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NeuroCult™ SM1 不含维生素A

添加物(50X)不含维生素A用于培养神经祖细胞
只有 %1
¥2,020.00

产品号 #(选择产品)

产品号 #05731_C

添加物(50X)不含维生素A用于培养神经祖细胞

产品优势

  • 去除维生素A,以支持神经祖细胞和可定制的分化工作流程;
  • 多功能细胞培养添加物;
  • 优化的无血清配方;
  • 原材料经过严格筛选,提高批次间的一致性

总览

NeuroCult™SM1 不含维生素A是一种无血清培养添加物,基于已发表的B27配方(Brewer等人)。J Neurosci Res., 1993),去除了维生素A。维生素A,也被称为视黄醇,可诱导神经干细胞的分化。NeuroCult™SM1不含维生素A与所选择的基础培养基结合使用,可用于原代和多能干细胞(PSC)衍生的神经祖细胞扩增,以及不需要维生素A的定制分化方案。

包含
• 抗氧化剂
• 胰岛素
• 其他成分
 
分类
添加剂
 
细胞类型
神经干/祖细胞,神经元,多能干细胞
 
种属
人,小鼠,大鼠
 
应用
细胞培养,分化,扩增,培养
 
品牌
NeuroCult
 
研究领域
药物发现和毒性检测,神经科学,干细胞生物学
 
制剂类别
无血清
 

产品说明书及文档

请在《产品说明书》中查找相关支持信息和使用说明,或浏览下方更多实验方案。

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
05731
Lot #
All
Language
English
Catalog #
100-1282
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
05731
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
100-1282
Lot #
All
Language
English

相关材料与文献

技术资料 (1)

文献 (2)

Near-infrared light induces neurogenesis and modulates anxiety-like behavior X. Qi et al. Stem Cell Research & Therapy 2024 Dec

Abstract

The hippocampus is associated with mood disorders,and the activation of quiescent neurogenesis has been linked to anxiolytic effects. Near-infrared (NIR) light has shown potential to improve learning and memory in human and animal models. Despite the vast amount of information regarding the effect of visible light,there is a significant gap in our understanding regarding the response of neural stem cells (NSCs) to NIR stimulation,particularly in anxiety-like behavior. The present study aimed to develop a new optical manipulation approach to stimulate hippocampal neurogenesis and understand the mechanisms underlying its anxiolytic effects. We used 940 nm NIR (40 Hz) light exposure to stimulate hippocampal stem cells in C57BL/6 mice. The enhanced proliferation and astrocyte differentiation of NIR-treated NSCs were assessed using 5-ethynyl-2’-deoxyuridine (EdU) incorporation and immunofluorescence assays. Additionally,we evaluated calcium activity of NIR light-treated astrocytes using GCaMP6f recording through fluorescence fiber photometry. The effects of NIR illumination of the hippocampus on anxiety-like behaviors were evaluated using elevated plus maze and open-field test. NIR light effectively promoted NSC proliferation and astrocyte differentiation via the OPN4 photoreceptor. Furthermore,NIR stimulation significantly enhanced neurogenesis and calcium-dependent astrocytic activity. Moreover,activating hippocampal astrocytes with 40-Hz NIR light substantially improved anxiety-like behaviors in mice. We found that flickering NIR (940 nm/40Hz) light illumination improved neurogenesis in the hippocampus with anxiolytic effects. This innovative approach holds promise as a novel preventive treatment for depression. The online version contains supplementary material available at 10.1186/s13287-024-04114-3.
GABA B Receptor Modulation of Membrane Excitability in Human Pluripotent Stem Cell‐Derived Sensory Neurons by Baclofen and α‐Conotoxin Vc1.1 M. S. Clair‐Glover et al. Journal of Neurochemistry 2025 Jan

Abstract

GABA B receptor (GABA B R) activation is known to alleviate pain by reducing neuronal excitability,primarily through inhibition of high voltage‐activated (HVA) calcium (Ca V 2.2) channels and potentiating G protein–coupled inwardly rectifying potassium (GIRK) channels. Although the analgesic properties of small molecules and peptides have been primarily tested on isolated murine dorsal root ganglion (DRG) neurons,emerging strategies to develop,study,and characterise human pluripotent stem cell (hPSC)‐derived sensory neurons present a promising alternative. In this study,hPSCs were efficiently differentiated into peripheral DRG‐induced sensory neurons (iSNs) using a combined chemical and transcription factor‐driven approach via a neural crest cell intermediate. Molecular characterisation and transcriptomic analysis confirmed the expression of key DRG markers such as BRN3A,ISLET1,and PRPH,in addition to GABA B R and ion channels including Ca V 2.2 and GIRK1 in iSNs. Functional characterisation of GABA B R was conducted using whole‐cell patch clamp electrophysiology,assessing neuronal excitability under current‐clamp conditions in the absence and presence of GABA B R agonists baclofen and α‐conotoxin Vc1.1. Both baclofen (100 μM) and Vc1.1 (1 μM) significantly reduced membrane excitability by hyperpolarising the resting membrane potential and increasing the rheobase for action potential firing. In voltage‐clamp mode,baclofen and Vc1.1 inhibited HVA Ca 2+ channel currents,which were attenuated by the selective GABA B R antagonist CGP 55845. However,modulation of GIRK channels by GABA B Rs was not observed in the presence of baclofen or Vc1.1,suggesting that functional GIRK1/2 channels were not coupled to GABA B Rs in hPSC‐derived iSNs. This study is the first to report GABA B R modulation of membrane excitability in iSNs by baclofen and Vc1.1,highlighting their potential as a future model for studying analgesic compounds.

更多信息

更多信息
物种 人, 大鼠, 小鼠
Contains • Antioxidants • Insulin • Other ingredients
配方 无血清
质量保证:

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