Sequential effect of aerobic training (T) on the plasticity of central oxytocinergic (otergic) system in normotensive and hypertensive rats

We investigate time-course training effects on OTergic pathways within autonomic areas, using BDNF as an index of neuronal plasticity. SHR and WKY were submitted to low-intensity T on treadmill (55% VO₂max) or kept sedentary (S) for 8 weeks. Resting heart rate (HR) was measured at weeks zero, 1, 2, 4 and 8. Fresh brains slices interesting hypothalamus and brain stem (~800 μm on dry ice) were obtained for punching the paraventricular nucleus (PVN), the dorsal and ventral brain stem (DBS and VBS). BDNF, OT, OT receptor mRNA expression were estimated by real time PCR. Other brains were fixed and cyoprotected; PVN, NTS and RVLM were sliced (30 μm) and incubated with anti-BDNF, anti-OT and 2^ary antibodies for immunofluorescence analysis (confocal microscopy). T equally improved treadmill performance and caused resting bradycardia (~12% reduction in both groups: SHR, from T₂ up to T₈; WKY at T₈). In trained WKY, PVN exhibited a precocious and transient BDNF expression increase (2.5-fold at T₁) with a late and smaller peak in DBS (1.5-fold at T₁–T₂). In trained SHR BDNF expression was smaller and/or appeared later (PVN=+1.4-fold, T₄–T₈; DBS=+1.5-fold, T₂–T₈); BDNF expression was also increased in the VBS (1.8-fold, T₁–T₈). In these areas BDNF protein content was similarly increased in WKY and SHR from T₁–T₂ up to T₈. BDNF changes were accompanied by increased T-induced OT content in the PVN (mRNA, 3 to 4-fold increase; protein 2.4 to 2.8-fold increase, starting at T₂) and OT receptor mRNA expression in the DBS and VBS (1.5 to 2.2-fold increase at T₂–T₈ and 1.3 to 1.6-fold increase at T₁–T₄, respectively). Results indicate that T-induced plasticity of central OTergic system occurs precociously in the PVN compared to other autonomic areas, is faster in WKY and precedes HR changes. Data also showed higher BDNF mRNA turnover in the SHR group.