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成年血清素能神经元中TrkB受体的缺失会增加大脑血清素水平，增强能量代谢并损害学习和记忆。

Depletion of TrkB Receptors From Adult Serotonergic Neurons Increases Brain Serotonin Levels, Enhances Energy Metabolism and Impairs Learning and Memory.

作者信息

Sahu Madhusmita P, Pazos-Boubeta Yago, Steinzeig Anna, Kaurinkoski Katja, Palmisano Michela, Borowecki Olgierd, Piepponen Timo Petteri, Castrén Eero

机构信息

Neuroscience Center, Helsinki Institute of Life Science HiLIFE, University of Helsinki, Helsinki, Finland.

Faculty of Philosopy and Social Sciences, Nicolaus Copernicus University in Toruń, Toruń, Poland.

出版信息

Front Mol Neurosci. 2021 Apr 15;14:616178. doi: 10.3389/fnmol.2021.616178. eCollection 2021.

DOI:10.3389/fnmol.2021.616178
PMID:33935645
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8082189/
Abstract

Neurotrophin brain-derived neurotrophic factor (BDNF) and neurotransmitter serotonin (5-HT) regulate each other and have been implicated in several neuronal mechanisms, including neuroplasticity. We have investigated the effects of BDNF on serotonergic neurons by deleting BDNF receptor TrkB from serotonergic neurons in the adult brain. The transgenic mice show increased 5-HT and Tph2 levels with abnormal behavioral phenotype. In spite of increased food intake, the transgenic mice are significantly leaner than their wildtype littermates, which may be due to increased metabolic activity. Consistent with increased 5-HT, the proliferation of hippocampal progenitors is significantly increased, however, long-term survival of newborn cells is unchanged. Our data indicates that BDNF-TrkB signaling regulates the functional phenotype of 5-HT neurons with long-term behavioral consequences.

摘要

神经营养因子脑源性神经营养因子（BDNF）和神经递质5-羟色胺（5-HT）相互调节，并参与了包括神经可塑性在内的多种神经元机制。我们通过在成年大脑的5-羟色胺能神经元中删除BDNF受体TrkB，研究了BDNF对5-羟色胺能神经元的影响。转基因小鼠表现出5-HT和色氨酸羟化酶2（Tph2）水平升高以及行为表型异常。尽管食物摄入量增加，但转基因小鼠比其野生型同窝小鼠明显更瘦，这可能是由于代谢活性增加所致。与5-HT增加一致，海马祖细胞的增殖显著增加，然而，新生细胞的长期存活率未发生变化。我们的数据表明，BDNF-TrkB信号传导调节5-羟色胺能神经元的功能表型，并产生长期行为后果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/17db960f628a/fnmol-14-616178-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/f8bcddc2db7e/fnmol-14-616178-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/2a0579ef9ea3/fnmol-14-616178-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/a0be94df6c99/fnmol-14-616178-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/17db960f628a/fnmol-14-616178-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/f8bcddc2db7e/fnmol-14-616178-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/2a0579ef9ea3/fnmol-14-616178-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/a0be94df6c99/fnmol-14-616178-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7483/8082189/17db960f628a/fnmol-14-616178-g004.jpg

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