Prebiotic feeding elevates central brain derived neurotrophic factor, N-methyl-D-aspartate receptor subunits and D-serine.
Prebiotic feeding elevates central brain derived neurotrophic factor, N-methyl-D-aspartate receptor subunits and D-serine.
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DOI：
10.1016/j.neuint.2013.10.006
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发表时间：
2013-12
影响因子：
4.2
通讯作者：
Burnet PW
中科院分区：
文献类型：
--
作者：
Savignac HM;Corona G;Mills H;Chen L;Spencer JP;Tzortzis G;Burnet PW
益生素喂养增加了大鼠海马区BDNF和NR1亚单位的mRNAs。GOS益生素增加了皮质NR1、d-丝氨酸和海马NR2A亚单位。GOS饲喂使大鼠血浆胃肠肽PYY水平升高。GOS血浆促进SH-SY5Y神经母细胞瘤细胞释放BDNF。PYY抗血清可阻断GOS胞浆分泌BDNF。肠道微生物区系对大脑化学的影响已经在啮齿动物身上得到了令人信服的证明。在没有肠道细菌的情况下，脑源性神经营养因子(BDNF)和N-甲基-d-天冬氨酸受体(NMDAR)亚单位的中枢表达减少，而口服益生菌增加了脑源性神经营养因子，并具有显著的抗焦虑作用。我们测试了益生菌化合物是否也影响大脑BDNF和NMDAR，这些化合物增加了固有的肠道微生物区系。此外，我们检测了益生素处理的大鼠血浆是否从人SH-SY5Y神经母细胞瘤细胞中释放BDNF，以提供作用机制的初步指示。给大鼠灌胃低聚果糖(FOS)、低聚半乳糖(GOS)或水5周，然后测定脑组织BDNF、NMDAR亚单位和与谷氨酸神经传递相关的氨基酸(谷氨酸、谷氨酰胺、丝氨酸和丙氨酸对映体)。与对照组相比，益生元增加了海马区BDNF和NR1亚单位的表达。GOS的摄入也增加了海马区NR2A亚单位和额叶皮质NR1和d-丝氨酸的含量。益生元没有改变大脑中谷氨酸、谷氨酰胺、L-丝氨酸、L-丙氨酸或d-丙氨酸的浓度，尽管GOS提高了血浆d-丙氨酸的水平。观察到摄入GOS后血浆多肽YY(PYY)水平升高。GOS大鼠血浆可促进SH-SY5Y细胞释放BDNF，但对PYY抗血清作用不明显。在SH-SY5Y细胞培养中加入人工合成的PYY，也能增加BDNF的分泌。我们得出结论，与益生菌一样，益生素介导的大鼠肠道微生物区系的增殖可能通过肠道激素的参与增加了脑组织BDNF的表达。GOS对中枢NMDAR信号成分的影响大于FOS，这可能反映了GOS对微生物区系的增殖能力。因此，我们的数据为进一步研究益生元在维持大脑健康和辅助治疗神经精神疾病中的效用提供了可靠的基础。
Prebiotic feeding elevated BDNF and NR1subunit mRNAs, in the rat hippocampus. The GOS prebiotic increased cortical NR1, d-serine, and hippocampal NR2A subunits. GOS feeding elevated plasma levels of the gut peptide PYY. GOS plasma increased BDNF release from human SH-SY5Y neuroblastoma cells. BDNF secretion from cells by GOS plasma was blocked by PYY antisera. The influence of the gut microbiota on brain chemistry has been convincingly demonstrated in rodents. In the absence of gut bacteria, the central expression of brain derived neurotropic factor, (BDNF), and N-methyl-d-aspartate receptor (NMDAR) subunits are reduced, whereas, oral probiotics increase brain BDNF, and impart significant anxiolytic effects. We tested whether prebiotic compounds, which increase intrinsic enteric microbiota, also affected brain BDNF and NMDARs. In addition, we examined whether plasma from prebiotic treated rats released BDNF from human SH-SY5Y neuroblastoma cells, to provide an initial indication of mechanism of action. Rats were gavaged with fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS) or water for five weeks, prior to measurements of brain BDNF, NMDAR subunits and amino acids associated with glutamate neurotransmission (glutamate, glutamine, and serine and alanine enantiomers). Prebiotics increased hippocampal BDNF and NR1 subunit expression relative to controls. The intake of GOS also increased hippocampal NR2A subunits, and frontal cortex NR1 and d-serine. Prebiotics did not alter glutamate, glutamine, l-serine, l-alanine or d-alanine concentrations in the brain, though GOSfeeding raised plasma d-alanine. Elevated levels of plasma peptide YY (PYY) after GOS intake was observed. Plasma from GOS rats increased the release of BDNF from SH-SY5Y cells, but not in the presence of PYY antisera. The addition of synthetic PYY to SH-SY5Y cell cultures, also elevated BDNF secretion. We conclude that prebiotic-mediated proliferation of gut microbiota in rats, like probiotics, increases brain BDNF expression, possibly through the involvement of gut hormones. The effect of GOS on components of central NMDAR signalling was greater than FOS, and may reflect the proliferative potency of GOS on microbiota. Our data therefore, provide a sound basis to further investigate the utility of prebiotics in the maintenance of brain health and adjunctive treatment of neuropsychiatric disorders.
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影响因子：
12.2
作者：
Messaoudi, Michael;Violle, Nicolas;Rougeot, Catherine
通讯作者：
Rougeot, Catherine
影响因子：
3.5
作者：
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影响因子：
4.3
作者：
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通讯作者：
Heimbach, James T.
影响因子：
4
作者：
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通讯作者：
Gaenzle, M. G.