Imipramine and fluoxetine prevent the stress-induced escape deficits in rats through a distinct mechanism of action

Efficacy of an Hypericum Perforatum (St. John's Wort) Extract in Preventing and Reverting a Condition of Escape Deficit in Rats

“…This interval is too short for the evaluation of ED reversal, since classical antidepressants require at least 4-6 days of continuous treatment to become active (Sherman et al 1982). Thus, the utilization of acute ED has been restricted to the assessment of the prevention liability of potential antidepressant treatments on the behavioral sequelae of stress (Gambarana et al 1995a). Acute ED is also an appropriate tool for the study of the effects of agonists and antagonists, specific for different receptor types, on the protective activity of antidepressant treatments.…”

“…The ED paradigm is a slight modification of the classical Learned Helplessness Syndrome which has already been described (De Montis et al 1995;Gambarana et al 1995a). In brief, the unavoidable shock session lasted 50 min.…”

“…Although several studies have investigated the possible mechanism of action of the antidepressant activity of H. perforatum extracts (Müller et al 1997Nahrstedt and Butterweck 1997;Chatterjee et al 1998;Laakmann et al 1998), no conclusive evidences on such activity have been reported either in humans or in animal models. Thus, we decided to assess the activity of a total extract of H. perforatum in three experimental models recently devised in our laboratory for the study of antidepressant treatments (Gambarana et al 1995a, De Montis et al 1995, Ghiglieri et al 1997.…”

“…The first model is an acute form of escape deficit (ED), the utilization of which is restricted to the evaluation of the protective activity of antidepressants on the behavioral sequelae of an unavoidable stress (Gambarana et al 1995a). The second is a chronic model of ED, which can be maintained indefinitely by the administration of tedious, mild stressors on alternate days (De Montis et al 1995), and which allows the study of ED reversal by antidepressant treatments (De Montis et al 1995).…”

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

“…Accordingly, the dopaminergic response to stress in the NAc, measured by voltammetry, is attenuated by the concurrent activation of dopaminergic terminals in the medial prefrontal cortex (mPFC), and this action is mediated, at least in part, by DA D 1 receptor stimulation (Doherty and Gratton 1996). Longterm exposure to different unavoidable stress protocols decreases DA output in the nucleus accumbens shell (NAcS) and in the mPFC (Di Chiara and Tanda 1997;Gambarana et al 1999b;Mangiavacchi et al 2001), and it impairs responsiveness to both aversive and pleasurable stimuli (Overmier and Seligman 1967;Papp et al 1991;Moreau et al 1992;Gambarana et al 1995;Ghiglieri et al 1997). The impaired responsiveness to environmental stimuli induced by exposure to chronic stress has been used to model two depressive symptoms, hyporeactivity and anhedonia, or lack of motivation, as stressed rats do not show an avoidance response when exposed to avoidable noxious stimuli ) and they do not acquire an appetitive behavior (Ghiglieri et al 1997) or a palatable food-induced place preference (Papp et al 1991).…”