- NeuroMab™ Anti-Tau Antibody,Clone NR3320P (Cat#: NRP-0422-P1760)
- NeuroMab™ Anti-TREM2 Antibody, Clone NR65P (Cat#: NRP-0422-P792)
- NeuroMab™ Anti-GARP Antibody,Clone NR3348P (Cat#: NRP-0422-P1639)
- NeuroMab™ Anti-pTau Antibody,Clone NR3595P (Cat#: NRP-0422-P1719)
- NeuroMab™ Anti-CD20 Antibody,Clone NR3021P (Cat#: NRP-0422-P1230)
- Tau Monoclonal Antibody (AT120, HT7 and BT2 clone) (Cat#: NK-2106-P008)
- NeuroMab™ Anti-ApoC3 BBB Shuttle Antibody,Clone NR1738P (Cat#: NRZP-1022-ZP3503)
- NeuroMab™ Rabbit Anti-LRRK2 Monoclonal Antibody (CBP1887) (Cat#: NAB-08-PZ735)
- NeuroMab™ Anti-GD2 Antibody,Clone NR3007P (Cat#: NRZP-1222-ZP767)
- NeuroMab™ Rabbit Anti-Alpha-synuclein (CBP1631) (Cat#: NAB-08-PZ079)
- Human Blood Brain Barrier Model (Cat#: NCL-2103-P187)
- Mouse Microglia Cell Line BV-2, Immortalized (Cat#: NCL2110P153)
- Human Brain Astroblastoma U-87 MG (Cat#: NCL2110P117)
- Human Glial (Oligodendrocytic) Hybrid Cell Line (MO3.13) (Cat#: NCL-2108P34)
- Human Brain Vascular Adventitial Fibroblasts (Cat#: NCL-21P6-014)
- Rat Retinal Muller Cell Line, Immortalized (Cat#: NCL-21P6-192)
- iNeu™ Human Neural Stem Cell Line (Cat#: NCL200552ZP)
- Mouse Glioma Cell Line GL-261-Luc (Cat#: NCL-2108P06)
- iNeu™ Human Oligodendrocyte Progenitor Cells (OPCs) (Cat#: NCL-2103-P49)
- iNeu™ Human Schwann Cell (Cat#: NCL-2103-P63)
- Beta Amyloid (1-42), Aggregation Kit (Cat#: NRZP-0323-ZP200)
- Human GFAP ELISA Kit [Colorimetric] (Cat#: NPP2011ZP383)
- Human Poly ADP ribose polymerase,PARP Assay Kit (Cat#: NRZP-1122-ZP62)
- Amyloid beta 1-42 Kit (Cat#: NRP-0322-P2170)
- Beta Amyloid (1-40), Aggregation Kit, TTF Assay (Cat#: NRZP-0323-ZP199)
- Human Tau Aggregation Kit (Cat#: NRP-0322-P2173)
- Alpha Synuclein Aggregation Kit (Cat#: NRZP-1122-ZP15)
- Alpha-Synuclein Aggregation Assay Kit (Cat#: NRZP-1122-ZP37)
- Dextran-CYanine5.5 (Cat#: NTA-2011-ZP118)
- pAAV-syn-jGCaMP8s-WPRE (Cat#: NTA-2106-P063)
- AAV-mDLX-CRE-tdTomato (Cat#: NRZP-0622-ZP721)
- pAAV-syn-jGCaMP8f-WPRE (Cat#: NTA-2106-P061)
- Dextran, Cy5 Labeled, 2000 kDa (Cat#: NRZP-0722-ZP22)
- rAAV-CAG-DIO-G-Flamp1 (Cat#: NRZP-0722-ZP719)
- PRV-CAG-EGFP (Cat#: NTA-2011-ZP14)
- rAAV-E-SARE-Cre-ERT2-PEST-WPRE-hGH polyA (Cat#: NTA-2010-TT342)
- pAAV-syn-FLEX-jGCaMP8m-WPRE (Cat#: NTA-2106-P065)
- AAV-EF1a-mCherry-flex-dtA (Cat#: NRZP-0622-ZP616)
- Human superoxide dismutase 1, soluble (SOD1) (NM_000454) ORF clone, TurboGFP Tagged (Cat#: NEP-0521-R0748)
- Human huntingtin (HTT) (NM_002111) ORF clone, Myc-DDK Tagged (Cat#: NEP-0521-R0497)
- Human huntingtin-associated protein 1 (HAP1) transcript variant 2 (NM_177977) ORF clone, Myc-DDK Tagged (Cat#: NEP-0521-R0676)
- Mouse SOD1 shRNA Silencing Adenovirus (Cat#: NV-2106-P14)
- Mouse Parkinson disease (autosomal recessive, early onset) 7 (Park7) (NM_020569) clone, Untagged (Cat#: NEP-0621-R0133)
- Human superoxide dismutase 3, extracellular (SOD3) (NM_003102) ORF clone, Untagged (Cat#: NEP-0521-R0808)
- Human presenilin 1 (PSEN1), transcript variant 2 (NM_007318) ORF clone, TurboGFP Tagged (Cat#: NEP-0421-R0140)
- Rat Parkinson disease (autosomal recessive, juvenile) 2, parkin (Park2) (NM_020093) ORF clone/lentiviral particle, Myc-DDK Tagged (Cat#: NEP-0621-R0041)
- Lenti of Human TAR DNA binding protein (TARDBP) (NM_007375) ORF clone, mGFP Tagged (Cat#: NEP-0521-R0832)
- Human apolipoprotein E (APOE) (NM_000041) ORF clone, Untagged (Cat#: NEP-0421-R0232)
- NeuroBiologics™ Mouse Cerebrospinal Fluid (Cat#: NRZP-0822-ZP497)
- NeuroBiologics™ Pig Cerebrospinal Fluid (Cat#: NRZP-0822-ZP498)
- NeuroBiologics™ Rat Cerebrospinal Fluid (Cat#: NRZP-0822-ZP496)
- NeuroBiologics™ Monkey Cerebrospinal Fluid (Cat#: NRZP-0822-ZP495)
- NeuroBiologics™ Human Cerebrospinal Fluid (Cat#: NRZP-0822-ZP491)
- NeuroPro™ Anti-TNFR BBB Shuttle Protein, HIRMab-TNFR (Cat#: NRZP-0423-ZP510)
- NeuroPro™ Anti-SGSH BBB Shuttle Protein, HIRMab-SGSH (Cat#: NRZP-0423-ZP505)
- NeuroPro™ Anti-EPO BBB Shuttle Protein, HIRMab-EPO (Cat#: NRZP-0423-ZP508)
- NeuroPro™ Anti-Erythropoietin BBB Shuttle Protein, cTfRMAb-EPO (Cat#: NRZP-0423-ZP499)
- NeuroPro™ Anti-IDUA BBB Shuttle Protein, HIRMab-IDUA (Cat#: NRZP-0423-ZP502)
- NeuroPro™ Anti-PON1 BBB Shuttle Protein, HIRMab-PON1 (Cat#: NRZP-0423-ZP507)
- NeuroPro™ Anti-GDNF BBB Shuttle Protein, cTfRMAb-GDNF (Cat#: NRZP-0423-ZP500)
- NeuroPro™ Anti-NAGLU BBB Shuttle Protein, HIRMab-NAGLU (Cat#: NRZP-0423-ZP506)
- NeuroPro™ Anti-GDNF BBB Shuttle Protein, HIRMab-GDNF (Cat#: NRZP-0423-ZP509)
- NeuroPro™ Anti-IDUA BBB Shuttle Protein, cTfRMAb-IDUA (Cat#: NRZP-0423-ZP498)
Multi-electrode Array (MEA) Technology
Multi-electrode array (MEA) platforms are becoming fundamental tools in neuroscience research fields. Creative Biolabs has 10+ years of experience providing CRO services with a skilled team of scientists who will work with you to promote your projects of interest.
Overview
An MEA is a device containing multiple microelectrodes through which extracellular voltage changes from neuronal networks can be measured. MEAs for in vitro studies typically include a petri dish with dozens to hundreds of embedded electrodes to allow multisite electrophysiological recording of biopsies or isolated cell cultures. MEA technology has several advantages, including high throughput and the ability to simultaneously record the activity of hundreds of neurons for long periods, and offers a wide range of MEA electrode designs. This has led to the growing popularity of MEA techniques for studying diseases or recreating reactions to drugs in the body. The MEA technique has also been used as a test-bed for neuroprosthetic devices since it allows direct stimulation of specific brain regions and multisite recordings of spatiotemporal dynamics.
MEA Technologies for Neuroscience
Currently, the main approach to studying neuronal circuitry-connectivity, physiology, and pathology under in vitro or in vivo conditions is to use substrate-integrated microelectrode arrays. Using cellular non-invasive extracellular MEAs for in vitro recording and multipoles for in vivo recording, greatly attenuated and time-filtered electrical signals can simultaneously record and stimulate large numbers of excitable cells for days or months without causing mechanical damage to the plasma membrane of neurons. For many years, MEAs have been widely adopted by many scientists for many types of neural experiments. For example, the application of MEAs to acute brain tissue both stimulated and recorded from multiple sites on acute hippocampus slice preparations. MEAs have also been used to study different properties of neural networks, such as network formation, network dynamics, and memory functions.
Fig.1 A schematic view of the MEA chip. (Chang, 2012)
Advantages of The MEA Technique
The MEA technique is a unique and well-established tool for studying the electrophysiological properties of living brain slices or cultured neuronal networks at the macro level, linking single-cell testing with behavioral studies. It is well-suited for studying synaptic plasticity, single unit activity, rhythmic activity, and pharmacological drug testing. The advantages of the MEA technique over traditional electrophysiology are:
- Gathering large amounts of spatial information within the network through multi-site records.
- A tremendous variety of research applications involving acute brain slices, organotypic slice cultures, and dissociated cell cultures.
- Multisite stimulation and recording within one slice.
- Long-term analysis of the spatiotemporal distribution of electrical activity at the network level.
MEA experiments have many purposes, from neuropharmacological testing for toxicity to cardiac experiments to neuronal plasticity. With Creative Biolabs’ complete suite of in vitro and in vivo solutions, we can be your one-stop shop in neurological diseases drug development. Our solutions range from study design consultancy to data generation and data interpretation. Contact us to discuss your next neuroscience project.
Reference
- Chang, Y.J.; et al. A low-cost multi-electrode array system for the simultaneous acquisition of electrophysiological signal and cellular morphology. Journal of Neuroscience and Neuroengineering. 2012, 1(2): 131-142.