Pharmacological modulation of the behavioral effects of social defeat in memory and learning in male mice

Autor:	María-Luisa Laorden, Maria Victoria Milanés, M. Carmen Blanco-Gandía, Pilar Almela, Marta Rodríguez-Arias, Cristina Núñez, Elena Martínez-Laorden, José Miñarro, Javier Navarro-Zaragoza, Sandra Montagud-Romero
Rok vydání:	2019
Předmět:	Male medicine.medical_specialty medicine.drug_class Mice Inbred Strains Tropomyosin receptor kinase B Anxiety Anxiolytic Social defeat Mice 03 medical and health sciences 0302 clinical medicine Cocaine Dopamine Uptake Inhibitors Memory Internal medicine medicine Animals Receptor trkB Maze Learning Social Behavior Pharmacology business.industry Dentate gyrus Azepines 030227 psychiatry Ventral tegmental area Endocrinology medicine.anatomical_structure Anxiogenic Benzamides medicine.symptom business Stress Psychological 030217 neurology & neurosurgery Basolateral amygdala
Zdroj:	Psychopharmacology. 236:2797-2810
ISSN:	1432-2072 0033-3158
DOI:	10.1007/s00213-019-05256-6
Popis:	Previous studies have demonstrated that repeated social defeat (RSD) stress only induces cognitive deficits when experienced during adulthood. However, RSD increases cocaine-rewarding effects in adult and adolescent mice, inducing different expressions of proBDNF in the ventral tegmental area. The aim of the present study was to evaluate the effect of cocaine administration in socially defeated adult or adolescent mice on learning, memory, and anxiety. Additionally, the role of BDNF was also studied. Adolescent and young adult mice were exposed to four episodes of social defeat or exploration (control), being treated with a daily injection of four doses of saline or 1 mg/kg of cocaine 3 weeks after the last social defeat. Other groups were treated with the TrkB receptor antagonist ANA-12 during this 21-day period. After this treatment, their cognitive and anxiogenic profiles were evaluated, along with the expression of BDNF, pCREB, and pERK1/2 in the dentate gyrus (DG) and basolateral amygdala (BLA). Cocaine induced an increased expression of pCREB and BDNF in the DG and BLA only in defeated animals. Although RSD did not affect memory, the administration of cocaine induced memory impairments only in defeated animals. Defeated adult mice needed more time to complete the mazes, and this effect was counteracted by cocaine administration. RSD induced anxiogenic effects only when experienced during adulthood and cocaine induced a general anxiolytic effect. Blockade of Trkb decreased memory retention without affecting spatial learning and modified anxiety on non-stressed mice depending on their age. Our results demonstrate that the long-lasting effects of social defeat on anxiety and cognition are modulated by cocaine administration. Our results highlight that the BDNF signaling pathway could be a target to counteract the effects of cocaine on socially stressed subjects.
Databáze:	OpenAIRE
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