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Related Experiment Videos

Electrophysiological studies with the spastic mutant mouse

A H Heller, M Hallett

    Brain Research
    |February 25, 1982
    PubMed
    Summary

    Genetically spastic mice show abnormal muscle activity. This study suggests a deficiency in spinal cord inhibition may cause these spasticity symptoms.

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    Recent developments in our understanding of motor control, corticomotoneuronal connections and the activation of motoneurons and motoneuronal pools.

    Supplements to Clinical neurophysiology·2003

    Area of Science:

    • Neuroscience
    • Genetics
    • Physiology

    Background:

    • The genetically spastic mouse (spa) is an autosomal recessive mutant.
    • Spastic homozygotes display abnormal electromyographic (EMG) activity.

    Purpose of the Study:

    • To investigate the neurophysiological basis of spasticity in the spa mouse model.
    • To explore the role of spinal cord pathways in the observed motor abnormalities.

    Main Methods:

    • Electromyographic (EMG) recordings were performed on spastic mice and control littermates.
    • Electrical stimulation of limbs was used to elicit responses.
    • Pharmacological agents (strychnine, picrotoxinin) were administered to normal mice.

    Main Results:

    • Spastic mice exhibited high-amplitude, repetitive EMG bursts during spontaneous activity.
    • Electrical stimulation evoked stereotyped EMG bursts in contralateral limbs of spastic mice, absent in controls.
    • Strychnine administration in normal mice mimicked the behavioral and EMG features of spastic homozygotes.

    Conclusions:

    • The spastic mouse phenotype is associated with abnormal spinal cord neuronal activity.
    • Symptoms suggest a potential deficiency in strychnine-sensitive inhibitory pathways, likely glycinergic, in the spinal cord.

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