Michal Morag

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Various medical conditions that involve activation of the immune system are associated with psychological and neuroendocrine changes that resemble the characteristics of depression. In this review we present our recent studies, designed to investigate the relationship between the behavioral effects of immune activation and depressive symptomatology. In the(More)
When exposed to infectious pathogens, human beings manifest variability in the incidence and severity of infection. This variability may partly depend on psychological variables, which have long been thought to contribute to the predisposition, onset, and course of various physical illnesses, including infectious diseases. The objective of the study was to(More)
A hypothesis was considered that anti-epileptic potency of sodium valproate (VPA) may be associated with its action via the benzodiazepine system. The ability of anti-petit mal drugs to suppress the slow secondary negative wave (SNW) of the visually evoked potential was used as a sensitive electrophysiological "tag" for comparison of VPA (200 mg/kg, i.p.)(More)
A double-blind prospective design was used to investigate the immediate and prolonged psychological effects of a specific viral infection, and the role of immune activation in mediating these effects. Subjects were 240 female teenager girls who were vaccinated with rubella vaccine. Based on analysis of levels of antibodies to rubella, subjects were divided(More)
A single dose (500 mg/kg, i.p.) of GABA-transaminase inhibitor, gamma-vinyl GABA (GVG), administered to Wistar rats caused time-related 2--3-fold enhancement of the slow negative wave (SNW) and sensory after-discharge (SAD) of the VEP. This effect was detectable at 1 h, reached plateau at 3--4 h and remained at this level 7 h after GVG. Sodium valproate(More)
Sodium Valproate (VPA) administered to rats in a dose of 10 or 200 mg/kg IP suppressed the slow negative wave (SNW) and photically-induced afterdischarge (SAD) of VEP (when they were present) within 15-30 min. The recovery of VEP amplitude began at 3 hr. This effect was antagonized by subconvulsive doses of convulsant benzodiazepine RO 5-3663 (2 mg/kg) and(More)