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Temporal Profiles of Nerve Growth Factor β‐Subunit Level in Rat Brain Regions After Transient Ischemia
Author(s) -
Shozuhara Hidetaka,
Onodera Hiroshi,
KatohSemba Rituko,
Kato Kanefusa,
Yamasaki Yasundo,
Kogure Kyuya
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb08888.x
Subject(s) - nerve growth factor , glial fibrillary acidic protein , ischemia , medicine , endocrinology , hippocampus , dentate gyrus , striatum , cerebral cortex , cortex (anatomy) , chemistry , biology , neuroscience , immunohistochemistry , dopamine , receptor
To determine the role of nerve growth factor (NGF) in ischemic brain damage, we measured the temporal and regional changes in the level of NGF in the hippo‐campal subfields, the cerebral cortex, the striatum, and the septum at 1, 2, 7, and 30 days after transient forebrain ischemia using a highly sensitive sandwich‐type enzyme im‐munoassay system for the β‐subunit of mouse 7S NGF (β‐NGF). We also analyzed glial fibrillary acidic protein immunoreactivity in the hippocampus to ascertain the contribution of reactive astrocytes to NGF production after an ischemic insult. In the CA1 subfield of the hippocampus, the level of β‐NGF decreased slightly 2 days after ischemia (not significant), at which time CA1 pyramidal cell loss began to occur, and increased by 40% 30 days after ischemia ( p < 0.05). A marked increase in glial fibrillary acidic pro‐tein‐positive astrocytes in the CA1 subfield 2–30 days after ischemia suggests that the reactive astrocytes participated in a gradual increase in the level of β‐NGF after recirculation. The level of β‐NGF in the dentate gyrus decreased transiently 2 days ( p < 0.05) and 7 days ( p < 0.01) after ischemia, followed by recovery to the level of control animals 30 days after ischemia. The level of β‐NGF in the septum gradually decreased 7 days (−27%, p < 0.05) and 30 days (−43%, p < 0.01) after ischemia. The levels of β‐NGF in the cerebral cortex and striatum remained unaltered throughout the observation period. These results suggest that the alteration of NGF content occurs not only in the CA1 subfield, where pyramidal cells are depleted, but also in areas with minimal histological damage. Septal decrease in NGF may reflect the reduction of retrograde NGF transport from hippocampus to septal cholinergic neurons.