Responses of axotomized afferents to blockade of nitric oxide synthesis after spinal nerve lesion in the rat

• Published in: Neuroscience letters Vol. 254; no. 1; pp. 33 - 36
• Main Authors: Häbler, Heinz-Joachim, Liu, Xianguo, Eschenfelder, Sebastian, Jänig, Wilfrid
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 18.09.1998; Elsevier
• Subjects: Animals; Axotomy; Biological and medical sciences; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction; Disease Models, Animal; Ganglia, Spinal - blood supply; Ganglia, Spinal - physiology; Male; Medical sciences; Nerve lesion; Nervous system (semeiology, syndromes); Neurology; Neurons, Afferent - physiology; Neuropathic pain; Nitric oxide; Nitric Oxide - antagonists & inhibitors; Nitric Oxide - biosynthesis; Primary afferent neuron; Rat; Rats; Rats, Wistar; Spinal Nerves - physiology; Rat; Primary afferent neuron; Nerve lesion; Nitric oxide; Neuropathic pain; Animal model; Nervous system diseases; Enzyme; Rodentia; Biosynthesis; Peripheral neuropathy; Spinal nerve; Nitric-oxide synthase; Vertebrata; Axotomy; Mammalia; Oxidoreductases; Lesion
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(98)00647-8

Lesioned afferents were tested for their responses to blockade of nitric oxide synthesis in the spinal nerve L5 lesion model for neuropathic pain in Wistar rats. Seven single fibers with spontaneous activity split from dorsal root L5 showed no response after non-selective blockade of nitric oxide synthesis with N G-nitro- l-arginine methyl ester whereas five were excited after 5–7 min. Three previously silent units were recruited. Blood flow in the dorsal root ganglion decreased. None of fifteen axotomized afferents tested responded to selective blockade of neuronal nitric oxide synthesis with 7-nitroindazole. It is concluded that neuronal nitric oxide is not involved in the generation of spontaneous activity in axotomized afferent neurons in this model. We suggest that the vasoconstriction induced by blockade of endothelial nitric oxide may be responsible for the excitatory responses.