title: Selective calcification of rat brain lesions caused by systemic administration of kainic acid.
abstract: Dystrophic calcification of previously damaged areas of nervous tissue occurs in a wide range of human diseases. The relationship between astroglial and microglial reactions and deposits of calcium salts was studied for up to five months in rats with a brain lesion produced by systemic administration of kainate. The morphology and atomic composition of the calcium salt deposits was also studied. Two types of lesions, sclerotic and liquefactive, were observed. In sclerotic lesions hyperplasia and hypertrophy of astrocytes partially substituted for the lost neurons, reaching a maximum in about twenty-five days after treatment. In liquefactive lesions, the astrocytic reaction occurred only around the liquefactive area. Microglial reaction was similar in both types of lesion and reached its highest expression in about twenty-five days. Calcium deposits were observed in the sclerotic but not in the liquefactive lesions. Clearly distinguishable granules of calcium salts were observed in sclerotic lesions under scanning electron microscopy after only five days post-injection. The size of calcified granules increased with time reaching 40 micro m or more in diameter at five months. The atomic composition of these deposits, studied by X-ray microanalysis, showed a time-dependent increase in calcium concentration. While there was no clear relationship between astroglial and microglial reactions and calcium salt deposits, the systemic injection of kainate produced progressively larger and more concentrated calcium deposits in sclerotic, but not in liquefactive lesions.
authors.affiliation: Institute of Neuroscience of Castilla y León, School of Medicine, University of Valladolid, Spain. gayoso@med.uva.es
authors.forename: M J
authors.initials: MJ
authors.lastname: Gayoso
authors.forename: A
authors.initials: A
authors.lastname: Al-Majdalawi
authors.forename: M
authors.initials: M
authors.lastname: Garrosa
authors.forename: B
authors.initials: B
authors.lastname: Calvo
authors.forename: L
authors.initials: L
authors.lastname: Díaz-Flores
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D001930:Brain Injuries / Q000139:chemically induced*; D002118:Calcium / Q000378:metabolism; D018690:Excitatory Amino Acid Agonists / Q000008:administration & dosage; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007608:Kainic Acid / Q000008:administration & dosage* / Q000378:metabolism; D037102:Lectins / Q000378:metabolism; D008297:Male; D017628:Microglia / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D018690:Excitatory Amino Acid Agonists; D005904:Glial Fibrillary Acidic Protein; D037102:Lectins; D007608:Kainic Acid; D002118:Calcium