Anxiolytic effects of GLYX-13 in animal models of posttraumatic stress disorder-like behavior.

In the present study, we investigated the effectiveness of GLYX-13, an NMDA receptor glycine site functional partial agonist, to alleviate the enhanced anxiety and fear response in both a mouse and rat model of stress-induced behavioral changes that might be relevant to posttraumatic stress disorder (PTSD). Studies over the last decades have suggested that the hyperactivity of hypothalamic-pituitary-adrenal (HPA) axis is one of the most consistent findings in stress-related disease. Herein, we used these animal models to further investigate the effect of GLYX-13 on the stress hormone levels and glucocorticoid receptor (GR) expression.

[Cardiovascular effect of intracerebroventricular injection of orexin-1 receptor antagonist in rats].

Objective: To study the cardiovascular effect of selective orexin-1 receptor (OX1R) antagonist SB408124 in anesthetized rats and explore the underlying mechanism by using intracerebroventricular (ICV) microinjection combined with immunohistochemical assay.

Methods: The changes of mean arterial blood pressure (MAP) and heart rate (HR) of male Sprague-Dawley rats were recorded during ICV microinjection of SB408124 with or without pretreatment of atropine methyl nitrate or hexamethonium bromide. Furthermore, tyrosine hydroxylase (TH) immunopositive neurons in the rostral ventrolateral medulla (RVLM) of the rat were detected with immunohistochemical assay after ICV microinjection of SB408124.

The action of a novel fluoroquinolone antibiotic agent antofloxacin hydrochloride on human-ether-à-go-go-related gene potassium channel.

The administration of certain fluoroquinolone antibacterials has recently been linked to QT interval prolongation, raising the clinical concerns over the cardiotoxicity of these agents. In this study, the effects of a novel fluoroquinolone, antofloxacin hydrochloride (AX) on human-ether-à-go-go-related gene (HERG) encoding potassium channels and the biophysical mechanisms of drug action were performed with whole-cell patch-clamp technique in transiently transfected HEK293 cells. The administration of AX caused voltage- and time-dependent inhibition of HERG K+ current (I(HERG/MiRP1)) in a concentration-dependent manner but did not markedly modify the properties of channel kinetics, including activation, inactivation, deactivation and recovery from inactivation as well.