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