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Motoneuron′s Vulnerability to Spinal Cord Injury: Changes in Nitric Oxide Synthase and Parvalbumin Immunoreactivity, pp. 465-481 $100.00
Authors:  Nadežda Lukáčová, Alexandra Dávidová, Andrea Schreiberová, Ľudmila Capková, Jozef Radoňak, Malgorzata Chalimoniuk and Jozef Langfort
Abstract:
Spinal cord transection interrupts neuronal pathways which are responsible for
synaptic connections between upper motor neurons in the brain and brain stem, and
lower motor neurons within the spinal cord. In addition, primary afferent inputs provide
part of synaptic drive to motoneurons and thus influence the pattern of motor activity
generated within the spinal cord. One subset of afferent fibers are the large-diameter,
fast-conducting Ia afferent fibers originating from muscle spindles and forming the basis
of the monosynaptic stretch reflex. These fibers carry proprioceptive impulses from the
muscles into the spinal cord and help to perform movement and to keep orthostatism of
the body. Recent experimental data from our laboratory indicated the colocalization of
parvalbumin, the calcium-binding protein and nitric oxide synthase, producing nitric
oxide in proprioceptive Ia fibres in dorsal column of lumbar and sacral spinal cord. It is
known that supraspinal input into the spinal motoneurons and related interneurons may lead to gradual development of exaggerated tendon reflexes, increased muscle tone, and
involuntary muscle spasms, i.e. the symptoms of prominent spasticity. This chapter
provides a general review of motoneuron′s vulnerability to spinal cord injury. We
performed immunohistochemical investigation in order to determine whether or not
parvalbumin and nitric oxid synthase are involved in the degeneration of motor neurons
and discuss the changes of these proteins in neuronal circuitry that underlies tail-flick
reflex. 


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Motoneuron′s Vulnerability to Spinal Cord Injury: Changes in Nitric Oxide Synthase and Parvalbumin Immunoreactivity, pp. 465-481