PDF(Pubmed)
Abstract：
Due to the assumed plasticity of immature brain, early in life brain alterations are thought to lead to better recoveries in comparison to the mature brain. Despite clinical needs, how neuronal networks and associated behaviors are affected by early in life brain stresses, such as pediatric concussions, have been overlooked. Here we provide first evidence in mice that a single early in life concussion durably increases neuronal activity in the somatosensory cortex into adulthood, disrupting neuronal integration while the animal is performing sensory-related tasks. This represents a previously unappreciated clinically relevant mechanism for the impairment of sensory-related behavior performance. Furthermore, we demonstrate that pharmacological modulation of the endocannabinoid system a year post-concussion is well-suited to rescue neuronal activity and plasticity, and to normalize sensory-related behavioral performance, addressing the fundamental question of whether a treatment is still possible once post-concussive symptoms have developed, a time-window compatible with clinical treatment.
摘要：
由于未成熟大脑的可塑性，与成熟的大脑相比，生命早期的大脑改变被认为会导致更好的恢复。尽管有临床需要,神经元网络和相关行为如何受到生命早期大脑压力的影响，比如小儿脑震荡，被忽视了。在这里，我们在小鼠中提供了第一个证据，即生命早期的脑震荡可以持久地增加体感皮层到成年期的神经元活动，在动物执行与感觉相关的任务时破坏神经元整合。这代表了先前未被理解的与感官相关的行为表现受损的临床相关机制。此外，我们证明脑震荡后一年内源性大麻素系统的药理调节非常适合挽救神经元活动和可塑性，并规范与感官相关的行为表现，解决了一个基本问题，即一旦出现脑震荡后症状，是否仍然可以进行治疗，与临床治疗相容的时间窗。
