Genetic study of glutamatergic neurotransmission in ventral hippocampus on baseline cardiovascular parameters, cardiac autonomic activity, baroreflex activity, neuroendocrine and behavioral parameters during chronic repeated stress

Abstract

Emotional stress causes a physiological and psychological imbalance in the body and it has been associated with several pathologies, including cardiovascular diseases and psychiatric disorders. Stressful stimuli cause cardiovascular changes, characterized by an increase in mean arterial pressure (MAP) and heart rate (HR), and HPA axis activation, with increases in plasma corticosterone and adrenocorticotrophin ACTH) plasma levels, and accompanied by emotional consequences, such as anxiety and depression-like effects. Prolonged or repeated exposure to real or potential threats initiates adaptive processes in order to minimize stress impact on the body. However, despite the importance of stress responses habittuation, neurobiological and neurochemical mechanisms involved in this process are still poorly understood. The ventral hippocampus (HV) is predominantly associated with stress, emotions and affection. In this sense, the role of hippocampus glutamatergic neurotransmission in physiological responses regulation to acute stress has been demonstrated. Therefore, the aim of present project is to evaluate the effect of chemogenetic silencing (through the use of DREADDs) of glutamatergic neurons in HV on changes of cardiovascular (systolic blood pressure - SBP, diastolic blood pressure - DBP, MAP, HR), cardiac autonomic activity (Intrinsic HR, cardiac sympathetic and parasympathetic activity), baroreflex, neuroendocrine (corticosterone and ACTH plasma concentrations) and behavioral (anxiogenic and depressive-like effect) in resting conditions caused by a chronic repeated stress protocol.