Brain injury leads to an excitatory phase followed by an inhibitory phase in the brain. The clinical sequelae caused by cerebral injury seem to be a response to remote functional inhibition of cerebral nuclei located far from the motor cortex but anatomically related to the injury site. It appears that such functional inhibition is mediated by an increase in lipid peroxidation (LP). To test this hypothesis, we report data from 80 rats that were allocated to the following groups: the sham group (n = 40), in which rats received an intracortical infusion of artificial cerebrospinal fluid (CSF); the injury group (n = 20), in which rats received CSF containing ferrous chloride (FeCl₂, 50 mM); and the recovery group (n = 20), in which rats were injured and allowed to recover. Beam-walking, sensorimotor and spontaneous motor activity tests were performed to evaluate motor performance after injury. Lipid fluorescent products (LFPs) were measured in the pons. The total pontine contents of glutamate (GLU), glutamine (GLN) and gamma-aminobutyric acid (GABA) were also measured. In injured rats, the motor deficits, LFPs and total GABA and GLN contents in the pons were increased, while the GLU level was decreased. In contrast, in recovering rats, none of the studied variables were significantly different from those in sham rats. Thus, motor impairment after cortical injury seems to be mediated by an inhibitory pontine response, and functional recovery may result from a pontine restoration of the GLN–GLU–GABA cycle, while LP may be a primary mechanism leading to remote pontine inhibition after cortical injury.

脑损伤导致大脑进入兴奋期，然后进入抑制期。脑损伤引起的临床后遗症似乎是对远离运动皮层但在解剖学上与损伤部位相关的大脑核团的远程功能抑制的反应。这种功能性抑制似乎是由脂质过氧化（LP）的增加介导的。为了检验这一假设，我们报告了 80 只大鼠的数据，这些大鼠被分配到以下组： 假手术组 (n = 40)，其中大鼠接受皮质内输注人工脑脊液 (CSF)；损伤组（n = 20），其中大鼠接受含有氯化亚铁（FeCl ₂, 50 mM); 和恢复组（n = 20），其中大鼠受伤并允许恢复。进行平衡木行走、感觉运动和自发运动活动测试，以评估受伤后的运动表现。在脑桥中测量脂质荧光产物（LFP）。还测量了谷氨酸（GLU）、谷氨酰胺（GLN）和γ-氨基丁酸（GABA）的脑桥总含量。在受伤的大鼠中，脑桥中的运动缺陷、LFPs以及总GABA和GLN含量增加，而GLU水平降低。相比之下，在康复大鼠中，所研究的变量与假手术大鼠中的变量没有显着差异。因此，皮质损伤后的运动障碍似乎是由抑制性脑桥反应介导的，而功能恢复可能是由于 GLN-GLU-GABA 循环的脑桥恢复所致。