肌肉低化大脑中的通道密度因髓基蛋白基因缺失而增加
J L Noebels1, P K Marcom, M H Jalilian-Tehrani
1Department of Neurology, Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030.
Nature
|August 1, 1991
概括
在发小鼠中缺乏髓基蛋白导致轴突中过多的通道. 这种轴突的可塑性有助于维持神经元刺激性和功能,尽管神经元髓化受损.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 性因素在刺激细胞成熟过程中调节离子通道表达.
- 髓罩影响轴突中的离子通道分布,但分子信号是未知的.
- 发 (shi) 突变小鼠由于基因删除而缺乏髓基本蛋白 (MBP).
研究的目的:
- 研究髓基蛋白 (MBP) 在调节轴突中的通道密度中的作用.
- 确定调解小寡细胞-轴膜相互作用的分子信号.
- 探索轴突的可塑性作为一个补偿机制在dysmyelinated条件下.
主要方法:
- 利用了shiverer突变小鼠模型,其中删除了髓基本蛋白质基因.
- 检查了突变大脑的大口径纤维通路中的离子通道拓.
- 评估了中枢神经系统投射神经元的功能兴奋性.
主要成果:
- 发的突变大脑表现出大量的通道在大口径的非髓化轴突中.
- 缺少MBP,而不仅仅是质-轴突接触,似乎对下调轴突管道至关重要.
- 成熟的神经元与非髓纤维增加通道密度,以维持刺激性.
结论:
- 髓基蛋白或相关的质信号对于调节轴突中的通道密度至关重要.
- 轴突的可塑性,特别是通道密度的增加,弥补了缺乏髓化.
- 这种可塑性可能解释了发小鼠中轻微的神经缺陷,并提供了从失髓性疾病中恢复的见解.
相关概念视频
Neural Regulation
Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
General Transcription Factors
Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Human Genetics
Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
The complex relationship between genetics and psychology is observable through common biological components such...
Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...


