Brain injury-induced neurological deficits typically develop on the contralateral side of the body and include abnormal posture, motor weakness, and spasticity. It is believed that the interruption of descending neural pathways that convey supraspinal commands to the motoneurons in the spinal cord is the main cause of these deficits. This long-standing paradigm was challenged by our recent findings: a unilateral injury of the hindlimb sensorimotor cortex of rats with prior complete transection of the spinal cord produced hindlimb postural asymmetry (HL-PA), asymmetric hindlimb withdrawal reflexes, and asymmetry in gene expression patterns in the lumbar spinal cord (Figure 1; Lukoyanov et al., 2021). Strikingly, the contralateral hindlimb was flexed as usually seen in rats with intact spinal cord after brain injury. Hypophysectomy abolished the injury-induced effects, whereas hindlimb postural asymmetry was induced by serum from animals with brain injury transfused into animals with the intact brains. Arg-vasopressin and β-endorphin, two pituitary neurohormones, induced the right side hindlimb responses in naïve animals, while their antagonists blocked HL-PA in rats with the left-brain injury. Thus, in addition to motor pathways descending from the brain to spinal circuits, the side-specific humoral signaling mediates the effects of unilateral brain injury (UBI) on hindlimb posture and reflex asymmetries.
- Brain injury, postural asymmetry, motor deficits
- postural asymmetry,
- motor deficits
- ntergenerational transmission