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

Abstract

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 (2g/kg or 4g/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 30min/day. At 45-60 days, CSD was recorded for 4h 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±0.18mm/min) than the sedentary group (3.80±0.18mm/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 2g/kg MSG, 4g/kg MSG, and saline, respectively; P<0.05). The amplitude (ranging from 14.3±5.9 to 18.7±6.2mV) and duration (46.7±11.1 to 60.5±11.6s) 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.

Pathogenesis of peritumoral hyperexcitability in an immunocompetent CRISPR-based glioblastoma model

“…SD arises experimentally from profound local metabolic stress (hypoxia, hypoglycemia, excess glutamate, and mitochondrial ATP depletion), which collapse membrane polarization levels and alter functional ionic gradients in neurons and astrocytes (28). Recurrent SD episodes are linked to prolonged ischemic tissue injury and have been shown to drive microglial infiltration in the neocortex and trigger seizures in disinhibited networks (18,(29)(30)(31).…”

Physical Exercise Preserves Adult Visual Plasticity in Mice and Restores it after a Stroke in the Somatosensory Cortex

“…Many molecular factors that changed after EE are also altered after physical exercise (Vivar et al, 2013 ); e.g., increased levels of BDNF (Berchtold et al, 2005 ), NGF (Neeper et al, 1996 ), and IGF (Carro et al, 2000 ). Interestingly, exposure of rats to either EE or treadmill exercise reduced the susceptibility to cortical spreading depression (Santos-Monteiro et al, 2000 ; Lima et al, 2014 ), thereby possibly contributing to reduced plasticity-impairing effects of a cortical PT-lesion after free access to a RW.…”

Effects of Physical Exercise on the Intestinal Mucosa of Rats Submitted to a Hypothalamic Obesity Condition

“…From day 0 to day 5 of life, each rat in the MSG and EMSG groups received a daily subcutaneous injection of monosodium glutamate (4 g/kg of body weight) according to Lima et al (). The S and E groups received saline injections during the same period of time.…”