Transcriptomics

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Alterations in Neuronal Gene Expression Profiles in Response to Experimental Demyelination and Axonal Transection


ABSTRACT: The pathological basis of multiple sclerosis involves damage to both myelin sheaths and axons. Demyelination and axonal transection are considered to cause reversible and irreversible neurological deficits respectively, gradually destroying the neuronal circuitry of the CNS. In order to analyse the individual effects of the pathological hallmarks of multiple sclerosis on neurons, the pontocerebellar pathway was targeted with either lysolecithin-induced chemical demyelination or complete pathway transection. Transcriptional changes in the pontocerebellar neuronal nuclei were investigated with microarrays at days 4, 10 and 37 post-intervention to identify underlying molecular responses. A common as well as unique set of injury response genes was identified in the transection and the demyelination conditions. The increased expression of activating transcription factor 3 (Atf3) and thyrotropin-releasing hormone (Trh) in both injury paradigms was validated by immunohistochemistry. Expression of Atf3 in a patient with Marburg’s variant of multiple sclerosis was also detected in the pons with large cerebellar demyelination, confirming the activation of the Atf3 pathway in a human disease sample as well. This experimental approach may be useful for the identification of pathways that could be targeted for remyelinative and neuroprotective drug development.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE12324 | GEO | 2008/08/05

SECONDARY ACCESSION(S): PRJNA113555

REPOSITORIES: GEO

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