當哺乳動物幼體脫離溫暖的母體,，來到一個陌生環(huán)境后，幼體在呼吸方面如何適應(yīng)這種突然轉(zhuǎn)變呢,？法國科研人員日前在老鼠身上檢驗出一種基因,，它能夠幫助新生幼鼠用肺呼吸。研究人員認為,，這正是哺乳動物出生后存活的關(guān)鍵所在,。
法國國家科研中心等機構(gòu)的研究人員在新一期法國《神經(jīng)學(xué)雜志》上報告說,，哺乳動物的胎兒都處在液體環(huán)境里并通過臍帶獲得氧，因此在出生前,，胎兒的肺部功能基本沒有,。此前的研究認為，哺乳動物幼體之所以一離開母體就能適應(yīng)環(huán)境,，主要得益于幾個神經(jīng)元回路,，其作用仿佛心臟起搏器，能夠激活呼吸系統(tǒng),，這樣幼體就能在出生后很快開始自主呼吸,。
法國國家科研中心的專家則近一步發(fā)現(xiàn)，一種名為TSHZ3的蛋白質(zhì)在神經(jīng)元的活動中發(fā)揮了關(guān)鍵作用,。實驗顯示,，如果老鼠幼崽細胞內(nèi)編碼合成TSHZ3蛋白質(zhì)的基因無法表達，那么小老鼠就會在出生幾分鐘后窒息而亡,。
未來,，法國科研人員希望深入了解TSHZ3蛋白質(zhì)編碼基因在呼吸系統(tǒng)障礙中發(fā)揮的作用，從而為睡眠窒息及相關(guān)醫(yī)學(xué)難題找到解決之道,。(生物谷Bioon.com)
生物谷推薦原文出處：
The Journal of Neuroscience doi:10.1523/JNEUROSCI.1765-10.2010
Teashirt 3 Regulates Development of Neurons Involved in Both Respiratory Rhythm and Airflow Control
Xavier Caubit,1,4 Muriel Thoby-Brisson,2 * Nicolas Voituron,3 * Pierre Filippi,1 * Michelle Bévengut,3 Hervé Faralli,1 Sébastien Zanella,3 Gilles Fortin,2 Gérard Hilaire,3 and Laurent Fasano1
1Unité Mixte de Recherche (UMR) 6216, Centre National de la Recherche Scientifique (CNRS), Université de la Méditerranée, Institut de Biologie du Développement de Marseille Luminy, Parc Scientifique de Luminy, 13288 Marseille Cedex 9, France, 2Neurobiology and Development, Unité Propre de Recherche 3294, Institute of Neurobiology A. Fessard, CNRS, 91198 Gif-sur-Yvette Cedex, France, 3MP3–Respiration, Centre de Recherche en Neurobiologie et Neurophysiologie de Marseille, UMR 6231, CNRS, Université Aix Marseille II and III, Faculté Saint Jér?me, 13397 Marseille Cedex 20, France, and 4Université de Provence, 13331 Marseille, France
Neonatal breathing in mammals involves multiple neuronal circuits, but its genetic basis remains unclear. Mice deficient for the zinc finger protein Teashirt 3 (TSHZ3) fail to breathe and die at birth. Tshz3 is expressed in multiple areas of the brainstem involved in respiration, including the pre-B?tzinger complex (preB?tC), the embryonic parafacial respiratory group (e-pF), and cranial motoneurons that control the upper airways. Tshz3 inactivation led to pronounced cell death of motoneurons in the nucleus ambiguus and induced strong alterations of rhythmogenesis in the e-pF oscillator. In contrast, the preB?tC oscillator appeared to be unaffected. These deficits result in impaired upper airway function, abnormal central respiratory rhythm generation, and altered responses to pH changes. Thus, a single gene, Tshz3, controls the development of diverse components of the circuitry required for breathing.
