近日，来自美国俄勒冈州卫生及科学大学的研究人员在神经科学杂志Neuroscience上发表文章称：他们首次证实了神经胶质细胞能抑制神经细胞的生长，这一科学发现对防治婴儿猝死综合征（Sudden Infant Death Syndrome，SIDS）来说一项重大突破研究。
研究人员观察了大脑的非神经元细胞-神经胶质细胞后发现它们非常强有力地调控脑干神经细胞的生长。事实上，神经胶质细胞实际上抑制脑干神经元的生长，且为建立神经网络，神经胶质细胞可能和神经营养因子起着同等重要的作用（神经营养因子是大脑发育和存活所必需的一个蛋白家族）。
早期研究表明：罹患婴儿猝死综合征的婴儿基本上存在有一个共同特征--大脑中神经胶质细胞的数量会明显增多，俄勒冈州卫生及科学大学的Agnieszka Balkowiec副教授认为这项最新研究成果证实了由于大脑神经胶质细胞的数量增加，导致了控制罹患婴儿猝死综合征的婴儿心肺功能的脑干神经元生长受到抑制，最终引发婴儿死亡。同时在这项研究中，工作人员发现神经胶质细胞要想调控脑干神经元的生长，就必须依赖于脑源性神经营养因子（Brain-Derived Neurotrophic Factor，BDNF）。
研究人员表示只有更好地进一步开展研究明确了神经胶质细胞及脑源性神经营养因子之间作用的相关机制，才能在治疗婴儿猝死综合征、高血压以及其他一些心肺控制的缺陷性疾病的治疗上取得十足的突破。（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.
