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Benjamin R. Brooks, MD; W. David Lust, PhD; John M. Andrews, MD; W. King Engel, MD

Arch Neurol. 1978;35(9):590-591.

Abstract
• Of the secondary messengers, cyclic guanosine monophosphate, but not cyclic adenosine monophosphate, was reduced by 80% in the cervical spinal cord and by 56% in the cerebellum of clinically affected homozygote "wobbler" mice compared to sex- and age-matched litter-mate clinically unaffected control mice. A neurotransmitter, gamma aminobutyric acid, and high-energy intermediates, adenosine triphosphate and phosphocreatine, were not significantly different in affected or unaffected mice.

Author Affiliations
From the Medical Neurology Branch (Drs Brooks and Engel) and the Section on Cellular Neurochemistry (Dr Lust), Laboratory of Neurochemistry, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, Md; and the Department of Neurology, University of California School of Medicine, Los Angeles (Dr Andrews).

Footnotes
Accepted for publication Jan 24, 1978.

Reprint requests to Building 10, Room 10D18, Clinical Center, National Institutes of Health, Bethesda, MD 20014 (Dr Engel).

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