近日,，來自美國(guó)俄勒岡州衛(wèi)生及科學(xué)大學(xué)的研究人員在神經(jīng)科學(xué)雜志Neuroscience上發(fā)表文章稱：他們首次證實(shí)了神經(jīng)膠質(zhì)細(xì)胞能抑制神經(jīng)細(xì)胞的生長(zhǎng)，這一科學(xué)發(fā)現(xiàn)對(duì)防治嬰兒猝死綜合征（Sudden Infant Death Syndrome,，SIDS）來說一項(xiàng)重大突破研究,。
研究人員觀察了大腦的非神經(jīng)元細(xì)胞-神經(jīng)膠質(zhì)細(xì)胞后發(fā)現(xiàn)它們非常強(qiáng)有力地調(diào)控腦干神經(jīng)細(xì)胞的生長(zhǎng),。事實(shí)上，神經(jīng)膠質(zhì)細(xì)胞實(shí)際上抑制腦干神經(jīng)元的生長(zhǎng),，且為建立神經(jīng)網(wǎng)絡(luò),，神經(jīng)膠質(zhì)細(xì)胞可能和神經(jīng)營(yíng)養(yǎng)因子起著同等重要的作用（神經(jīng)營(yíng)養(yǎng)因子是大腦發(fā)育和存活所必需的一個(gè)蛋白家族）。
早期研究表明：罹患嬰兒猝死綜合征的嬰兒基本上存在有一個(gè)共同特征--大腦中神經(jīng)膠質(zhì)細(xì)胞的數(shù)量會(huì)明顯增多,，俄勒岡州衛(wèi)生及科學(xué)大學(xué)的Agnieszka Balkowiec副教授認(rèn)為這項(xiàng)最新研究成果證實(shí)了由于大腦神經(jīng)膠質(zhì)細(xì)胞的數(shù)量增加，導(dǎo)致了控制罹患嬰兒猝死綜合征的嬰兒心肺功能的腦干神經(jīng)元生長(zhǎng)受到抑制,，最終引發(fā)嬰兒死亡,。同時(shí)在這項(xiàng)研究中，工作人員發(fā)現(xiàn)神經(jīng)膠質(zhì)細(xì)胞要想調(diào)控腦干神經(jīng)元的生長(zhǎng),，就必須依賴于腦源性神經(jīng)營(yíng)養(yǎng)因子（Brain-Derived Neurotrophic Factor,，BDNF）。
研究人員表示只有更好地進(jìn)一步開展研究明確了神經(jīng)膠質(zhì)細(xì)胞及腦源性神經(jīng)營(yíng)養(yǎng)因子之間作用的相關(guān)機(jī)制,，才能在治療嬰兒猝死綜合征,、高血壓以及其他一些心肺控制的缺陷性疾病的治療上取得十足的突破。（生物谷Bioon.com）
doi:10.1016/j.neuroscience.2012.01.013
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Glia determine the course of brain-derived neurotrophic factor-mediated dendritogenesis and provide a soluble inhibitory cue to dendritic growth in the brainstem
J.L. Martina, b, A.L. Browna, 1, A. Balkowiec
Cardiorespiratory control neurons in the brainstem nucleus tractus solitarius (NTS) undergo dramatic expansion of dendritic arbors during the early postnatal period, when functional remodeling takes place within the NTS circuitry. However, the underlying molecular mechanisms of morphological maturation of NTS neurons are largely unknown. Our previous studies point to the neurotrophin brain-derived neurotrophic factor (BDNF), which is abundantly expressed by NTS-projecting primary sensory neurons, as a candidate mediator of NTS dendritogenesis. In the current study, we used neonatal rat NTS neurons in vitro to examine the role of BDNF in the dendritic development of neurochemically identified subpopulations of NTS neurons. In the presence of abundant glia, BDNF promoted NTS dendritic outgrowth and complexity, with the magnitude of the BDNF effect dependent on neuronal phenotype. Surprisingly, BDNF switched from promoting to inhibiting NTS dendritogenesis upon glia depletion. Moreover, glia depletion alone led to a significant increase in NTS dendritic outgrowth. Consistent with this result, astrocyte-conditioned medium (ACM), which promoted hippocampal dendritogenesis, inhibited dendritic growth of NTS neurons. The latter effect was abolished by heat-inactivation of ACM, pointing to a diffusible astrocyte-derived negative regulator of NTS dendritic growth. Together, these data demonstrate a role for BDNF in the postnatal development of NTS neurons, and reveal novel effects of glia on this process. Moreover, previously documented dramatic increases in NTS glial proliferation in victims of sudden infant death syndrome (SIDS) underscore the importance of our findings and the need to better understand the role of glia and their interactions with BDNF during NTS circuit maturation. Furthermore, while it has previously been demonstrated that the specific effects of BDNF on dendritic growth are context-dependent, the role of glia in this process is unknown. Thus, our data carry important implications for mechanisms of dendritogenesis likely beyond the NTS.
