title: [Induction of noradrenergic supersensitivity following cordotomy in neonatal rat spinal motoneurons].
abstract: Patients with spinal cord lesions frequently show autonomic hyperreflexia. The mechanism of autonomic hyperreflexia has been thought to be an acute general autonomic overactivity in response to cutaneous or visceral stimuli, but it remains uncertain. Several kinds of experiments suggest that amplified spinal sympathetic reflexes in the decentralized cord are attributable to the denervation supersensitivity of denervated neurons, which is a well-known phenomenon in denervated muscle fibers. In the present study, changes in the supersensitivity of motoneurons after cordotomy were studied in the spinal cord of neonatal rats. Responses to bath-applied noradrenaline (NA) were recorded from a ventral root of the isolated spinal cord of 6-day-old rats. In normal spinal cords, NA induced depolarization in motoneurons dose-dependently. alpha 1-antagonist prazosin (3 microM) inhibited the deporalization induced by NA, and alpha 2-antagonist rauwolscine (1 microM) potentiated it. In one group of rats, cordotomy was performed 4 days after birth by complete transection of the spinal cord at vertebrate 8th-10th thoracic level, and NA response was examined two days later (when they were 6 days old). In cordotomized rats, NA-induced depolarization was increased with respect to both amplitude and duration. alpha 1- as well as alpha 2-antagonists inhibited the NA response in the spinalized rats. Especially, both antagonists shortened the duration of NA response as compared to normal level. It is concluded that the denervation supersensitivity to NA appears 2 days after cordotomy in the spinal motoneurons of neonatal rats and that the supersensitivity to NA is attributable to the upregulation of both alpha 1- and alpha 2-adrenoceptors on the motoneurons, indicating that a new type of alpha 2-adrenoceptor function appears.
authors: Department of Anesthesiology, Nippon Medical School, Tokyo, Japan.
authors: H
authors: H
authors: Kadotani
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001342:Autonomic Nervous System Diseases / Q000209:etiology; D002818:Cordotomy; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D009046:Motor Neurons / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology*; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D018340:Receptors, Adrenergic, alpha-1 / Q000187:drug effects / Q000378:metabolism; D018341:Receptors, Adrenergic, alpha-2 / Q000187:drug effects / Q000378:metabolism; D012021:Reflex, Abnormal; D015854:Up-Regulation; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D015016:Yohimbine; D009638:Norepinephrine; D011224:Prazosin