Involvement of endoplasmic reticulum stress in the necroptosis ofmicroglia/macrophages after spinal cord injury.

Abstract—In decerebrate cats, the electromyogram (EMG)\nactivity of the forelimb extensor triceps brachii (TB) increases\nduring side-down roll tilt of the whole animal (vestibulospinal\nreflex, VSR) at about 0.15 Hz. (10°), while decreases\nduring side up tilt. On the other hand, the TB activity\nincreases during dorsal flexion of the ipsilateral forepaw\n(0.15 Hz, 5°–10°), but decreases during ventral flexion. In six\nexperiments, these stimuli were synergistically associated\n(side-down tilt coincided with dorsal flexion of the forepaw),\nso that the EMG modulation of the TB activity was greater\nthan that induced by the individual stimuli. During a 3-h\nperiod of this sustained stimulation, the amplitude of the pure\nVSR progressively increased to reach the maximum value at\nthe end of the third hour and persisted unmodified during the\npost-adaptation period (1 h). In three experiments, animal tilt\nand forepaw rotation were antagonistically associated (sidedown tilt coincided with ventral flexion of the forepaw). In these instances the VSR gain remained on the average stable, but, at the end of the 3-h period of combined stimulation, a proportion of TB responses to animal tilt howed a phase reversal. In a digitigrade animal like the cat, a dorsal flexion of the wrist is associated with a decrease in limb length and would occur when the extensor tone is not appropriate to support body weight; we propose, therefore, that somatosensory volleys elicited by wrist rotation modify the gain of VSR so as to maintain postural stability. Inactivation, on the side of muscle recording, of the corticocerebellar region which projects to the lateral vestibular nucleus of Deiters, by local microinjection of the GABA-A agonist muscimol (0.5 l at 16 g/l), decreased the already adapted gain of VSR. In conclusion, the results of this study suggest that somatosensory reafferent inputs to the cerebellar vermis are used to plastically modify the gain of VSR, when external forces produce changes in the final posture of the foot during animal tilt.