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

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% VO 2 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 (T 2 vs T 8 in WKY); BP fall in SHR (−7%) was evident at T 8 –T 12 . T was accompanied by increased GAD expression in the PVN (+1.6‐fold in both groups, T 1 –T 8 ); changes in RVLM and NTS appeared later (T 8 –T 12 ). 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 (Y WKY =−0.005x+2.9, r=−0.45; Y SHR =− 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.