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This Article Full Text Full Text (PDF) All Versions of this Article: 100/2/723    most recent 90218.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Lyalka, V. F. Articles by Deliagina, T. G. PubMed PubMed Citation Articles by Lyalka, V. F. Articles by Deliagina, T. G.

Effect of Intrathecal Administration of Serotoninergic and Noradrenergic Drugs on Postural Performance in Rabbits With Spinal Cord Lesions

¹Department of Neuroscience, Karolinska Institute, Stockholm, Sweden; and ²Pavlov Institute of Physiology, St. Petersburg, Russia

Submitted 1 February 2008; accepted in final form 16 May 2008

Our previous studies have shown that extensive spinal lesions at T₁₂ in the rabbit [ventral hemisection (VHS) or 3/4-section that spares one ventral quadrant (VQ)] severely damaged the postural system. When tested on the platform periodically tilted in the frontal plane, VHS and VQ animals typically were not able to perform postural corrective movements by their hindlimbs, although EMG responses (correctly or incorrectly phased) could be observed. We attempted to restore postural control in VHS and VQ rabbits by applying serotoninergic and noradrenergic drugs to the spinal cord below the lesion through the intrathecal cannula. It was found that serotonin and quipazine (5-HT_1,2,3 agonist) did not re-establish postural corrective movements. However, when applied during a 10-day period after lesion, these drugs produced a twofold increase of the proportion of correct EMG responses to tilts. It was also found that methoxamine (₁ noradrenergic agonist), as well as the mixture of methoxamine and quipazine, did not re-establish postural corrective movements and did not increase the proportion of correct EMG responses. Serotonin (at later stages) and methoxamine induced periodical bursting in EMGs, suggesting activation of spinal rhythm-generating networks. Appearance of bursting seems to perturb normal operation of postural mechanisms, as suggested by methoxamine-induced abolishment of postural effects of quipazine. When applied in an intact animal, none of the tested drugs affected the value of postural corrections or evoked periodical bursting. We conclude that activation of the serotoninergic system (but not the noradrenergic one) causes selective enhancement of spinal postural reflexes during the earlier postlesion period.