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Receptor alterations associated with spinal motoneuron degeneration in Bovine Akabane disease
Author(s) -
Gundlach Andrew L.,
Grabara Corrine S. G.,
Johnston Graham A. R.,
Harper Peter A. W.
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410270510
Subject(s) - amyotrophic lateral sclerosis , biology , neuroscience , anterior horn cell , strychnine , motor neuron , receptor , glycine receptor , spinal cord , anatomy , pathology , medicine , disease , glycine , biochemistry , amino acid
Akabane disease in cattle is characterized by congenital abnormalities including arthrogryposis, which is characterized by a depletion of spinal ventral horn motoneurons, a loss of axons, and depletion of myelin in the lateral and ventral tracts. These neuropathological changes produced major reductions (70–80%) in the density of muscarinic cholinergic, glycine/strychnine, and central‐type benzodiazepine receptors in the ventral horn motor nuclei. The density of peripheral‐type benzodiazepine receptors and adenosine A 1 receptors was dramatically increased (250–300%) in the lateral and ventral spinal columns, reflecting the proliferation of glial cells. Bovine Akabane disease represents a useful model for assessing the processes and consequences of neuronal degeneration and demyelination and has implications for human diseases such as amyotrophic lateral sclerosis.