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Fluo-4 (potassium salt)

目录号 : GC49741

一种细胞不可渗透的荧光钙指示剂

Fluo-4 (potassium salt) Chemical Structure

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10 x 50 µg
¥2,570.00
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500 µg
¥2,570.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

Fluo-4 is a cell-impermeable fluorescent calcium indicator. It binds to calcium (Kd = 355 nM) and displays excitation/emission maxima of 490/515 nm, respectively.

N/A

Chemical Properties

Cas No. N/A SDF Download SDF
Canonical SMILES O=C1C(F)=CC2=C(C3=CC(OCCOC4=CC(C)=CC=C4N(CC([O-])=O)CC([O-])=O)=C(N(CC([O-])=O)CC([O-])=O)C=C3)C5=C(C=C(C(F)=C5)[O-])OC2=C1.[K+].[K+].[K+].[K+].[K+]
分子式 C36H25F2N2O13 • 5K 分子量 927.1
溶解度 N/A 储存条件 -20°C
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1 mg 5 mg 10 mg
1 mM 1.0786 mL 5.3932 mL 10.7863 mL
5 mM 0.2157 mL 1.0786 mL 2.1573 mL
10 mM 0.1079 mL 0.5393 mL 1.0786 mL
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Research Update

A simple and fast method to image calcium activity of neurons from intact dorsal root ganglia using fluorescent chemical Ca2+ indicators

Mol Pain 2017 Jan-Dec;13:1744806917748051.PMID:29212403DOI:10.1177/1744806917748051.

Chemical calcium indicators have been commonly used to monitor calcium (Ca2+) activity in cell bodies, i.e., somata, of isolated dorsal root ganglion neurons. Recent studies have shown that dorsal root ganglion somata play an essential role in soma-glia interactions and actively participate in the transmission of nociceptive signals. It is therefore desirable to develop methods to study Ca2+ activity in neurons and glia in intact dorsal root ganglia. In our previous studies, we found that incubation of intact dorsal root ganglia with acetoxymethyl dye resulted in efficient Ca2+ dye loading into glial cells but limited dye loading into neurons. Here, we introduce a useful method to load Ca2+ dyes in intact dorsal root ganglion neurons through electroporation. We found that electroporation greatly facilitated loading of Fluo-4 acetoxymethyl, Oregon green bapta-1-488 acetoxymethyl, and Fluo-4 pentapotassium salt into dorsal root ganglion neurons. In contrast, electroporation did not further facilitate dye loading into glia. Using electroporation followed by incubation of acetoxymethyl form Ca2+ dye, we can load acetoxymethyl Ca2+ dye well in both neurons and glia. With this approach, we found that inflammation induced by complete Freund's adjuvant significantly increased the incidence of neuron-glia interactions in dorsal root ganglia. We also confirmed the actions of capsaicin and morphine on Ca2+ responses in dorsal root ganglion neurons. Thus, by promoting the loading of Ca2+ dye in neurons and glia through electroporation and incubation, Ca2+ activities in neurons and neuron-glia interactions can be well studied in intact dorsal root ganglia.

Dopamine reduces odor- and elevated-K(+)-induced calcium responses in mouse olfactory receptor neurons in situ

J Neurophysiol 2004 Apr;91(4):1492-9.PMID:14657189DOI:10.1152/jn.00670.2003.

Although D2 dopamine receptors have been localized to olfactory receptor neurons (ORNs) and dopamine has been shown to modulate voltage-gated ion channels in ORNs, dopaminergic modulation of either odor responses or excitability in mammalian ORNs has not previously been demonstrated. We found that <50 microM dopamine reversibly suppresses odor-induced Ca2+ transients in ORNs. Confocal laser imaging of 300-microm-thick slices of neonatal mouse olfactory epithelium loaded with the Ca(2+)-indicator dye Fluo-4 AM revealed that dopaminergic suppression of odor responses could be blocked by the D2 dopamine receptor antagonist sulpiride (<500 microM). The dopamine-induced suppression of odor responses was completely reversed by 100 microM nifedipine, suggesting that D2 receptor activation leads to an inhibition of L-type Ca2+ channels in ORNs. In addition, dopamine reversibly reduced ORN excitability as evidenced by reduced amplitude and frequency of Ca2+ transients in response to elevated K(+), which activates voltage-gated Ca2+ channels in ORNs. As with the suppression of odor responses, the effects of dopamine on ORN excitability were blocked by the D2 dopamine receptor antagonist sulpiride (<500 microM). The observation of dopaminergic modulation of odor-induced Ca2+ transients in ORNs adds to the growing body of work showing that olfactory receptor neurons can be modulated at the periphery. Dopamine concentrations in nasal mucus increase in response to noxious stimuli, and thus D2 receptor-mediated suppression of voltage-gated Ca2+ channels may be a novel neuroprotective mechanism for ORNs.