Functional plasticity in the respiratory drive to thoracic motoneurons in the segment above a chronic lateral spinal cord lesion
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Functional plasticity in the respiratory drive to thoracic motoneurons in the segment above a chronic lateral spinal cord lesion. / Ford, T W; Anissimova, Natalia P; Meehan, Claire Francesca; Kirkwood, P A.
In: Journal of Neurophysiology, Vol. 115, No. 1, 01.01.2016, p. 554-567.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Functional plasticity in the respiratory drive to thoracic motoneurons in the segment above a chronic lateral spinal cord lesion
AU - Ford, T W
AU - Anissimova, Natalia P
AU - Meehan, Claire Francesca
AU - Kirkwood, P A
N1 - Copyright © 2016 the American Physiological Society.
PY - 2016/1/1
Y1 - 2016/1/1
N2 - A previous neurophysiological investigation demonstrated an increase in functional projections of expiratory bulbospinal neurons (EBSNs) in the segment above a chronic lateral thoracic spinal cord lesion that severed their axons. We have now investigated how this plasticity might be manifested in thoracic motoneurons by measuring their respiratory drive and the connections to them from individual EBSNs. In anesthetized cats, simultaneous recordings were made intracellularly from motoneurons in the segment above a left-side chronic (16 wk) lesion of the spinal cord in the rostral part of T8, T9, or T10 and extracellularly from EBSNs in the right caudal medulla, antidromically excited from just above the lesion but not from below. Spike-triggered averaging was used to measure the connections between pairs of EBSNs and motoneurons. Connections were found to have a very similar distribution to normal and were, if anything (nonsignificantly), weaker than normal, being present for 42/158 pairs, vs. 55/154 pairs in controls. The expiratory drive in expiratory motoneurons appeared stronger than in controls but again not significantly so. Thus we conclude that new connections made by the EBSNs following these lesions were made to neurons other than α-motoneurons. However, a previously unidentified form of functional plasticity was seen in that there was a significant increase in the excitation of motoneurons during postinspiration, being manifest either in increased incidence of expiratory decrementing respiratory drive potentials or in an increased amplitude of the postinspiratory depolarizing phase in inspiratory motoneurons. We suggest that this component arose from spinal cord interneurons.
AB - A previous neurophysiological investigation demonstrated an increase in functional projections of expiratory bulbospinal neurons (EBSNs) in the segment above a chronic lateral thoracic spinal cord lesion that severed their axons. We have now investigated how this plasticity might be manifested in thoracic motoneurons by measuring their respiratory drive and the connections to them from individual EBSNs. In anesthetized cats, simultaneous recordings were made intracellularly from motoneurons in the segment above a left-side chronic (16 wk) lesion of the spinal cord in the rostral part of T8, T9, or T10 and extracellularly from EBSNs in the right caudal medulla, antidromically excited from just above the lesion but not from below. Spike-triggered averaging was used to measure the connections between pairs of EBSNs and motoneurons. Connections were found to have a very similar distribution to normal and were, if anything (nonsignificantly), weaker than normal, being present for 42/158 pairs, vs. 55/154 pairs in controls. The expiratory drive in expiratory motoneurons appeared stronger than in controls but again not significantly so. Thus we conclude that new connections made by the EBSNs following these lesions were made to neurons other than α-motoneurons. However, a previously unidentified form of functional plasticity was seen in that there was a significant increase in the excitation of motoneurons during postinspiration, being manifest either in increased incidence of expiratory decrementing respiratory drive potentials or in an increased amplitude of the postinspiratory depolarizing phase in inspiratory motoneurons. We suggest that this component arose from spinal cord interneurons.
KW - Animals
KW - Cats
KW - Female
KW - Laminectomy
KW - Male
KW - Medulla Oblongata
KW - Motor Neurons
KW - Neural Pathways
KW - Neuronal Plasticity
KW - Respiration
KW - Spinal Cord
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1152/jn.00614.2015
DO - 10.1152/jn.00614.2015
M3 - Journal article
C2 - 26490290
VL - 115
SP - 554
EP - 567
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 1
ER -
ID: 176952331