通过激发性和抑制性神经元中的突触增强来显著调节Ih
Lotte J Herstel1,2, Corette J Wierenga3,2
1Biology Department, Faculty of Science, Utrecht University, Utrecht 3584 CH, the Netherlands.
eNeuro
|October 15, 2024
概括
与激发性神经元不同的是,突触可塑性降低抑制性海马内部神经元中的高极化激活周期性核酸门 (HCN) 通道的调节. 这表明HCN通道在调节神经网络活动方面有着不同的作用.
科学领域:
- 神经科学是一个神经科学.
- 细胞神经科学 细胞神经科学
- 离子通道生理学 离子通道生理学
背景情况:
- 树突离子通道,特别是高极化激活的循环核酸门通道 (HCN) 对于神经元刺激性和突触集成至关重要.
- HCN通道介导向内电流 (Ih),并且已知受激发性神经元中的突触可塑性调节.
- 在抑制性神经元中树突性HCN通道的作用和调节在很大程度上仍未被描述.
研究的目的:
- 研究和比较海马CA1金字塔神经元 (刺激性) 和层辐射体 (sRad) 内神经元 (抑制性) 中通过突触可塑性对Ih的调制.
- 阐明海马体内不同神经元群体中HCN通道的差异调节.
主要方法:
- 利用小鼠器官类型培养来研究海马CA1金字塔神经元和sRad内部神经元.
- 系统地比较了Ih特性对激发性和抑制性神经元之间突触强化反应的调制.
- 电生理学记录以评估IH特性和HCN通道功能.
主要成果:
- 它的特性在抑制和激发性海马神经元之间是可比的,影响静止膜潜力和发射模式.
- 突触可塑性导致sRad内部神经元中HCN通道的下调,独立于突触强化的强度.
- 相比之下,激发性神经元表现出基于突触强化强度的HCN通道的双向调制.
结论:
- 在突触可塑性之后,海马刺激神经元和抑制神经元之间的HCN通道调节显著不同.
- 内部神经元中观察到的HCN通道的下调表明,它在调节海马网络活动中起着独特的功能作用.
- 这些发现突出了不同细胞类型中控制内在神经元特性的专门机制.
相关概念视频
Excitatory and Inhibitory Effects of Neurotransmitters
9.8K
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...
9.8K
The Role of Ion Channels in Neuronal Computation
3.1K
A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential....
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential....
3.1K
Long-term Potentiation
2.7K
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when...
Hebbian LTP
LTP can occur when...
2.7K
Integration of Synaptic Events
1.5K
Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability...
1.5K
Ligand-Gated Ion Channel Receptor: Gating Mechanism
2.1K
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...
2.1K
Chemical Synapses
8.7K
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...
8.7K


