The cellular mRNA expression of GABA and glutamate receptors in spinal motor neurons of SOD1 mice

S. Petri*, S. Schmalbach, J. Grosskreutz, K. Krampfl, C. Grothe, R. Dengler, L. Van Den Bosch, W. Robberecht, J. Bufler

*Corresponding author for this work
20 Citations (Scopus)

Abstract

ALS is a fatal neurodegenerative disorder characterized by a selective loss of upper motor neurons in the motor cortex and lower motor neurons in the brain stem and spinal cord. About 10% of ALS cases are familial, in 10-20% of these, mutations in the gene coding for superoxide dismutase 1 (SOD1) can be detected. Overexpression of mutated SOD1 in mice created animal models which clinically resemble ALS. Abnormalities in glutamatergic and GABAergic neurotransmission presumably contribute to the selective motor neuron damage in ALS. By in situ hybridization histochemistry (ISH), we investigated the spinal mRNA expression of the GABAA and AMPA type glutamate receptor subunits at different disease stages on spinal cord sections of mutant SOD1 mice and control animals overexpressing wild-type SOD1 aged 40, 80, 120 days and at disease end-stage, i.e. around 140 days) (n = 5, respectively). We detected a slight but statistically significant decrease of the AMPA receptor subunits GluR3 and GluR4 only in end stage disease animals.

Original languageEnglish
JournalJournal of the Neurological Sciences
Volume238
Issue number1-2
Pages (from-to)25-30
Number of pages6
ISSN0022-510X
DOIs
Publication statusPublished - 15.11.2005
Externally publishedYes

Research Areas and Centers

  • Centers: Center for Neuromuscular Diseases

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