摘要 : 美國(guó)加利福尼亞大學(xué)歐文分校的神經(jīng)科學(xué)家珍妮弗·切爾尼亞夫斯基和約翰·古佐夫斯基說(shuō)，大腦炎癥可以很快干擾我們提取類似但不同經(jīng)歷的復(fù)雜記憶的能力。他們的研究成果發(fā)表在美國(guó)《神經(jīng)科學(xué)學(xué)報(bào)》上。

美國(guó)加利福尼亞大學(xué)歐文分校的神經(jīng)科學(xué)家珍妮弗·切爾尼亞夫斯基和約翰·古佐夫斯基說(shuō)，大腦炎癥可以很快干擾我們提取類似但不同經(jīng)歷的復(fù)雜記憶的能力。

他們的研究成果發(fā)表在美國(guó)《神經(jīng)科學(xué)學(xué)報(bào)》上。該研究弄清了免疫系統(tǒng)如何示意稱為“細(xì)胞因子”的分子損害海馬體中神經(jīng)元之間的通信。海馬體是大腦中的一個(gè)區(qū)域，它對(duì)于分辨記憶很重要。該研究有助于人們認(rèn)識(shí)接受*的人和存在自身免疫疾病或神經(jīng)組織退化疾病的人出現(xiàn)認(rèn)知缺陷的原因。

古佐夫斯基說(shuō)：“我們的研究在免疫系統(tǒng)活化、神經(jīng)回路功能改變和受損的分辨記憶之間建立了。該研究的一些推論或許對(duì)多發(fā)性硬化癥等慢性疾病的患者有益。這類患者會(huì)出現(xiàn)記憶缺損。該研究甚至對(duì)癌癥患者也有好處。”

他認(rèn)為，一個(gè)有趣現(xiàn)象是，海馬體中“細(xì)胞因子”水平增加只會(huì)影響復(fù)雜分辨記憶，這種記憶能讓我們區(qū)分大致上類似的經(jīng)歷，例如我們?cè)诠ぷ鲿r(shí)做了什么或晚餐吃了什么。由海馬體處理的較簡(jiǎn)單的記憶形式——類似于記住你工作的地點(diǎn)——卻沒(méi)有因?yàn)榇竽X炎癥而改變。

該研究或許還能讓我們認(rèn)識(shí)*相關(guān)的心智現(xiàn)象——“*腦”。遭遇“*腦”問(wèn)題的癌癥患者會(huì)難以有效處理信息。歐文分校的神經(jīng)腫瘤學(xué)家發(fā)現(xiàn)，*會(huì)損害大腦中一些干細(xì)胞，這些干細(xì)胞本來(lái)會(huì)成長(zhǎng)為用于創(chuàng)建和儲(chǔ)存記憶的神經(jīng)元。

原文摘要：

Acute Neuroinflammation Impairs Context Discrimination Memory and Disrupts Pattern Separation Processes in Hippocampus

Jennifer Czerniawski and John F. Guzowski

Although it is known that immune system activation can impair cognition, no study to date has linked cognitive deficits during acute neuroinflammation to dysregulation of task-relevant neuronal ensemble activity. Here, we assessed both neural circuit activity and context discrimination memory retrieval, in a within-subjects design, of male rats given systemic administration of saline or lipopolysaccharide (LPS). Rats were exposed over several days to two similar contexts: one of which was paired with weak foot shock and the other was not. After reaching criteria for discriminative freezing, rats were given systemic LPS or saline injection and tested for retrieval of context discrimination 6 h later. Importantly, LPS administration produced an acute neuroinflammatory response in dorsal hippocampus at this time (as assessed by elevation of proinflammatory cytokine mRNA levels) and abolished retrieval of the previously acquired discrimination. The impact of neuroinflammation on hippocampal CA3 and CA1 neural circuit activity was assessed using theArc/Homer1a cellular analysis of temporal activity by fluorescence in situ hybridization imaging method. Whereas the saline-treated subjects discriminated and had low overlap of hippocampal ensembles activated in the two contexts, LPS-treated subjects did not discriminate and had greater ensemble overlap (i.e., reduced orthogonalization). Additionally, retrieval of standard contextual fear conditioning, which does not require context discrimination, was not affected by pretesting LPS administration. Together, the behavioral and circuit analyses data provide compelling evidence that LPS administration impairs context discrimination memory by disrupting cellular pattern separation processes within the hippocampus, thus linking acute neuroinflammation to disruption of specific neural circuitfunctions and cognitive impairment.