BrainPhys™原代神经元试剂盒

BrainPhys™ 原代神经元无血清培养试剂盒

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产品号 #（选择产品）

产品号 #05794_C

BrainPhys™ 原代神经元无血清培养试剂盒

产品优势

更贴近大脑的细胞外环境；
增强神经元功能，具突触活性的神经元比例更高；
无需更换培养基和电击细胞的情况下进行功能分析；
支持ES/iPS细胞和中枢神经系统（CNS）来源的神经元的长期培养；
严格的原料筛选和质量控制可确保最大的减少批次间的差异

产品组分包括

NeuroCult™神经元铺板培养基，100 mL（产品号：#05713）；
NeuroCult™SM1神经元添加物，10 mL（产品号：#05711）；
BrainPhys™神经元培养基，500 mL（产品号：#05790）

立即询价

总览

在完全无血清的原代神经元培养基中培养中枢神经系统 (CNS) 神经元，该培养基经过优化，可促进而非抑制神经元的活性和成熟。

为了方便起见，BrainPhys™原代神经元培养试剂盒包含无血清的BrainPhys™神经元培养基（基础培养基）、NeuroCult™ SM1神经元添加物和NeuroCult™神经元铺板培养基，从而为您的原代组织来源神经元提供完整的培养体系。BrainPhys™神经元培养基基于Bardy和Gage的配方（Bardy et al. PNAS, 2015），可模拟中枢神经系统（CNS）的细胞外环境，以产生更高比例的突触活性神经元。NeuroCult™ SM1神经元添加物基于Brewer's B27配方（Brewer et al. J Neurosci Res., 1993），可在短期和长期无血清培养中维持细胞健康并促进神经突生长和分支。

为了避免因更换培养基而对细胞造成冲击，您也可以在进行功能性检测（例如基于微电极阵列的记录或活细胞荧光成像）时使用BrainPhys™培养基。

查看我们的其他资源，了解更多关于BrainPhys™产品线的信息。

实验数据

Table 1. Properties of Culture Media (C Bardy et al. Proc Natl Acad Sci USA, 2015)

Check-mark denotes physiological conditions and supported activities according to C Bardy et al. Proc Natl Acad Sci USA, 2015.

Rodent Neurons Matured in BrainPhys™ Neuronal Medium

Figure 1. Protocol for Plating and Culturing Primary Neurons with the SM1 Culture System

Primary rodent tissue dissociated in papain was plated in NeuroCult™ Neuronal Plating Medium, supplemented with NeuroCult™ SM1 Neuronal Supplement, L-Glutamine, and L-Glutamic Acid. On day 5, primary neurons were transitioned to BrainPhys™ Neuronal Medium, supplemented with NeuroCult™ SM1 Neuronal Supplement, by performing half-medium changes every 3 - 4 days.

Primary Neuronal Cultures Matured in BrainPhys™ Neuronal Medium Have Greater Numbers of Neurons

Figure 2. The SM1 Culture System Supports Long-Term Culture of Rodent Neurons

Primary E18 rat cortical neurons were cultured in the SM1 Culture System. A large number of viable neurons are visible after (A) 21 and (B) 35 days, as demonstrated by their bright neuronal cell bodies, and extensive neurite outgrowth and branching. Neurons are evenly distributed over the culture surface with minimal cell clumping.

Rodent Neuronal Cultures Matured in BrainPhys™ Neuronal Medium Show Improved Excitatory and Inhibitory Synaptic Activity

Figure 3. Pre- and Post-Synaptic Markers are Expressed in Rodent Neurons Cultured in the SM1 Culture System

Primary E18 rat cortical neurons were cultured in the SM1 Culture System. At 21 DIV, neurons are phenotypically mature, as indicated by the presence of an extensive dendritic arbor, and appropriate expression and localization of pre-synaptic synapsin (A,C; green) and post-synaptic PSD-95 (A,B; red) markers. Synapsin is concentrated in discrete puncta distributed along the somata and dendritic processes, as defined by the dendritic marker MAP2 (A,D; blue).

Expression of Pre-Synaptic Markers in Rodent Neurons Matured in BrainPhys™ Neuronal Medium

Figure 4. The SM1 Culture System Supports Increased Cell Survival

(A) Primary E18 rat cortical neurons were cultured in the SM1 Culture System or a Competitor Culture System for 21 days. Neurons cultured in the SM1 Culture System have a significantly higher number of viable cells compared to the competitor culture system (n = 4; mean ± 95% CI; *p < 0.05). (B) Primary E18 rat cortical neurons were cultured in Neurobasal® supplemented with NeuroCult™ SM1 Neuronal Supplement (SM1) or competitor B27-like supplements (Competitor 1,2,3) for 21 days. Cultures supplemented with NeuroCult™ SM1 Neuronal Supplement have an equal number of neurons compared to competitor-supplemented cultures. Bars represent standard error of mean.

Raster plots showing activity of neurons cultured in BrainPhys and SM1 versus commercial media

Figure 5. BrainPhys™ Supports Improved Neuronal Activity and More Consistent Network Bursting in Long-Term Culture

Raster plots from MEA recordings show the firing patterns of primary E18 rat cortical neurons across 8 electrodes at Weeks 2, 4, 6 and 8. Neurons were either cultured with a Commercial Medium with Supplements, Commercial Medium Plus with Supplements, BrainPhys™ and SM1, or BrainPhys™ and SM1 with 15 mM glucose. Detected spikes (black lines), single channel bursts (blue lines; a collection of at least 5 spikes, each separated by an ISI of no more than 100 ms), and network bursts (magenta boxes; a collection of at least 50 spikes from a minimum of 35% of participating electrodes across each well, each separated by an ISI of no more than 100 ms) were recorded for each medium. (A-D) Neurons cultured with Commercial Medium exhibited network bursting in Week 2 but no spiking activity was detected in subsequent timepoints. (E-H) In Commercial Medium Plus-cultured neurons, a high number of spikes and regular network bursting were detected at Week 2. A decreased number of spikes and inconsistent network bursting were observed in later time points, corresponding to the drop in MFR seen in Figure 4. (I-L) Without glucose, individual spiking was observed at Weeks 2 and 4 with BrainPhys™ and SM1 but network bursting was not detected until Weeks 6 and 8. (M-T) In contrast, neurons cultured with BrainPhys™ and SM1 with 15 mM glucose demonstrated strong spiking activity and consistent network bursting at all timepoints. MEA = microelectrode array; ISI = inter-spike interval; MFR = mean firing rate

MEA data showing mean firing rate of rodent primary neurons cultured in BrainPhys and SM1 versus commercial media

Figure 6. Glucose Supplementation in BrainPhys™ Maintains Neuronal Activity Over 8 Weeks in Culture

Primary E18 rat cortical neurons were cultured with BrainPhys™ and SM1 or other commercially available culture systems for 8 weeks. Neuronal activity can be detected at Day 9 with BrainPhys™, whereas activity is not detected until Day 14 in cultures maintained in either of the Commercial Media with Commercial Supplements. For Commercial Medium and Supplement-cultured neurons, mean firing rate remains low throughout culture. In contrast, a “peak-drop” activity pattern is observed in the Commercial Medium Plus condition, where mean firing rate increases rapidly within 2 days, followed by a drop in activity in the next 2 - 4 days. BrainPhys™and SM1 Kit with 15 mM glucose maintains the highest level of activity throughout the 8-week culture period.

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

Document Type

Product Information Sheet

Product Name

BrainPhys™ Primary Neuron Kit

Catalog #

05794

Lot #

All

Language

English

Document Type

Safety Data Sheet 1

Product Name

BrainPhys™ Primary Neuron Kit

Catalog #

05794

Lot #

All

Language

English

Document Type

Safety Data Sheet 2

Product Name

BrainPhys™ Primary Neuron Kit

Catalog #

05794

Lot #

All

Language

English

Document Type

Safety Data Sheet 3

Product Name

BrainPhys™ Primary Neuron Kit

Catalog #

05794

Lot #

All

Language

English

文献 (51)

Development and Dynamic Regulation of Mitochondrial Network in Human Midbrain Dopaminergic Neurons Differentiated from iPSCs. E. Gabriel et al. Stem cell reports 2016 JAN

Abstract

Mitochondria are critical to neurogenesis,but the mechanisms of mitochondria in neurogenesis have not been well explored. We fully characterized mitochondrial alterations and function in relation to the development of human induced pluripotent stem cell (hiPSC)-derived dopaminergic (DA) neurons. Following directed differentiation of hiPSCs to DA neurons,mitochondria in these neurons exhibit pronounced changes during differentiation,including mature neurophysiology characterization and functional synaptic network formation. Inhibition of mitochondrial respiratory chains via application of complex IV inhibitor KCN (potassium cyanide) or complex I inhibitor rotenone restricted neurogenesis of DA neurons. These results demonstrated the direct importance of mitochondrial development and bioenergetics in DA neuronal differentiation. Our study also provides a neurophysiologic model of mitochondrial involvement in neurogenesis,which will enhance our understanding of the role of mitochondrial dysfunctions in neurodegenerative diseases.

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A viral strategy for targeting and manipulating interneurons across vertebrate species. Dimidschstein J et al. Nature neuroscience 2016 DEC

Abstract

A fundamental impediment to understanding the brain is the availability of inexpensive and robust methods for targeting and manipulating specific neuronal populations. The need to overcome this barrier is pressing because there are considerable anatomical,physiological,cognitive and behavioral differences between mice and higher mammalian species in which it is difficult to specifically target and manipulate genetically defined functional cell types. In particular,it is unclear the degree to which insights from mouse models can shed light on the neural mechanisms that mediate cognitive functions in higher species,including humans. Here we describe a novel recombinant adeno-associated virus that restricts gene expression to GABAergic interneurons within the telencephalon. We demonstrate that the viral expression is specific and robust,allowing for morphological visualization,activity monitoring and functional manipulation of interneurons in both mice and non-genetically tractable species,thus opening the possibility to study GABAergic function in virtually any vertebrate species.

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Recent Zika Virus Isolates Induce Premature Differentiation of Neural Progenitors in Human Brain Organoids. E. Gabriel et al. Cell stem cell 2017 JAN

Abstract

The recent Zika virus (ZIKV) epidemic is associated with microcephaly in newborns. Although the connection between ZIKV and neurodevelopmental defects is widely recognized,the underlying mechanisms are poorly understood. Here we show that two recently isolated strains of ZIKV,an American strain from an infected fetal brain (FB-GWUH-2016) and a closely-related Asian strain (H/PF/2013),productively infect human iPSC-derived brain organoids. Both of these strains readily target to and replicate in proliferating ventricular zone (VZ) apical progenitors. The main phenotypic effect was premature differentiation of neural progenitors associated with centrosome perturbation,even during early stages of infection,leading to progenitor depletion,disruption of the VZ,impaired neurogenesis,and cortical thinning. The infection pattern and cellular outcome differ from those seen with the extensively passaged ZIKV strain MR766. The structural changes we see after infection with these more recently isolated viral strains closely resemble those seen in ZIKV-associated microcephaly.

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