生物谷：一直以來，科學(xué)家認(rèn)為大腦神經(jīng)軸突（axon）的作用只是用來在腦細(xì)胞間傳遞信號,。美國科學(xué)家近日研究發(fā)現(xiàn)，神經(jīng)軸突的作用不僅僅限于傳遞信號,，在適當(dāng)?shù)拇碳は?，它還可以加強(qiáng)或減弱信號的作用。該發(fā)現(xiàn)有望為精神分裂癥等精神病患者帶來福音,。相關(guān)論文在線發(fā)表于8月19日的《自然—神經(jīng)學(xué)》上,。
該項(xiàng)研究由加州大學(xué)歐文分校聽覺研究中心的神經(jīng)生物學(xué)副教授Raju Metherate領(lǐng)導(dǎo)完成。起初,，他和研究小組想確定的是,，煙堿（nicotine）改變了在大腦池體（cell body）中處理的信息，但是,，一系列的實(shí)驗(yàn)失敗使他們將研究重點(diǎn)轉(zhuǎn)向了神經(jīng)軸突,。研究小組檢測了小鼠大腦中與聽覺有關(guān)的區(qū)域，該區(qū)域的腦細(xì)胞通過神經(jīng)軸突與大腦皮層相連,。他們用煙堿刺激神經(jīng)軸突,，以確定它怎樣影響信號在腦細(xì)胞和大腦皮層之間的傳遞。結(jié)果發(fā)現(xiàn),，如果不使用煙堿,，腦細(xì)胞發(fā)出的信號大約有35％到達(dá)了大腦皮層；如果使用煙堿,，這一數(shù)字則大約為70％,。
Metherate表示，迄今為止,，科學(xué)家一直認(rèn)為在大腦皮層中,，信號僅僅只在池體中進(jìn)行加工處理。此次的研究表明,，神經(jīng)軸突也是一個(gè)處理信息的地方,。他說：“我們過去以為神經(jīng)軸突就像廣播電線一樣，用來傳輸信號。但是現(xiàn)在發(fā)現(xiàn),，如果你刺激神經(jīng)軸突,，信號就會發(fā)生改變，就像廣播調(diào)頻一樣,。”他認(rèn)為,，煙堿的作用可能在于激活了神經(jīng)軸突上的相關(guān)蛋白。而此次的發(fā)現(xiàn)可以說是一種關(guān)于大腦工作方式的全新理念,。
此次研究具有重要的實(shí)踐意義,。比如精神分裂等精神病一直被認(rèn)為是由于大腦不同部位交流紊亂造成的，此次研究將有助于為這些患者提供有效治療手段,。（科學(xué)網(wǎng) 梅進(jìn)/編譯）
原始出處:
Published online: 19 August 2007; | doi:10.1038/nn1956
Nicotinic control of axon excitability regulates thalamocortical transmission
Hideki Kawai, Ronit Lazar & Raju Metherate
Department of Neurobiology and Behavior and Center for Hearing Research, University of California, Irvine, 2205 McGaugh Hall, Irvine, California 92697-4550, USA.
Correspondence should be addressed to Raju Metherate [email protected]
The thalamocortical pathway, a bundle of myelinated axons that arises from thalamic relay neurons, carries sensory information to the neocortex. Because axon excitation is an obligatory step in the relay of information from the thalamus to the cortex, it represents a potential point of control. We now show that, in adult mice, the activation of nicotinic acetylcholine receptors (nAChRs) in the initial portion of the auditory thalamocortical pathway modulates thalamocortical transmission of information by regulating axon excitability. Exogenous nicotine enhanced the probability and synchrony of evoked action potential discharges along thalamocortical axons in vitro, but had little effect on synaptic release mechanisms. In vivo, the blockade of nAChRs in the thalamocortical pathway reduced sound-evoked cortical responses, especially those evoked by sounds near the acoustic threshold. These data indicate that endogenous acetylcholine activates nAChRs in the thalamocortical pathway to lower the threshold for thalamocortical transmission and to increase the magnitude of sensory-evoked cortical responses. Our results show that a neurotransmitter can modulate sensory processing by regulating conduction along myelinated thalamocortical axons.
