Lectinhistochemistry and ultrastructure of microglial response to monosodium glutamate-mediated neurotoxicity in the arcuate nucleus

Citation
B. Pelaez et al., Lectinhistochemistry and ultrastructure of microglial response to monosodium glutamate-mediated neurotoxicity in the arcuate nucleus, HIST HISTOP, 14(1), 1999, pp. 165-174
Citations number
49
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
HISTOLOGY AND HISTOPATHOLOGY
ISSN journal
02133911 → ACNP
Volume
14
Issue
1
Year of publication
1999
Pages
165 - 174
Database
ISI
SICI code
0213-3911(199901)14:1<165:LAUOMR>2.0.ZU;2-5
Abstract
In this study we describe the most relevant morphological features of the m icroglial reaction that takes place in the arcuate nucleus (AN) after neuro toxic injury induced by a single subcutaneous injection of monosodium gluta mate (MSG) in neonatal rats. The time course of the reaction was evaluated by lectin-histochemistry. Microglial/macrophagic cells were labelled with t he lectin obtained from Lycopersicon esculentum and with Bq isolectin from Griffonia simplicifolia. The microglial response was also studied by ultras tructural observations. The histochemical study revealed the presence of fe w reactive microglial cells at 6 h post-injection. These cells were intense ly stained and had a globular morphology but contained no neuronal debris i nside them when observed under the electron microscope. At 12 h post-inject ion, the number of microglial cells had increased and, at the same time, in tense phagocytic activity was observed ultrastructurally. The microglial re action peaked at 24 and 36 h post-injection, when the number of microglial/ macrophagic cells was maximum, although the ultrastructural observations sh owed that at 36 h the amount of debris ingested by macrophages was decrease d with respect to animals sacrificed at 24 h. Finally, at 4 days after neur otoxic injection the number and morphology of microglial cells were similar to those observed in the control rats. The ultrastructural study also reve aled the existence of microglial cell mitosis in the territory of the AN to gether with a strong increase in the number of supraependymal cells resembl ing macrophages in the third ventricle during the lesion. Our data demonstr ate that activated microglial cells initially extend throughout the damaged territory, but from 24-36 h onwards they are especially patent in the vent rolateral portions of the AN.