Examining SLV-323, a novel NK1 receptor antagonist, in a chronic psychosocial stress model for depression

Abstract

The novel NK1R antagonist SLV-323 has certain antidepressant-like effects in a valid animal model of depression.

Astroglial Plasticity in the Hippocampus is Affected by Chronic Psychosocial Stress and Concomitant Fluoxetine Treatment

“…Similar findings have been reported in animals submitted to chronic stress (Ohl et al, 2000;van der Hart et al, 2002;Alonso et al, 2004;Czéh et al, 2005a). The exact mechanisms responsible for this hippocampal volume loss have not yet been identified.…”

“…The first experimental phase ('Stress') lasted 7 days, during which the animals of the Stress and the Stress + Fluoxetine group were submitted to daily psychosocial conflict. The psychosocial stress procedure was carried out according to our standard protocol (for details see Czéh et al, 2001Czéh et al, , 2005a. The second experimental phase consisted of the fluoxetine treatment for 4 weeks (28 days), while animals remained in the psychosocial conflict situation.…”

Localized proton MRS of animal brain in vivo: Models of human disorders

“…The latter two drugs had an even more enhancing effect on brain metabolites than tianeptine and also led to elevated Ins concentrations [104]. Similar treatment results were obtained for the novel NK 1 receptor antagonist SLV-323 [276]. Taken together, the proton MRS results confirm a direct neurobiologic effect of chronic stress and suggest a similar protective effect for different classes of antidepressants.…”

Regulation of Adult Neurogenesis and Plasticity by (Early) Stress, Glucocorticoids, and Inflammation

“…Hence, stimulation of neurogenesis has been regarded as a promising strategy for identifying new antidepressant targets. Accordingly, when tested in chronic stress paradigms, several candidate antidepressant compounds, like corticotrophinreleasing factor (CRF-1), vasopressin (V1b) or GR antagonist (Alonso et al 2003;Oomen et al 2007;Surget et al 2008), tianeptine (Czéh et al 2001), or selective neurokinin 1 (NK-1) receptor antagonists (Czéh et al 2005), could indeed normalize inhibitory effects of stress on proliferation or neurogenesis.…”