許多甘氨酸突觸中γ-氨基丁酸與甘氨酸共存,。在2008年2月28日的《神經(jīng)元》（Neuron）封面文章中,，Lu等人證明了γ-氨基丁酸直接調(diào)節(jié)甘氨酸受體對甘氨酸的應(yīng)答響應(yīng),，從而產(chǎn)生適宜聽覺功能的快速抑制作用,。囊泡中同時(shí)包含強(qiáng)弱激動劑是進(jìn)行突觸后微調(diào)的作用機(jī)制。
神經(jīng)元放電模式是通過集中神經(jīng)興奮與抑制形成,，在程度和持續(xù)時(shí)間上都非常精確,。在聽覺腦干核里，甘氨酸抑制劑以其快速衰減動力學(xué)而著稱,，但作用機(jī)制一直不為人所知,。
在最新研究中，科學(xué)家通過甘氨酸與天然或重組的甘氨酸受體相互作用,，發(fā)現(xiàn)該作用的衰減時(shí)間是通過γ-氨基丁酸增加而增加的,，其中γ-氨基丁酸是甘氨酸受體的弱局部激動劑。激動劑接觸期間的系統(tǒng)變異顯示,，快速突觸時(shí)段可能是在亞毫秒級尺度上,，在生理濃度下與甘氨酸和γ-氨基丁酸的混合物接觸而達(dá)成。相應(yīng)地,，突觸前的終端一般包含兩個(gè)發(fā)送器,，通過耗盡γ-氨基丁酸的終端來減緩甘氨酸突觸電流。
因此,，與甘氨酸共釋放的γ-氨基丁酸,，通過直接作用于甘氨酸受體與縮短有效抑制的時(shí)間的方式來加速甘氨酸的傳遞。研究人員猜測,，也許將強(qiáng)弱激動劑包裹在囊泡中是一個(gè)普遍的方法,，通過這種方式突觸前神經(jīng)元可以調(diào)節(jié)突觸后的反應(yīng)持續(xù)時(shí)間。（科學(xué)網(wǎng) 武彥文/編譯）
生物谷推薦原始出處：
（Neuron）,，Vol 57, 524-535, 28 February 2008,，Tao Lu, Laurence O. Trussell
Glycinergic Transmission Shaped by the Corelease of GABA in a Mammalian Auditory Synapse
Tao Lu, Maria E. Rubio, and Laurence . Trussell
Summary
The firing pattern of neurons is shaped by the convergence of excitation and inhibition, each with finely tuned magnitude and duration. In an auditory brainstem nucleus, glycinergic inhibition features fast decay kinetics, the mechanism of which is unknown. By applying glycine to native or recombinant glycine receptors, we show that response decay times are accelerated by addition of GABA, a weak partial agonist of glycine receptors. Systematic variation in agonist exposure time revealed that fast synaptic time course may be achieved with submillisecond exposures to mixtures of glycine and GABA at physiological concentrations. Accordingly, presynaptic terminals generally contained both transmitters, and depleting terminals of GABA slowed glycinergic synaptic currents. Thus, coreleased GABA accelerates glycinergic transmission by acting directly on glycine receptors, narrowing the time window for effective inhibition. Packaging both weak and strong agonists in vesicles may be a general means by which presynaptic neurons regulate the duration of postsynaptic responses.
