TY - JOUR
T1 - Response of rat cerebral cortical astrocytes to freeze‐ or cobalt‐induced injury
T2 - An immunocytochemical and gap‐FRAP study
AU - Anders, Juanita J.
AU - Niedermair, Suzanne
AU - Ellis, Elaine
AU - Salopek, Maureen
PY - 1990
Y1 - 1990
N2 - Astrocytic response in the immediate vicinity of freeze‐ and cobalt‐induced lesions has been examined at the light and ultrastructural level. However, the temporal and spatial distribution of astrocytic reactivity throughout the rat cerebral cortex, using glial fibrillary acidic protein (GFAP) immunolabeling, has not been examined. The first purpose of this study was to establish the chronological distribution of astrocytic reactivity, as measured by changes in GFAP immunoreactivity, following freeze‐ or cobalt‐induced injury to the rat cerebral cortex. Cobalt metal also has been proposed to have a direct effect on astrocytes and has been shown to stimulate in vitro astrocytes to become reactive. The second purpose of this report was to determine if cobalt had an effect on in vitro astrocytic gap junctional dye coupling as measured by fluorescence recovery after laser‐photobleaching (gap‐FRAP). Although the chronological development of the increased GFAP immunoreactivity was different for the freeze‐ and cobalt‐induced lesions, astrocytes initially showed an increase in GFAP immunoreactivity in the region surrounding these lesions. This initial response was followed by a spread of increased GFAP immunoreactivity throughout certain regions of the ipsilateral cerebral hemisphere and then by a restriction of the increased immunolabeling to the lesion site. Cobalt also had a direct effect on in vitro astrocytes as demonstrated by the inhibition of astrocytic gap junctional dye coupling. Based on gap‐FRAP analysis, cobalt significantly blocked fluorescence recovery (2.5%) as compared to the fluorescence recovery in control astrocytes (26%). It is proposed that the initial increase in GFAP immunoreactivity may be due to decreased gap junctional activity.
AB - Astrocytic response in the immediate vicinity of freeze‐ and cobalt‐induced lesions has been examined at the light and ultrastructural level. However, the temporal and spatial distribution of astrocytic reactivity throughout the rat cerebral cortex, using glial fibrillary acidic protein (GFAP) immunolabeling, has not been examined. The first purpose of this study was to establish the chronological distribution of astrocytic reactivity, as measured by changes in GFAP immunoreactivity, following freeze‐ or cobalt‐induced injury to the rat cerebral cortex. Cobalt metal also has been proposed to have a direct effect on astrocytes and has been shown to stimulate in vitro astrocytes to become reactive. The second purpose of this report was to determine if cobalt had an effect on in vitro astrocytic gap junctional dye coupling as measured by fluorescence recovery after laser‐photobleaching (gap‐FRAP). Although the chronological development of the increased GFAP immunoreactivity was different for the freeze‐ and cobalt‐induced lesions, astrocytes initially showed an increase in GFAP immunoreactivity in the region surrounding these lesions. This initial response was followed by a spread of increased GFAP immunoreactivity throughout certain regions of the ipsilateral cerebral hemisphere and then by a restriction of the increased immunolabeling to the lesion site. Cobalt also had a direct effect on in vitro astrocytes as demonstrated by the inhibition of astrocytic gap junctional dye coupling. Based on gap‐FRAP analysis, cobalt significantly blocked fluorescence recovery (2.5%) as compared to the fluorescence recovery in control astrocytes (26%). It is proposed that the initial increase in GFAP immunoreactivity may be due to decreased gap junctional activity.
KW - Gap junctional dye coupling
KW - GFAP
KW - In vivo and in vitro astrocytes
UR - http://www.scopus.com/inward/record.url?scp=0025619286&partnerID=8YFLogxK
U2 - 10.1002/glia.440030606
DO - 10.1002/glia.440030606
M3 - Article
C2 - 2148550
AN - SCOPUS:0025619286
SN - 0894-1491
VL - 3
SP - 476
EP - 486
JO - GLIA
JF - GLIA
IS - 6
ER -