Crossed reciprocal inhibition evoked by electrical stimulation of the lamprey spinal cord

Citation
P. Fagerstedt et al., Crossed reciprocal inhibition evoked by electrical stimulation of the lamprey spinal cord, EXP BRAIN R, 134(2), 2000, pp. 147-154
Citations number
51
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL BRAIN RESEARCH
ISSN journal
00144819 → ACNP
Volume
134
Issue
2
Year of publication
2000
Pages
147 - 154
Database
ISI
SICI code
0014-4819(200009)134:2<147:CRIEBE>2.0.ZU;2-6
Abstract
Activation of a motoneuron pool is often accompanied by inhibition of the a ntagonistic pool through a system of reciprocal inhibition between the two parts of the neuronal network controlling the antagonistic pools. In the pr esent study, we describe the activity of such a system in the isolated spin al cord of the lamprey, when a tonic motel output is evoked by extracellula r stimulation (0.5-1 s train of pulses, 20 Hz) of either end of the spinal cord. With two electrodes symmetrically positioned in relation to the midli ne, stimulation with either of them separately elicited prolonged (1-5 s) i psilateral ventral root activity. Activity could be abolished by stronger, simultaneously applied, stimulation of the contralateral side of the cord, suggesting that reciprocal inhibition between hemisegments operates when a tonic motor output is generated. Simultaneous stimulation of both sides of the spinal cord with a single electrode with a large tip (300-400 mu m in d iameter), positioned over the anatomical midline, elicited inconsistent rig ht-side, left-side, or bilateral ventral root responses. A minor displaceme nt (10-20 mu m) to the left or right from the mid line resulted in activati on of ipsilateral motoneurons, whereas the contralateral motoneurons were s ilent. These findings indicate that a small asymmetry in the excitatory dr ive to the left and right spinal hemisegments can be further amplified by r eciprocal inhibition between the hemisegments. Longitudinal splitting of th e spinal cord along the midline resulted in reduced reciprocal inhibition b etween the hemisegments separated by the lesion. The reduction was proporti onal to the extent of the split. The inhibition was abolished when the spli t reached nine segments in length. From these experiments, the longitudinal distribution of the commissural axons responsible for inhibition of contra lateral motor output could be estimated.