title: Temporal and regional profile of neuronal and glial cellular injury after induction of kaolin hydrocephalus.
abstract: To study regional and temporal pattern of glial and neuronal reaction to induction of kaolin hydrocephalus in adult rats. Enzyme- and immunohistochemistry was performed in 20 adult rats with kaolin-hydrocephalus after 2, 4, 6 and 8 weeks to glial glutamatergic transmission activity (GLDH) and neuronal nitrous oxide synthetic activity (nNOS). Also, glial fibrillary acidic protein (GFAP), 68 kd neurofilament protein (NF68) and synaptophysin (SYN38) and basic fibroblastic growth-factor (bFGF) were stained. Results were quantified by imaging analysis (SCION IMAGE) and expressed as relative immunopositive area. After 2 weeks, nNos-activity increased in cortical and hippocampal neurones (CA1 and CA3) and GLDH-activity also showed increases, most significant in periventricular white matter (25.7 +/- 3.8 vs. 15.5 +/- 4.9; p < 0.001) and hippocampus (p < 0.01). After 4 or 6 weeks, global cortical GLDH-activity showed further marked increases (25.7 +/- 3.9 vs. 11.3 +/- 1.5; p < 0.05), while sustained structural changes have occurred: GFAP decreased in periventricular (3.3 +/- 0.5 vs. 6.3 +/- 1.2; p < 0.01), hippocampal and cortical astrocytes (0.9 +/- 0.34 vs. 5.0 +/- 0.7%; p < 0.01), whereas NF68 in cortical efferent neurones increased (6.5 +/- 1.5% vs. 4.7 +/- 0.1; p < 0.01) followed by a decrease in cortical and hippocampal (CA1) SYN 38 (p < 0.05). Acute glial and neuronal reactions were almost functional and in chronic stages sustained structural changes predominated. Since neuronal reactions were pronounced in selective vulnerable areas glial reaction was not restricted to periventricular astrocytes.
authors.affiliation: Department of Neurosurgery, Medical School and Nordstadt Hospital, Hannover, Germany.
authors.forename: P
authors.initials: P
authors.lastname: Klinge
authors.forename: A
authors.initials: A
authors.lastname: Mühlendyck
authors.forename: S
authors.initials: S
authors.lastname: Lee
authors.forename: W
authors.initials: W
authors.lastname: Lüdemann
authors.forename: S
authors.initials: S
authors.lastname: Groos
authors.forename: M
authors.initials: M
authors.lastname: Samii
authors.forename: T
authors.initials: T
authors.lastname: Brinker
mesh_terms: D000818:Animals; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D006624:Hippocampus / Q000201:enzymology / Q000473:pathology; D006849:Hydrocephalus / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D007616:Kaolin; D009457:Neuroglia / Q000187:drug effects / Q000473:pathology*; D009474:Neurons / Q000187:drug effects / Q000473:pathology*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D051381:Rats; D017207:Rats, Sprague-Dawley; D016708:Synaptophysin / Q000378:metabolism; D013997:Time Factors
chemical_list: D016708:Synaptophysin; D016222:Fibroblast Growth Factor 2; D007616:Kaolin; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat