Impact of Intermittent Restraint Stress and Recovery on Gene Expression of Ion Transporters in Brain/Gut Axis of Mice

Stress evokes characteristic ion osmotic homeostatic disturbance in vertebrates, including mammals. In contrast, vertebrates have developed a mechanism to regain their disturbed physiological homeostasis during a recovery phase or ease response. Despite the well-known ion regulatory disturbance that occurs during the stress response, the mechanisms of stress and ease response during ion osmotic regulation in mammals still need to be better understood. Thus, we hypothesised that intermittent restraint stress and its recovery might rely on transporter function in mice's brains and gut segments. The impact of intermittent restraint stress and its recovery on the major ion regulatory proteins and synuclein alpha was examined in mice's brain/gut axis to understand how the role of ion transporters and brain/gut axis respond to stress and ease response. The mRNA expression of ion transporter genes (Na⁺/K⁺-ATPase (Atp1a3), Ca²⁺transporting ATPase (Atp2b2), sodium/calcium exchanger (Slc8a1), serotonin receptor 3A (Htr3a), and synuclein alpha (Snca)) in the brain segments cortex, hippocampus and cerebellum, and anterior ileum were quantified after intermittent restraint stress and recovery. Atp1a3, and Htr3a genes activated in all brain segments upon restraint stress but deactivated upon recovery. The Snca and Htr3a may act as stress and ease markers as they respond differentially to stress and recovery. Our data thus support the hypothesis that ion-transporter-aided cellular communication operates across mice's brain/gut axis during stress and ease response.