近日,，來自弗吉尼亞州立邦連大學（VCU）的研究者表示,，輕度的腦部損傷可以導致長達數日的大腦功能明顯異常,，這就能解釋為什么因為運動、事故等引發(fā)的腦部損傷患者會出現(xiàn)神經學上的某些癥狀,。相關研究成果刊登在了5月份的雜志Journal of Neuroscience上,。
研究者致力于外傷性腦部損傷研究（TBI），研究者試圖去理解并研究經過創(chuàng)傷后的患者大腦結構和功能性的改變,，這個問題目前研究者并不清楚,。以前的研究表明，輕度的外傷腦部損傷可以導致患者出現(xiàn)長時間的神經問題,，包括認知過程緩慢,、意識模糊,、慢性頭痛、外傷性神經癥以及抑郁癥,。
由Kimberle M.Jacobs教授領導VCU的研究團隊運用高精尖的生物成像以及電生理學方法,，揭示了輕度的腦部損傷可以引起大腦軸突結構性的破壞以及改變神經元的運動方式。軸突是大腦中的神經纖維,，負責在大腦中傳導電脈沖,，研究小組用輕度外傷性腦損傷模型進行研究，并且對大腦中活的外皮質層的神經元進行形態(tài)學上的相關研究,。
研究者的發(fā)現(xiàn)對于推動該領域研究有極大幫助,，并且提供了一套生物成像和電生理學的方法來評估TBI的改變以及潛在的治療調節(jié)方法，另外研究者也研究了是否重復性的腦部損傷可以加重原先的腦部異常等癥狀,。（生物谷：T.Shen編譯）
doi:10.1523/JNEUROSCI.0881-12.2012
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Electrophysiological Abnormalities in Both Axotomized and Nonaxotomized Pyramidal Neurons following Mild Traumatic Brain Injury
John E. Greer, John T. Povlishock, and Kimberle M. Jacobs
Mild traumatic brain injury (mTBI) often produces lasting detrimental effects on cognitive processes. The mechanisms underlying neurological abnormalities have not been fully identified, in part due to the diffuse pathology underlying mTBI. Here we employ a mouse model of mTBI that allows for identification of both axotomized and intact neurons in the living cortical slice via neuronal expression of yellow fluorescent protein. Both axotomized and intact neurons recorded within injured cortex are healthy with a normal resting membrane potential, time constant (τ), and input resistance (Rin). In control cortex, 25% of cells show an intrinsically bursting action potential (AP) firing pattern, and the rest respond to injected depolarizing current with a regular-spiking pattern. At 2 d postinjury, intrinsic bursting activity is lost within the intact population. The AP amplitude is increased and afterhyperpolarization duration decreased in axotomized neurons at 1 and 2 d postinjury. In contrast, intact neurons also show these changes at 1 d, but recover by 2 d postinjury. Two measures suggest an initial decrease in excitability in axotomized neurons followed by an increase in excitability within intact neurons. The rheobase is significantly increased in axotomized neurons at 1 d postinjury. The slope of the plot of AP frequency versus injected current is larger for intact neurons at 2 d postinjury. Together, these results demonstrate that intact and axotomized neurons are both affected by mTBI, resulting in different changes in neuronal excitability that may contribute to network dysfunction following TBI.
