因诺西1,4,5-三酸盐诱导的Ca2+释放是一种由透细胞中的光Ca2+控制的稳定状态现象
L Missiaen1, H De Smedt, G Droogmans
1Laboratorium voor Fysiologie, KUL Campus Gasthuisberg, Leuven, Belgium.
Nature
|June 18, 1992
概括
低的伊诺西1,4,5-三酸盐 (InsP3) 度会导致储存中的 (Ca2+) 迅速释放. 进一步释放速度较慢,这表明随着储量耗尽,存储对InsP3变得不那么敏感,支持稳定状态释放机制.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 身体生理学 身体生理学
背景情况:
- 伊诺西1,4,5-三酸盐 (InsP3) 触发了细胞内 (Ca2+) 的快速释放.
- 双相Ca2+释放有两个建议的机制:全或无或稳定状态释放.
- 之前的研究表明InsP3受体异质性在体外.
研究的目的:
- 研究由InsP3.3.引起的双相Ca2+释放的机制.
- 为了确定Ca2+储存量耗尽是否影响InsP3灵敏度.
主要方法:
- 实验使用透的A7r5光滑肌细胞进行.
- 细胞在没有Ca2+的介质中进行化,并加载45Ca2+.
- 测量了InsP3诱导的Ca2+释放,然后进行重新加载和重新刺激.
主要成果:
- 最初释放后剩余的Ca2+的数量独立于最初的储存Ca2+水平.
- 部分耗尽的库存显示对InsP3.3的敏感性降低.
- 重装储存器恢复了InsP3的敏感性,允许进一步释放Ca2+.
结论:
- 从储存中的Ca2+释放通过稳定状态机制发生.
- 储存的Ca2+含量会影响InsP3的敏感性,而耗尽会降低它.
- 这一发现使双相Ca2+释放与InsP3受体特性相协调.
相关概念视频
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...
Feedback Regulation of Calcium Concentration
Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Calmodulin-dependent Signaling
Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Ligand-Gated Ion Channel Receptor: Gating Mechanism
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...
Relaxation of Skeletal Muscles
The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
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...


