位于每個(gè)神經(jīng)纖維根部的“軸突起始段” (AIS)（在那里,，成簇的鈉通道產(chǎn)生動(dòng)作勢(shì),，后者隨后沿軸突傳播）,，是從事神經(jīng)可激發(fā)性之性質(zhì)研究的神經(jīng)科學(xué)家的關(guān)注焦點(diǎn),。作為一個(gè)神經(jīng)脈沖的來(lái)源,，它似乎是調(diào)控神經(jīng)活動(dòng)的一個(gè)邏輯點(diǎn)。本期Nature上兩篇論文證實(shí),，AIS是一個(gè)內(nèi)在的神經(jīng)彈性來(lái)源,。
生物谷啟用新域名 www.bioon.net
Matthew Grubb 和 Juan Burrone發(fā)現(xiàn)，電活動(dòng)可逆地改變AIS在培養(yǎng)的海馬神經(jīng)元中的位置,。他們提出，由此所導(dǎo)致的內(nèi)在可激發(fā)性的增加在發(fā)育過(guò)程中可能會(huì)微調(diào)神經(jīng)可激發(fā)性,，同時(shí)也為癲癇的控制指出了潛在目標(biāo),。Hiroshi Kuba、Yuki Oichi 和Harunori Ohmori發(fā)現(xiàn),，在消除了聲音刺激的鳥聽覺(jué)神經(jīng)元中,，AIS的尺寸增加。同樣,，內(nèi)在可激發(fā)性會(huì)增加,、并且可能有助于聽覺(jué)通道的維持。這樣的神經(jīng)彈性也許可補(bǔ)償某些形式的失聰,。（生物谷Bioon.net）
生物谷推薦原文出處：
Nature doi:10.1038/nature09160
Activity-dependent relocation of the axon initial segment fine-tunes neuronal excitability
Matthew S. Grubb& Juan Burrone
In neurons, the axon initial segment (AIS) is a specialized region near the start of the axon that is the site of action potential initiation1, 2, 3, 4, 5, 6. The precise location of the AIS varies across and within different neuronal types7, 8, and has been linked to cells’ information-processing capabilities8; however, the factors determining AIS position in individual neurons remain unknown. Here we show that changes in electrical activity can alter the location of the AIS. In dissociated hippocampal cultures, chronic depolarization with high extracellular potassium moves multiple components of the AIS, including voltage-gated sodium channels, up to 17?μm away from the soma of excitatory neurons. This movement reverses when neurons are returned to non-depolarized conditions, and depends on the activation of T- and/or L-type voltage-gated calcium channels. The AIS also moved distally when we combined long-term LED (light-emitting diode) photostimulation with sparse neuronal expression of the light-activated cation channel channelrhodopsin-2; here, burst patterning of activity was successful where regular stimulation at the same frequency failed. Furthermore, changes in AIS position correlate with alterations in current thresholds for action potential spiking. Our results show that neurons can regulate the position of an entire subcellular structure according to their ongoing levels and patterns of electrical activity. This novel form of activity-dependent plasticity may fine-tune neuronal excitability during development.
