Transient upregulation of NCAM mRNA in astrocytes in response to entorhinal cortex lesions and ischemia
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Transient upregulation of NCAM mRNA in astrocytes in response to entorhinal cortex lesions and ischemia. / Jucker, M; Mondadori, C; Mohajeri, H; Bartsch, U; Schachner, M.
In: MOL BRAIN RES, Vol. 28, No. 1, 01.1995, p. 149-56.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Transient upregulation of NCAM mRNA in astrocytes in response to entorhinal cortex lesions and ischemia
AU - Jucker, M
AU - Mondadori, C
AU - Mohajeri, H
AU - Bartsch, U
AU - Schachner, M
PY - 1995/1
Y1 - 1995/1
N2 - Axonal sprouting and synaptic reorganization play an important role in the adaptation of the CNS to injury. However, the molecular mechanisms underlying this neuronal plasticity are poorly understood. In the present study we used in situ hybridization to examine the expression of NCAM mRNA in normal hippocampus, and in response to entorhinal cortex (EC) lesions and transient global ischemia. Both neurons and astrocytes were labeled by digoxygenin-tagged cRNA probes which recognize all three major NCAM isoforms of the adult CNS. In contrast, NCAM180-specific probes labeled only neurons in the hippocampus. After unilateral EC lesion, a transient and anatomically restricted upregulation of NCAM120/140 mRNA in reactive astrocytes in the denervated molecular layer of the dentate gyrus was observed. This increase was only present 2-4 days after the lesion whereas the GFAP mRNA increase was present up to 30 days postlesion. Following global ischemia a similar, transient increase of NCAM120/140 mRNA labeling of reactive astrocytes was observed; this increase was anatomically restricted to CA1, where neuronal loss occurred. Results suggest that the transient upregulation of NCAM120/140 mRNA in reactive astrocytes shortly after injury might be an important molecular mechanism in the cascade of events underlying neuronal plasticity in the adult CNS.
AB - Axonal sprouting and synaptic reorganization play an important role in the adaptation of the CNS to injury. However, the molecular mechanisms underlying this neuronal plasticity are poorly understood. In the present study we used in situ hybridization to examine the expression of NCAM mRNA in normal hippocampus, and in response to entorhinal cortex (EC) lesions and transient global ischemia. Both neurons and astrocytes were labeled by digoxygenin-tagged cRNA probes which recognize all three major NCAM isoforms of the adult CNS. In contrast, NCAM180-specific probes labeled only neurons in the hippocampus. After unilateral EC lesion, a transient and anatomically restricted upregulation of NCAM120/140 mRNA in reactive astrocytes in the denervated molecular layer of the dentate gyrus was observed. This increase was only present 2-4 days after the lesion whereas the GFAP mRNA increase was present up to 30 days postlesion. Following global ischemia a similar, transient increase of NCAM120/140 mRNA labeling of reactive astrocytes was observed; this increase was anatomically restricted to CA1, where neuronal loss occurred. Results suggest that the transient upregulation of NCAM120/140 mRNA in reactive astrocytes shortly after injury might be an important molecular mechanism in the cascade of events underlying neuronal plasticity in the adult CNS.
KW - Animals
KW - Astrocytes
KW - Brain Ischemia
KW - Calcium-Binding Proteins
KW - Cell Adhesion Molecules, Neuronal
KW - Cerebellar Nuclei
KW - Entorhinal Cortex
KW - Gene Expression
KW - Hippocampus
KW - Immunohistochemistry
KW - In Situ Hybridization
KW - Leukocyte L1 Antigen Complex
KW - Male
KW - RNA, Messenger
KW - Rats
KW - Rats, Sprague-Dawley
KW - Up-Regulation
KW - Journal Article
M3 - SCORING: Journal article
C2 - 7707869
VL - 28
SP - 149
EP - 156
IS - 1
ER -
