Facilitation of postural limb reflexes with epidural stimulation in spinal rabbits. / Musienko, P. E.; Zelenin, P. V.; Orlovsky, G. N.; Deliagina, T. G.
In: Journal of Neurophysiology, Vol. 103, No. 2, 02.2010, p. 1080-1092.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Facilitation of postural limb reflexes with epidural stimulation in spinal rabbits
AU - Musienko, P. E.
AU - Zelenin, P. V.
AU - Orlovsky, G. N.
AU - Deliagina, T. G.
PY - 2010/2
Y1 - 2010/2
N2 - It is known that after spinalization animals lose their ability to maintain lateral stability when standing or walking. A likely reason for this is a reduction of the postural limb reflexes (PLRs) driven by stretch and load receptors of the limbs. The aim of this study was to clarify whether spinal networks contribute to the generation of PLRs. For this purpose, first, PLRs were recorded in decerebrated rabbits before and after spinalization at T12. Second, the effects of epidural electrical stimulation (EES) at L7 on the limb reflexes were studied after spinalization. To evoke PLRs, the vertebrate column of the rabbit was fixed, whereas the hindlimbs were positioned on the platform. Periodic lateral tilts of the platform caused antiphase flexion - extension limbs movements, similar to those observed in intact animals keeping balance on the tilting platform. Before spinalization, these movements evoked PLRs: augmentation of extensor EMGs and increase of contact force during limb flexion, suggesting their stabilizing postural effects. Spinalization resulted in almost complete disappearance of PLRs. After EES, however, the PLRs reappeared and persisted for up to several minutes, although their values were reduced. The post-EES effects could be magnified by intrathecal application of quipazine (5-HT agonist) at L4 - L6. Results of this study suggest that the spinal cord contains the neuronal networks underlying PLRs; they can contribute to the maintenance of lateral stability in intact subjects. In acute spinal animals, these networks can be activated by EES, suggesting that they are normally activated by a tonic supraspinal drive.
AB - It is known that after spinalization animals lose their ability to maintain lateral stability when standing or walking. A likely reason for this is a reduction of the postural limb reflexes (PLRs) driven by stretch and load receptors of the limbs. The aim of this study was to clarify whether spinal networks contribute to the generation of PLRs. For this purpose, first, PLRs were recorded in decerebrated rabbits before and after spinalization at T12. Second, the effects of epidural electrical stimulation (EES) at L7 on the limb reflexes were studied after spinalization. To evoke PLRs, the vertebrate column of the rabbit was fixed, whereas the hindlimbs were positioned on the platform. Periodic lateral tilts of the platform caused antiphase flexion - extension limbs movements, similar to those observed in intact animals keeping balance on the tilting platform. Before spinalization, these movements evoked PLRs: augmentation of extensor EMGs and increase of contact force during limb flexion, suggesting their stabilizing postural effects. Spinalization resulted in almost complete disappearance of PLRs. After EES, however, the PLRs reappeared and persisted for up to several minutes, although their values were reduced. The post-EES effects could be magnified by intrathecal application of quipazine (5-HT agonist) at L4 - L6. Results of this study suggest that the spinal cord contains the neuronal networks underlying PLRs; they can contribute to the maintenance of lateral stability in intact subjects. In acute spinal animals, these networks can be activated by EES, suggesting that they are normally activated by a tonic supraspinal drive.
UR - http://www.scopus.com/inward/record.url?scp=76649123583&partnerID=8YFLogxK
U2 - 10.1152/jn.00575.2009
DO - 10.1152/jn.00575.2009
M3 - Article
C2 - 20018835
AN - SCOPUS:76649123583
VL - 103
SP - 1080
EP - 1092
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 2
ER -
ID: 92593338