加利福尼大學歐文分校的研究人員發(fā)現(xiàn),，持續(xù)幾個小時的短時間壓力就可以損害大腦中與學習和記憶有關(guān)區(qū)域腦細胞的溝通,。
據(jù)每日科學報道，以往人們知道,，持續(xù)幾周或幾個月的嚴重壓力可損傷大腦學習和記憶區(qū)域中細胞的通信交流,，但這次研究首次提出了短時間壓力會產(chǎn)生相似影響的證據(jù)。
“壓力在我們生活中常見,，不可避免,。” 加利福尼大學歐文醫(yī)學院神經(jīng)學主任泰利Z.巴拉姆博士說。“我們這一發(fā)現(xiàn)為當前開發(fā)預防這種不良影響的藥物起到重要作用,，也有助于了解為什么有些人在壓力狀態(tài)下健忘或者很難記住一些事情,。”
在這項研究中，巴拉姆和同事發(fā)現(xiàn)了壓力產(chǎn)生這種作用的一個新的途徑,。他們發(fā)現(xiàn),，與其說是壓力激素皮質(zhì)醇產(chǎn)生了這種作用，倒不如說是巨大的壓力激活了促腎上腺素釋放激素（CRH）破壞了大腦的連接和儲存記憶的過程,。
學習和記憶與突觸有關(guān),。腦細胞通過突觸進行通信交流。這些突觸呈特殊的枝狀突起在神經(jīng)元上,，稱作樹突棘,。
在對小鼠的研究中發(fā)現(xiàn)，大腦中的主要學習和記憶中樞海馬釋放CRH導致了這些樹突棘的快速蛻變,，從而削弱了突觸的結(jié)合力和儲存記憶的能力,。
研究發(fā)現(xiàn)，抑制CRH與受體的相互作用就可以消除壓力對海馬細胞中與學習和記憶有關(guān)的樹突棘的損害。
此外,，研究人員用低劑量的合成CRH替換壓力對樹突棘的作用,，觀察樹突棘的恢復情況。“一旦去掉CRH,，樹突棘似乎又恢復了原來情況,。”巴拉姆說。
巴拉姆還說,，有一些可以抑制CRH受體的藥物正在開發(fā)中,，這項研究將在把這些藥物用于壓力相關(guān)的學習和記憶力喪失的治療上發(fā)揮重要作用。
這項研究發(fā)表在3月12日出版的《神經(jīng)學雜志》（The Journal of Neuroscience）上,。（來源：中國公眾科技網(wǎng)）
生物谷推薦原始出處：
（The Journal of Neuroscience）,，28(11):2903-2911，Yuncai Chen,，Tallie Z. Baram
Rapid Loss of Dendritic Spines after Stress Involves Derangement of Spine Dynamics by Corticotropin-Releasing Hormone
Yuncai Chen,1 Céline M. Dubé,1 Courtney J. Rice,2 and Tallie Z. Baram1,2
Departments of 1Pediatrics and 2Anatomy/Neurobiology, University of California Irvine, Irvine, California 92697-4475
Correspondence should be addressed to Dr. Tallie Z. Baram, Departments of Pediatrics and Anatomy/Neurobiology, University of California Irvine, Medical Sciences I, ZOT: 4475, Irvine, CA 92697-4475. Email: [email protected]
Chronic stress causes dendritic regression and loss of dendritic spines in hippocampal neurons that is accompanied by deficits in synaptic plasticity and memory. However, the responsible mechanisms remain unresolved. Here, we found that within hours of the onset of stress, the density of dendritic spines declined in vulnerable dendritic domains. This rapid, stress-induced spine loss was abolished by blocking the receptor (CRFR1) of corticotropin-releasing hormone (CRH), a hippocampal neuropeptide released during stress. Exposure to CRH provoked spine loss and dendritic regression in hippocampal organotypic cultures, and selective blockade of the CRFR1 receptor had the opposite effect. Live, time-lapse imaging revealed that CRH reduced spine density by altering dendritic spine dynamics: the peptide selectively and reversibly accelerated spine retraction, and this mechanism involved destabilization of spine F-actin. In addition, mice lacking the CRFR1 receptor had augmented spine density. These findings support a mechanistic role for CRH–CRFR1 signaling in stress-evoked spine loss and dendritic remodeling.
