Gene expression profiling in perilesional and contralateral areas after ischemia in rat brain.
Structural and functional reorganization in the vicinity of damaged neocortex and other connected brain areas seems to be responsible for postlesional functional recovery. To better understand the molecular mechanisms underlying this type of plasticity, gene expression patterns were analyzed by using DNA macroarrays comprising 1176 genes. Circumscribed unilateral infarcts consistently affecting the forelimb area of the motor cortex were induced photochemically in adult rats. Ten days after lesioning, cortical gene expression fingerprints were evaluated from an area adjacent to the lesion as well as two contralateral areas of motor and somatosensory cortex. Discrete regions showed distinct expression patterns. Upregulation was observed of different members of transcription factors, immediate early genes, neuronal signaling as well as neuronal growth and structure-associated genes, ipsilaterally (six genes) and/or contralaterally (eight genes in the motor and seven in the somatosensory cortex). In contrast, downregulations were restricted to ipsilateral areas and included genes coding for ion channels, transport proteins, mediators of metabolic pathways, and intracellular transducers (14 genes). A subset of these regulations were further confirmed by real-time polymerase chain reaction (TaqMan assay). At least part of the detected regulations, in particular those of the contralateral hemisphere, are likely to underlie plasticity processes.
Keyvani
Kathy
K
Institute of Neuropathology, University of Muenster, Muenster, Germany.
Witte
Otto W
OW
Paulus
Werner
W
D000818:Animals; D001921:Brain / Q000503:physiopathology*; D002545:Brain Ischemia / Q000235:genetics*; D016172:DNA Fingerprinting; D020869:Gene Expression Profiling; D008297:Male; D009044:Motor Cortex / Q000503:physiopathology; D009473:Neuronal Plasticity; D020411:Oligonucleotide Array Sequence Analysis; D051381:Rats; D017208:Rats, Wistar; D013003:Somatosensory Cortex / Q000503:physiopathology