration of WAY 100635 and fluoxetine. All results suggest that (1) compared to the 5-HT1B receptor, the 5-HT1A receptor signal plays the dominant role in improving the anti-immobility effect

of fluoxetine in the IFN-alpha-induced depression; (2) combination of the 5-HT(1)A antagonist with subactive fluoxetine can be helpful in IFN-alpha-induced depression treatment.”
“Background: Donepezil hydrochloride (CAS 120014-06-4) is a piperidine-based reversible inhibitor of the enzyme acetylcholinesterase (AChE). It is postualted to exert its therapeutic effect by enchancing cholinergic function. This accomplished by increasing the concentration of acetylcholine (ACh) through reversible inhibition of its hydrolysis by AChE.

Objective: The aim of this study was to assess the bioequivalence of a new donepezil 10 mg formulation (test formulation) vs. the reference product, as required by European regulatory authorities for the marketing of a generic product. Additionally, the applicability of the truncated area under the plasma concentration curve (AUC) approach to this drug and under these test conditions was determined.