Acta Vet. Brno 2016, 85: 337-341

https://doi.org/10.2754/avb201685040337

The immunoreactivity of satellite glia of the spinal ganglia of rats treated with monosodium glutamate

Aleksandra Ewa Krawczyk, Jadwiga Jaworska-Adamu

University of Life Sciences, Faculty of Veterinary Medicine, Department of Animal Anatomy and Histology, Lublin, Poland

Received March 30, 2016
Accepted December 19, 2016

Satellite glia of the peripheral nervous system ganglia provide metabolic protection to the neurons. The aim of this study was to determine the effects of monosodium glutamate administered parenterally to rats on the expression of glial fibrillary acidic protein, S-100β protein and Ki-67 antigen in the satellite glial cells. Adult, 60-day-old male rats received monosodium glutamate at two doses of 2 g/kg b.w. (group 1) and 4 g/kg b.w. (group 2) subcutaneously for 3 consecutive days. Animals in the control group (group C) were treated with corresponding doses of 0.9% sodium chloride. Immediately after euthanasia, spinal ganglia of the lumbar region were dissected. Immunohistochemical peroxidase anti-peroxidase reactions were performed on the sections containing the examined material using antibodies against glial fibrillary acidic protein, S-100β and Ki-67. Next, morphological and morphometric analyses of immunopositive and immunonegative glia were conducted. The data were presented as the mean number of cells with standard deviation. Significant differences were analysed using ANOVA (P < 0.05). In all 63-day-old rats, immunopositivity for the examined proteins glia was observed. Increased number of cells expressing glial fibrillary acidic protein was demonstrated in group 2, whereas the number of S-100β-positive glia grew in the groups with the increasing doses of monosodium glutamate. The results indicate the early stage reactivity of glia in response to increased levels of glutamate in the extracellular space. These changes may be of a neuroprotective nature under the conditions of excitotoxicity induced by the action of this excitatory neurotransmitter.

References

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