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相关概念视频

Chemical Synapses01:26

Chemical Synapses

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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...
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Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

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Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
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Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

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When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
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Long-term Depression01:03

Long-term Depression

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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
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Synaptic Signaling01:09

Synaptic Signaling

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Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
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Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

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Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
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相关实验视频

Updated: Jun 21, 2025

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
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陶介导的突触功能障碍与HCN通道病变结合在一起.

Despoina Goniotaki1, Francesco Tamagnini2, Luca Biasetti3

  • 1Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology & Neuroscience, Maurice Wohl Clinical Neuroscience Institute, King's College London, London, UK.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|July 12, 2024
PubMed
概括

病态的变异症改变了高极化激活的循环核酸门 (HCN) 通道,导致突触缺陷. 这项研究将功能障碍与HCN通道变化联系起来,影响阿尔茨海默病和小鼠模型中的神经元功能.

关键词:
痴呆症 痴呆症是一种痴呆症.超极化激活的循环核酸门通道.神经退行症的神经退行症压力下降的压力下降.有关突触的突触.陶氏病变是一种病变.

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相关实验视频

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科学领域:

  • 神经科学是一个神经科学.
  • 分子生物学分子生物学
  • 细胞生物学 细胞生物学

背景情况:

  • 包括阿尔茨海默氏症 (AD) 在内的病症涉及异常的处理,导致突触功能障碍.
  • 超极化激活的循环核酸门 (HCN) 通道与各种神经退行性疾病有关.

研究的目的:

  • 在神经退行症的背景下,研究病理和HCN通道之间的功能联系.
  • 阐明变化如何影响HCN通道表达和功能.

主要方法:

  • 在海马组织上进行了组织学,生物化学,超结构和功能分析.
  • 研究包括死后阿尔茨海默病 (AD) 海马,年龄匹配的对照,Tau35小鼠和Tau35初级海马神经元.

主要成果:

  • 在死后AD海马和Tau35小鼠中观察到特定HCN通道的高表达.
  • 35小鼠表现出渐进的异常,包括酸化的增加,增强的HCN通道表达,减少树突分支和突触密度.
  • 图35主要神经元显示HCN通道表达增加,膜电压"松"发生变化,突触活动发生变化.

结论:

  • 病态在病变中直接影响HCN通道,导致结构和功能突触缺陷.
  • 这些发现支持了一个模型,其中HCN通道的tau介导的变化驱动整个网络的突触异常.