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 2ary 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.
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© 2010 Published by Elsevier Inc.