Sequential Effects of Training (T) on GABAergic Neurons in Central Autonomic Areas

Abstract

We showed previously the efficacy of T to alter neuronal plasticity of OTergic preautonomic circuitry. Here we identify the sequential effects of T on GABAergic neurons in central autonomic areas of normotensive and hypertensive rats. WKY and SHR were trained (55% VO2 max, 5 days/week, 1h/day) or kept sedentary (S) for 12 weeks. At weeks 0, 1, 2, 4, 8 and 12, after pressure (BP) and heart rate (HR) recordings, rats were anesthetized and perfused (PBS or PFA 4%) for brain removal. Punches of fresh PVN, NTS and RVLM were used for GAD mRNA expression (RT‐PCR, HPRT as reporter gene); fixed brains were processed for GAD immunofluorescence (ir). Compared to PVN, GAD expression was lower in the VBS (−37%) and higher in the NTS (+20%), mainly in SHR (+94%). T‐induced resting bradycardia (−10%) appeared earlier in SHR (T2 vs T8 in WKY); BP fall in SHR (−7%) was evident at T8–T12. T was accompanied by increased GAD expression in the PVN (+1.6‐fold in both groups, T1–T8); changes in RVLM and NTS appeared later (T8–T12). GADir confirmed both the presence of GABAergic neurons in autonomic areas and the effects of training. PVN GAD expression was positively correlated with resting bradycardia (YWKY=−0.005x+2.9, r=−0.45; YSHR=− 0.010x+5.1, r=−0.73, P<0.05). T‐induced improvement of PVN GABAergic signaling contributes to the appearance of resting bradycardia, a characteristic marker of training.