関連する実験動画
Updated: Jun 10, 2026
11:35
Flash Photolysis of Caged Compounds in the Cilia of Olfactory Sensory Neurons
Published on: October 29, 2011
イノシトール1,4,5-トリスホスファートによって誘発されたCa2+の放出は,浸透性細胞における光のCa2+によって制御される安定状態現象である
L Missiaen1, H De Smedt, G Droogmans
1Laboratorium voor Fysiologie, KUL Campus Gasthuisberg, Leuven, Belgium.
Nature
|June 18, 1992
まとめ
低濃度のイノシトール1,4,5-トリフォスファート (InsP3) は,貯蔵中のカルシウム (Ca2+) の急速な放出を引き起こします. さらに放出は遅いので,貯蔵庫が枯渇するにつれてInsP3に対する感受性が低下し,安定状態放出メカニズムをサポートすることを示唆しています.
科学分野:
- 細胞生物学 細胞生物学
- バイオケミストリー バイオケミストリー
- 生理学 生理学とは
背景:
- イノシトール1,4,5-トリフォスファート (InsP3) は,細胞内カルシウム (Ca2+) の急速な放出を誘発する.
- 二相Ca2+放出には,すべてまたは何もないまたは安定状態の放出という2つのメカニズムが提案されています.
- 以前の研究では,InsP3受容体の異質性を in vitroで示した.
研究 の 目的:
- InsP3.3によって引き起こされる二相Ca2+放出のメカニズムを調査する.
- Ca2+貯蔵庫の枯渇がInsP3の感受性に影響するかどうかを判断する.
主な方法:
- 実験は,透析されたA7r5滑らかな筋肉細胞を用いて行われました.
- 細胞は,Ca2+ のない媒介で化され,45Ca2+ で充填されました.
- InsP3誘発のCa2+放出が測定され,再充填と再刺激が続いた.
主要な成果:
- 最初の放出後に残るCa2+の量は,最初の貯蔵Ca2+レベルとは無関係でした.
- 部分的に枯渇した貯蔵庫は,InsP3.3に対する感度が低下したことを示した.
- リローディングストアはInsP3の感受性を回復させ,さらにCa2+が放出されるようにした.
結論:
- 貯蔵庫からCa2+が放出されるのは,安定状態のメカニズムによって起こります.
- 貯蔵中のCa2+含有量は,InsP3の感受性に影響し,枯渇により感受性が低下する.
- この発見は,二相Ca2+放出とInsP3受容体の性質を調和させるものである.
関連する概念動画
01:26Chemical 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...
01:27Feedback 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...
01:16Calmodulin-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,...
01:30Ligand-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...
01:29Relaxation 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.
01:26Chemical 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...