Spreading depression features and Iba1 immunoreactivity in the cerebral cortex of developing rats submitted to treadmill exercise after treatment with monosodium glutamate

Physical exercise and excessive consumption of monosodium glutamate (MSG) can affect the morphological and electrophysiological organization of the brain during development. However, the interaction of both factors remains unclear. We analyzed the effect of this interaction on the excitability-related phenomenon known as cortical spreading depression (CSD) and the microglial reaction expressed as Iba1-immunolabeled cells in the rat motor cortex. MSG (2. g/kg or 4. g/kg) was administered every other day during the first 14 postnatal days. Treadmill exercise started at 21-23 days of life and lasted 3 weeks, 5 days/week, for 30. min/day. At 45-60 days, CSD was recorded for 4. h at two cortical points and the CSD parameters (velocity, amplitude, and duration of the negative potential change) calculated. Confirming previous observations, exercised rats presented with lower CSD velocities (3.29. ±. 0.18. mm/min) than the sedentary group (3.80. ±. 0.18. mm/min; P<. 0.05). MSG increased CSD velocities in the exercised rats compared to saline-treated and exercised animals in a dose-dependent manner (3.49. ±. 0.19, 4.05. ±. 0.18, and 3.27. ±. 0.26 for 2. g/kg MSG, 4. g/kg MSG, and saline, respectively; P<. 0.05). The amplitude (ranging from 14.3. ±. 5.9 to 18.7. ±. 6.2. mV) and duration (46.7. ±. 11.1 to 60.5. ±. 11.6. s) of the negative slow potential shift of the CSD were similar in all groups. Both exercise and MSG treatment increased Iba1 immunolabeling. The results confirm that physical exercise decelerates CSD propagation. However, it does not impede the CSD-accelerating action of MSG. These effects were accompanied by a cortical microglia reaction. Therefore, the data suggest that treadmill exercise early in life can influence the development of cortical electrical activity. © 2013 ISDN.