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Zinc status and peripheral nerve function in guinea pigs.

B L O'Dell¹, J Conley-Harrison, C Besch-Williford

¹Department of Biochemistry, University of Missouri, Columbia 65211.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|August 1, 1990

Summary

Zinc deficiency in guinea pigs causes neurological signs and impaired nerve conduction velocity (NCV). This study reveals reduced Na,K-ATPase activity in peripheral nerves, offering a model for neuropathy research.

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Area of Science:

Neuroscience
Biochemistry
Nutritional Science

Background:

Zinc deficiency can lead to neurological symptoms in guinea pigs.
These symptoms include abnormal posture, locomotion, and hypersensitivity.

Purpose of the Study:

To investigate the electrophysiological and biochemical basis of neuropathy in zinc-deficient guinea pigs.
To correlate nerve function with clinical signs and identify specific molecular defects.

Main Methods:

Electrophysiological measurements (nerve conduction velocity) in vivo and in vitro.
Biochemical assays of Na,K-ATPase activity and sodium channel binding (saxitoxin).
Comparison between zinc-deficient, repleted, and control guinea pigs.

Main Results:

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Zinc-deficient guinea pigs exhibited decreased motor nerve conduction velocity (NCV).
A strong correlation was observed between reduced NCV and the severity of clinical neurological signs.
Nerves from deficient animals showed decreased Na,K-ATPase activity, but sodium channel numbers remained unaffected.

Conclusions:

Neuropathy in zinc deficiency is linked to impaired peripheral nerve conduction velocity.
Reduced Na,K-ATPase activity is a key biochemical defect contributing to this neuropathy.
The zinc-deficient guinea pig serves as a valuable model for studying peripheral neuropathies.