title: Differential susceptibility of senile and lesion-induced astrogliosis to phosphatidylserine.
abstract: The susceptibility of age- and lesion-induced astrogliosis to the treatment with phosphatidylserine was investigated with the use of GFAP immunoblotting. The existence of age-induced upregulation of GFAP content was confirmed in the hippocampus, septum, and corpus callosum of the rat. The Ptd-Ser treatment of the aged rats further increased the GFAP content in the hippocampus and corpus callosum. The GFAP content increase in the corpus callosum was additionally illustrated by the upregulation in GFAP immunostaining. In the septum no further elevation of GFAP was observed after Ptd-Ser treatment, and in the striatum the compound elicited significant GFAP content increase, absent in the untreated aged rat brain striatum. In the intact adult rat brain no effect of Ptd-Ser on GFAP content was observed; neither did the compound elicit any modulation of the astrogliosis related to the mechanical lesion of the brain in the septum, hippocampus, cortex, and striatum. In the corpus callosum, Ptd-Ser potentiated the GFAP content increase related to the mechanical lesion, pointing to the structure-related heterogeneity of astrocytic population. Because it has been previously found that Ptd-Ser partly reverses one of the aspects of rodent brain aging, the aging-induced decrease of the acetylcholine release, the possibility exists that the effects of Ptd-Ser administration on glia and neurons in the aged brain may be related.
authors.affiliation: Department of Neurophysiology, Nencki Institute of Experimental Biology, Warszawa, Poland.
authors.forename: W
authors.initials: W
authors.lastname: Jegliński
authors.forename: G
authors.initials: G
authors.lastname: Pepeu
authors.forename: B
authors.initials: B
authors.lastname: Oderfeld-Nowak
mesh_terms: D000375:Aging / Q000473:pathology*; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000502:physiology*; D001921:Brain / Q000473:pathology; D001923:Brain Chemistry / Q000502:physiology; D001930:Brain Injuries / Q000378:metabolism / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D010718:Phosphatidylserines / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D015854:Up-Regulation / Q000502:physiology
chemical_list: D005904:Glial Fibrillary Acidic Protein; D010718:Phosphatidylserines