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J Psychiatr Res ; 154: 224-232, 2022 10.
Artículo en Inglés | MEDLINE | ID: mdl-35961178

RESUMEN

BACKGROUND: Single Prolonged Stress (SPS) is a valid animal model that reflects the core of post-traumatic stress disorder (PTSD) phenotypes. Although SPS has been a pivotal tool, it can bring ethics approval difficulties due to the use of ether as a stressor. The present study evaluated if changing a chemical (ether) with a social stressor resembles the PTSD hallmark symptoms. METHODS: Female and male young adult rats were distributed in Sham and Social-SPS groups. Rats in Social-SPS groups were subjected to stress, whereas those in Sham groups remained undisturbed. One set of animals performed the behavioral tests, elevated plus-maze (EPM) and Y-maze. Plasma corticosterone levels and cortical and hippocampal molecular protein contents were analyzed. Another set of animals performed the dexamethasone suppression test. RESULTS: A significant decrease in the percentage of time spent and the number of entries in open arms and an increase in anxiety index in the EPM were observed in rats of the social-SPS groups. In the Social-SPS groups, rats reduced the spontaneous alternations in Y-maze. The Social-SPS exposure enhanced the HPA-axis feedback and increased glucocorticoid receptor contents in the cerebral cortex and hippocampus of rats. A decrease in the content of synaptic integrity-related proteins, synaptophysin, and PSD-95, were found in the cortex and hippocampus of rats subjected to social-SPS. There were no statistical differences between males and females in any parameter analyzed. LIMITATIONS: The absence of a task to recap criterion E 'arousal' and predictive validity experiments. CONCLUSIONS: This study reveals that social-SPS recapitulated the main clusters required for a candidate animal model of PTSD.


Asunto(s)
Trastornos por Estrés Postraumático , Animales , Femenino , Masculino , Ratas , Corticosterona , Dexametasona , Modelos Animales de Enfermedad , Éter/metabolismo , Hipocampo/metabolismo , Receptores de Glucocorticoides/metabolismo , Trastornos por Estrés Postraumático/metabolismo , Sinaptofisina/metabolismo
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