Innervation and properties of the rat FDSBQ muscle: an animal model to evaluate voluntary muscle strength after incomplete spinal cord injury.
Muscles innervated from spinal segments close to the site of a human spinal cord injury are often under voluntary control but are weak because they are partially paralyzed and partially denervated. Our objective was to develop an animal model of this clinical condition to evaluate strategies to improve voluntary muscle strength. To do so, we examined the spinal and peripheral innervation of the flexor digitorum superficialis brevis quinti (FDSBQ) muscle of the rat foot, characterized the muscle and motor unit properties, and located the FDSBQ motoneurons. Retrograde labeled motoneurons were in L4 to L6 spinal cord. Unilateral stimulation of L4 to S1 ventral roots and recording of evoked force showed that FDSBQ motor axons exited via two ventral roots (L5 and L6 or L6 and S1) in 38% of rats and via one ventral root in 62% of rats. FDSBQ motor axons traveled via two peripheral nerves, the lateral plantar (76% of axons) and sural nerves (24%). Each ventral root contributed motor axons to each nerve branch. Thus, by combining conduction block of one peripheral nerve to induce partial muscle paralysis and ventral root section to induce partial denervation, it is possible to produce in one rat muscle the consequences of many human cervical spinal cord injuries. FDSBQ muscles and motor units were mainly fast-twitch, fatigable, and composed of fast-type muscle fibers. The narrow range of motor unit forces (1-13 mN), the low mean twitch force (5.1 +/- 0.3 mN), and the large number of motoneurons (31 +/- 4) suggest that rat FDSBQ muscle is a good model of distal human musculature which is frequently influenced by spinal cord injury. We conclude that the FDSBQ muscle and its innervation provide a useful animal model in which to study the consequences of many spinal cord injuries which spare some descending inputs but also induce substantial motoneuron death near the lesion.
Thomas
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Department of Neurological Surgery, University of Miami School of Medicine, Miami, Florida, 33136, USA.
Esipenko
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V
Xu
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Madsen
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Gordon
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T
D000818:Animals; D001369:Axons / Q000502:physiology; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005071:Evoked Potentials; D005260:Female; D007839:Functional Laterality; D006614:Hindlimb; D006801:Humans; D009046:Motor Neurons / Q000502:physiology*; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000294:innervation* / Q000502:physiology / Q000503:physiopathology; D010243:Paralysis / Q000503:physiopathology*; D010525:Peripheral Nerves / Q000502:physiology / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D013126:Spinal Nerve Roots / Q000502:physiology* / Q000503:physiopathology; D013497:Sural Nerve / Q000502:physiology / Q000503:physiopathology