Chronic mild stress induces anhedonic behavior and changes in glutamate release, BDNF trafficking and dendrite morphology only in stress vulnerable rats. The rapid restorative action of ketamine

Publication date: Available online 2 April 2019Source: Neurobiology of StressAuthor(s): Paolo Tornese, Nathalie Sala, Daniela Bonini, Tiziana Bonifacino, Luca La Via, Marco Milanese, Giulia Treccani, Mara Seguini, Alessandro Ieraci, Jessica Mingardi, Jens R. Nyengaard, Stefano Calza, Giambattista Bonanno, Gregers Wegener, Alessandro Barbon, Maurizio Popoli, Laura MusazziAbstractDepression is a debilitating mental disease, characterized by persistent low mood and anhedonia. Stress represents a major environmental risk factor for depression; the complex interaction of stress with genetic factors results in different individual vulnerability or resilience to the disorder. Dysfunctions of the glutamate system have a primary role in depression. Clinical neuroimaging studies have consistently reported alterations in volume and connectivity of cortico-limbic areas, where glutamate neurons and synapses predominate. This is confirmed by preclinical studies in rodents, showing that repeated stress induces morphological and functional maladaptive changes in the same brain regions altered in humans. Confirming the key role of glutamatergic transmission in depression, compelling evidence has shown that the non-competitive NMDA receptor antagonist, ketamine, induces, at sub-anesthetic dose, rapid and sustained antidepressant response in both humans and rodents.We show here that the Chronic Mild Stress model of depression induces, only in stress-vulnerable rats, depressed-like anhedonic beh...
Source: Neurobiology of Stress - Category: Neuroscience Source Type: research