Inhibitory interneurons show early dysfunction in a SOD1 mouse model of amyotrophic lateral sclerosis

Author:

Cavarsan Clarissa F.12,Steele Preston R.123,Genry Landon T.123,Reedich Emily J.12,McCane Lynn M.3,LaPre Kay J.12,Puritz Alyssa C.4,Manuel Marin12,Katenka Natallia5,Quinlan Katharina A.124

Affiliation:

1. George and Anne Ryan Institute for Neuroscience University of Rhode Island Kingston RI USA

2. Department of Biomedical and Pharmaceutical Sciences College of Pharmacy University of Rhode Island Kingston RI USA

3. Interdisciplinary Neuroscience Program University of Rhode Island Kingston RI USA

4. Department of Physiology Northwestern University Feinberg School of Medicine Chicago IL USA

5. Department of Computer Science and Statistics University of Rhode Island Kingston RI USA

Funder

Target ALS

National Institute of Neurological Disorders and Stroke

Publisher

Wiley

Subject

Physiology

Reference82 articles.

1. Long‐term measurement of muscle denervation and locomotor behavior in individual wild‐type and ALS model mice;Akay T.;Journal of Neurophysiology,2014

2. Expression of the glycinergic system during the course of embryonic development in the mouse spinal cord and its co-localization with GABA immunoreactivity

3. Locomotor deficits in a mouse model of ALS are paralleled by loss of V1-interneuron connections onto fast motor neurons

4. Morphological differences between wild-type and transgenic superoxide dismutase 1 lumbar motoneurons in postnatal mice

5. Plasma glutamate and glycine levels in patients with amyotrophic lateral sclerosis;Andreadou E.;In Vivo,2008

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