Effect of interruption of bulbospinal pathways on lordosis, posture, and locomotion.

The effect of interruption of descending bulbospinal projections arising from (i) the medial medullary reticular formation: nucleus reticularis gigantocellularis (NGC) and nucleus reticularis magnocellularis (NMC), (ii) nucleus raphe magnus, and (iii) nucleus subceruleus on the lordosis reflex, posture, and locomotion was examined. After interruption of descending NGC-NMC fibers, time-dependent deficits in lordosis were observed during the first two postoperative weeks with subsequent reflex recovery. A syndrome of postural and locomotor deficits occurred after NGC-NMC lesions. Postoperatively, postural reflexes were dominated by increased extensor tone which resulted in limb hyperextension. Specific time-dependent deficits in the control of extensor and flexor muscle groups involved in locomotion resulted in a motor syndrome that is detailed. After interruption of NMC fibers alone, no postural or locomotor deficits occurred and effects on lordosis were limited to the first few postoperative days. The NMC data suggested that the majority of the functional deficits seen after NGC plus NMC lesions were due to destruction of the NGC descending projections. Interruption of NSC bulbospinal fibers resulted in a significant depletion of spinal cord noradrenaline (NA) but not serotonin (5-HT). Functional deficits, when present, were limited to the first few postoperative days. Although interruption of descending NRM fibers resulted in a significant depletion of spinal cord 5-HT concentrations, greater depletions occurred in the NGC plus NMC group. No functional deficits were observed in the NRM group. These data suggest that interruption of NGC-NMC fibers destroyed the descending output from neurons which integrate the hormonal and sensory information necessary for lordosis.