Expression of full-length trkB receptors by reactive astrocytes after chronic CNS injury

被引:34
作者
McKeon, RJ [1 ]
Silver, J
Large, TH
机构
[1] Emory Univ, Dept Anat & Cell Biol, Atlanta, GA 30322 USA
[2] Case Western Reserve Univ, Dept Neurosci, Cleveland, OH 44106 USA
关键词
astrocyte; microglia; neurotrophin; neurotrophin receptor; trk; CNS injury; regeneration;
D O I
10.1006/exnr.1997.6698
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Growth factors, including members of the neurotrophin family, are expressed by neuronal and glial elements following injury to the CNS. In order to assess the capacity for glial cells to respond to neurotrophins at sites of chronic injury, full-lengths trkB receptors were localized following implantation of a nitrocellulose filter into the cerebral cortex for 30 days. Northern analysis demonstrated that filter implants contained cells expressing transcripts for full-length and truncated trkB receptors, in contrast to the predominant expression of truncated trkB receptors by cultured astrocytes. In situ hybridization and immunohistochemistry using probes to the trkB kinase domain colocalized full-length receptors with GFAP-immunopositive reactive astrocytes adjacent to and within the filter implant. In contrast, OX-42-immunopositive microglia/macrophages were not stained for full-length trkB. These data indicate that reactive astrocytes can express functional trkB receptors following a chronic insult to the cerebral cortex and support the hypothesis that neurotrophins may regulate astrocytic responses to injury. (C) 1997 Academic Press.
引用
收藏
页码:558 / 567
页数:10
相关论文
共 47 条
[1]   IN-SITU HYBRIDIZATION OF TRKB AND TRKC RECEPTOR MESSENGER-RNA IN RAT FOREBRAIN AND ASSOCIATION WITH HIGH-AFFINITY BINDING OF [I-125] BDNF, [I-125] NT-4/5 AND [I-125] NT-3 [J].
ALTAR, CA ;
SIUCIAK, JA ;
WRIGHT, P ;
IP, NY ;
LINDSAY, RM ;
WIEGAND, SJ .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1994, 6 (09) :1389-1405
[2]   NERVE GROWTH-FACTOR AND ITS LOW-AFFINITY RECEPTOR PROMOTE SCHWANN-CELL MIGRATION [J].
ANTON, ES ;
WESKAMP, G ;
REICHARDT, LF ;
MATTHEW, WD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (07) :2795-2799
[3]  
BALASINGAM V, 1994, J NEUROSCI, V14, P846
[4]  
Baxter GT, 1997, J NEUROSCI, V17, P2683
[5]  
BECK KD, 1993, J NEUROSCI, V13, P4001
[6]   NEUROTROPHIN-5 - A NOVEL NEUROTROPHIC FACTOR THAT ACTIVATES TRK AND TRKB [J].
BERKEMEIER, LR ;
WINSLOW, JW ;
KAPLAN, DR ;
NIKOLICS, K ;
GOEDDEL, DV ;
ROSENTHAL, A .
NEURON, 1991, 7 (05) :857-866
[7]  
CONDORELLI DF, 1994, J NEUROCHEM, V63, P509
[8]   Trk receptor alterations in Alzheimer's disease [J].
Connor, B ;
Young, D ;
Lawlor, P ;
Gai, W ;
Waldvogel, H ;
Faull, RLM ;
Dragunow, M .
MOLECULAR BRAIN RESEARCH, 1996, 42 (01) :1-17
[9]   DIFFERENTIAL REGULATION OF CATALYTIC AND NONCATALYTIC TRKB MESSENGER-RNAS IN THE RAT HIPPOCAMPUS FOLLOWING SEIZURES INDUCED BY SYSTEMIC ADMINISTRATION OF KAINATE [J].
DUGICHDJORDJEVIC, MM ;
OHSAWA, F ;
OKAZAKI, T ;
MORI, N ;
DAY, JR ;
BECK, KD ;
HEFTI, F .
NEUROSCIENCE, 1995, 66 (04) :861-877
[10]  
Eide FF, 1996, J NEUROSCI, V16, P3123