近日，來自弗吉尼亞州立邦連大學(xué)（VCU）的研究者表示,，輕度的腦部損傷可以導(dǎo)致長達(dá)數(shù)日的大腦功能明顯異常，這就能解釋為什么因?yàn)檫\(yùn)動(dòng),、事故等引發(fā)的腦部損傷患者會(huì)出現(xiàn)神經(jīng)學(xué)上的某些癥狀。相關(guān)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(jīng)過創(chuàng)傷后的患者大腦結(jié)構(gòu)和功能性的改變,，這個(gè)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(dǎo)致患者出現(xiàn)長時(shí)間的神經(jīng)問題,，包括認(rèn)知過程緩慢、意識(shí)模糊,、慢性頭痛,、外傷性神經(jīng)癥以及抑郁癥。
由Kimberle M.Jacobs教授領(lǐng)導(dǎo)VCU的研究團(tuán)隊(duì)運(yùn)用高精尖的生物成像以及電生理學(xué)方法,，揭示了輕度的腦部損傷可以引起大腦軸突結(jié)構(gòu)性的破壞以及改變神經(jīng)元的運(yùn)動(dòng)方式,。軸突是大腦中的神經(jīng)纖維，負(fù)責(zé)在大腦中傳導(dǎo)電脈沖,，研究小組用輕度外傷性腦損傷模型進(jìn)行研究,，并且對大腦中活的外皮質(zhì)層的神經(jīng)元進(jìn)行形態(tài)學(xué)上的相關(guān)研究。
研究者的發(fā)現(xiàn)對于推動(dòng)該領(lǐng)域研究有極大幫助,，并且提供了一套生物成像和電生理學(xué)的方法來評估TBI的改變以及潛在的治療調(diào)節(jié)方法,，另外研究者也研究了是否重復(fù)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.
