Leptin and Remyelination

Leptin Promotes Proliferation of OPCs

Demyelination occurs in many diseases of the Central Nervous System (CNS) including Multiple Sclerosis and Parkinson's Disease. Here researchers show that Leptin plays a role in the proliferation of Oligodendrocyte Precursor Cells (OPCs): These cells are critical for keeping the myelin sheath on Neurons of the CNS healthy and happy.  Ken Matoba, Rieko Muramatsu & Toshihide Yamashita. Leptin sustains spontaneous remyelination in the adult central nervous system. Scientific Reports 7, Article number: 40397 (2017) doi:10.1038/srep40397.

Our LepRB Antibody is used in this study to stain OPCs.

Figures: (a) Representative image of cultured OPCs stained with antibodies against LepRb (green) and PDGFRα (red). Scale bar: 25 μm. (b) Relative BrdU incorporation into the OPC obtained from the brain (left graph) and spinal cord (right graph). Cells were treated with recombinant leptin for 48 h (n = 4). (Left graph) P = 0.005993 (control vs 10 ng/mL), 0.045616 (control vs 100 ng/mL), (Right graph) P = 0.004456 (control vs 10 ng/mL), 0.017859 (control vs 100 ng/mL). (c) Relative BrdU incorporation into the OPC after leptin stimulation (10 ng/ml) with U0126 (20 μM), a MEK inhibitor (n = 4 for brain OPCs, n = 3 for spinal cord OPCs). (Left graph) P = 0.019753 (control vs leptin), 0.039433 (leptin vs leptin + U0126), (Right graph) P = 0.045545 (control vs leptin), 0.04486 (leptin vs leptin + U0126). (d) Representative images of western blotting (upper panels) and quantitative analysis of ERK phosphorylation (lower graph) are shown. OPCs were treated with leptin (10 ng/ml) under indicated periods (n = 3). P = 0.006352 (2 min), 0.016571 (5 min), 0.017675 (10 min), 0.024100 (15 min), 0.081342 (30 min).

We are in the process of looking for Labs to sponsor Neuromics' to isolate and purify adult human OPCs in return for receiving 2,000,000 cells. Stay tuned.

Human Astroglia and Schwann Cells-BBB Model

Broadening our Capabilities

At the core of our solutions are many options for primary human cells. We are especially pleased that we have growing capabilities to provide new cells to researchers studying autoimmune neuro-degenerative diseases like ALS and MS with the addition of:
Schwann Cells

Human Schwann Cells (HSwC) are isolated from human spinal nerve. HSwC are cryopreserved at passage one and delivered frozen. Each vial contains >5 x 10^5 cells in 1 ml volume. HSwC are characterized by immunofluorescence with antibodies specific to S100, GFAP, and CD90. HSwC are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast, and fungi. HSwC can to further expand for 10 population doublings in our Schwann Growth medium (cat # SGM001).
Human Astrocytes

 Human Brain Astrocytes cultured with AlphaBioCoat.
Human Blood Brain Barrier Model
I will continue to post updates here.

Mouse and Human Motor Neurons

Designed for Neuro-muscular Diseases Research

Clients have been using our easy to culture and research proven GFP Labeled Mouse Motor Neurons for Neuro-muscular disease research. This includes the inclusion of the cells in several ALS drug discovery programs being conducted by large Pharma.

Image: GFP+ mMN Mouse Motor Neurons at 2 days post thaw 20X.

I am pleased to announce the addition of Human Motor Neurons to our Primary Human, Mouse and Rat Neurons, Astrocytes and Neuron-Astroglial co-culture solutions.

Image: Human alpha-Motor Neurons

Questions?  Do not hesitate to contact me directly, Pete Shuster, CEO and Owner, Neuromics, pshuster@neuromics.com and direct phone: 612-801-1007. Thank you.

Apoptosis and Neurodegeneration

Towards the Development of Disease Specific Assays
Neurodegenerative diseases are becoming increasingly prevalent, especially in the Western societies, with larger percentage of members living to an older age. They have to be seen not only as a health problem, but since they are care-intensive, they also carry a significant economic burden.

Apoptotic pathways are induced in many of these diseases and are key culprits in disease progression.

Figure: Schematic representation of apoptotic pathways. Apoptosis triggered by internal (intrinsic) or external (extrinsic) stress signals that is activated by binding of ligands (e.g. FasL, APO-2L, TRAIL, TNF) to cell surface receptors (e.g. Fas, DR4, DR5, TNF-R1). The intrinsic apoptosis pathway might be triggered by p53 upon DNA damage following exposure to cellular stress. In the intrinsic pathway, death signal reaches mitochondria, leading to release of cytochrome c, which can binds to Apaf1. The cytochrome c/Apaf1 make a complex with pro-caspase-9 (in the presence of dATP), activates caspase-9, which promotes caspase-3 activation, eventually leading to cell death. The extrinsic pathway is initiated through the stimulation of the members of tumor necrosis factor receptor (TNF-R) family (transmembrane death receptors) by their respective ligands. These receptors activate pro-caspases-8, -10 by recruiting the endogenous adaptor protein FADD. Procaspase-8, -10 cleave themselves to form activated caspase-8 or -10. Ultimately, effector enzymes such as caspase-3, -6, -7 are activated in this cascade to mediate apoptosis. Likewise, there can be cross-talk between the intrinsic and extrinsic pathways. For example caspase-8 may cleave Bid to form tBid that is a strong activator of the intrinsic/mitochondrial apoptotic pathway. The intrinsic pathway is usually activated by the recruitment of BAX and BAK to outer mitochondrial membrane, causing cytochrome c release formation of apoptosome and subsequent activation of caspase-9. Activated caspase-9 proteolytically activates caspases-3, -6, and -7. Moreover, some of the effector caspases also can activate caspase-8, forming a positive amplification loop. doi:10.1016/j.pneurobio.2013.10.004.

Working with the Apoptosis Experts at Immunochemistry Technologies and Human Astroglial-Neuron Biosensors Experts at ArunA Biomedical, we plan on  developing disease specific assays. Here's a map of the general process.

Larger Image

We welcome feedback and input on your interests. You can email rose@neuromics.com. We will continue to post updates on exciting new developments.

GFP Labeled Motor Neurons and MEA

Big Upcoming Webinar

We have been strategically partnering with ArunA Biomedical to improve how we serve Neuro-drug discovery and Neurotox research community. I am especially excited about how well are our GFP Labeled Mouse Neurons are working in many different and unique research applications. They have proved an important tool in the study of neuro-muscular diseases like ALS, Parkinson's and Multiple Sclerosis.

I am pleased to announce a coming Webinar: “GFP+ Motor Neurons: Development and in-vitro Functional Assessment” Wednesday June 10th, 11:30 AM EDT-Register Today!

Download Flyer. I will continue to post unique assays developed for our Astro-glial Neuron solutions.

Solutions for Studying Neuro-degeneration

Data Rich and Frequently Published

The Neuromics' brand is built, in part, by our proven ability to provide solutions for the study of neuro-degeneration. These include:

• Neuronal-Glial Markers
• Primary Neurons and Astrocytes
• Apoptosis Research Reagents
• Transfection Reagents

A recent example shows the use of one of  MAP-2 markers to study hearing decline with age: Radtke-schuller S, Seeler S and Grothe B(2015) Restricted loss of olivocochlear but not vestibular efferent neurons in the senescent gerbil (Meriones unguiculatus). Front. Aging Neurosci. 7:4. doi:10.3389/fnagi.2015.00004.

Figure: Lipofuscin granules in MSO neurons of an aged gerbil. MSO neurons are MAP2 immunostained (Alexa Fluor 647, red). Lipofuscin granules have been excited with the DAPI excitation wavelengths and appear blue. Confocal images show a maximum projection of image stacks in A and a single optical image of 0.3 µm thickness in the enlargement in B. Scale bar in A: 50 µm and 20 µm in B.

We stand ready to serve you. Should you have interest or questions, do not hesitate to contact me directly: Pete Shuster-Owner/CEO-pshuster@neuromics.com or direct phone: 612-801-1007. Thank you.

Schwann Cell-Sensory Neurons-PNS Markers

Data-Publications
These markers a important tools for the study of Neuro-muscular diseases like Amyotrophic Lateral Sclerosis (ALS) and Multiple Sclerosis (MS).

For Neuromuscular Disease Researchers, we have some of the best Schwann Cell and Sensory/Peripheral Neuron Markers in the business.

Images: Rat mixed neuron/glial cultures stained with Peripherin (green channel) and Neurofilament alpha-internexin/NF66 (green channel). These cultures contain mostly neurons which are rich in alpha-internexin, and a subgroup which have a large amount of peripherin also, such as the prominent cell in the middle of the micrograph. Since this cell expresses large amounts of peripherin and alpha-internexin, the green and red signals superimpose to produce a golden cell. Blue is a DNA stain. Protocol on data-sheet.

Here're recent publications referencing use of these markers:
Leah R. Reznikov, Qian Dong, Jeng-Haur Chena, Thomas O. Moninger, Jung Min Park, Yuzhou Zhang, Jianyang Du, Michael S. Hildebrand, Richard J. H. Smith, Christoph O. Randak, David A. Stoltz, and Michael J. Welsh. CFTR-deficient pigs display peripheral nervous system defects at birth. www.pnas.org/cgi/doi/10.1073/pnas.1222729110...goat anti-p75 (1:500; Neuromics)...

Gayle M. Passmore, Joanne M. Reilly, Matthew Thakur, Vanessa N. Keasberry, Stephen J. Marsh, Anthony H. Dickenson and David A. Brown. Functional significance of M-type potassium channels in nociceptive cutaneous sensory endings. Fronteirs in Molecular Science. doi: 10.3389/fnmol.2012.00063. ...neurofilament H (1:1000,Neuromics,USA)...

Leigh A Nattkemper, Zhong-Qiu Zhao, Anna J Nichols, Alexandru D P Papoiu, Carol A Shively, Zhou-Feng Chen and Gil Yosipovitch. Over-Expression of the Gastrin-Releasing Peptide in Cutaneous Nerve Fibers and its Receptor in Spinal Cord in Primates with Chronic Itch. Journal of Investigative Dermatology accepted article preview 4 April 2013; doi: 10.1038/jid.2013.166...Protein Gene Product 9.5 (PGP9.5; Neuromics, Edina, MN).

Wiebke Kallenborn-Gerhardt, Katrin Schröder, Domenico Del Turco, Ruirui Lu, Katharina Kynast, Judith Kosowski, Ellen Niederberger, Ajay M. Shah, Ralf P. Brandes, Gerd Geisslinger, and Achim Schmidtko. NADPH Oxidase-4 Maintains Neuropathic Pain after Peripheral Nerve Injury. The Journal of Neuroscience, 25 July 2012, 32(30): 10136-10145; doi: 10.1523/​JNEUROSCI.6227-11.2012...chicken anti-P-Zero or MPZ (1:500; Neuromics)...

Images: Micrographs depicting SSeCKS colocalization with myelination markers (CNPase and Pzero). (A) SSeCKS (red) and CNPase (green) in the lumbar spinal cord dorsal horn. The labeling appears discrete with minimal colocalization. (B) SSeCKS (red) and Pzero (green) in the L4 dorsal root ganglia. A lack of co-localization is observed and Pzero can be seen localized to putative axonal elements (arrow). (C) SSeCKS (red) and Pzero (green) in the sciatic nerve. As in the dorsal root ganglia, a lack of co-localization is observed. Both SSeCKS and Pzero can be seen localized to axonal elements. (D) SSeCKS (red) and Pzero (green) in glabrous skin of the hind-paw, fibers displaying colocalization (yellow) can be observed (arrow). Irmen et al. Journal of Brachial Plexus and Peripheral Nerve Injury 2008 3:8 doi:10.1186/1749-7221-3-8.

I will post new data and pubs as they become available.

OPC Markers!

Effective Oligodendrocyte, Oligodendroglial Oligodendrocyte Lineage Markers are important for determining the differentiate state of Oligodendrocyte Precursor Cells. This is important for the study of de and re-myelination of neurons and the discovery of potential therapeutic targets for diseases like MS and ALS.

Here researchers use our Olig2 antibody to study the differentiation state of Fetal Human Oligodendrocyte Progenitor Cells: Crystal R. McClain, Fraser J. Sim and Steven A. Goldman. Pleiotrophin Suppression of Receptor Protein Tyrosine Phosphatase-β/ζ Maintains the Self-Renewal Competence of Fetal Human Oligodendrocyte Progenitor Cells. The Journal of Neuroscience, 24 October 2012, 32(43): 15066-15075; doi: 10.1523/​JNEUROSCI.1320-12.2012.
Abstract: Oligodendrocyte progenitor cells (OPCs) persist in human white matter, yet the mechanisms by which they are maintained in an undifferentiated state are unknown. Human OPCs differentially express protein tyrosine phosphatase receptor β/ζ (PTPRZ1) and its inhibitory ligand, pleiotrophin, suggesting the maintenance of an autocrine loop by which PTPRZ1 activity is tonically suppressed. PTPRZ1 constitutively promotes the tyrosine dephosphorylation of β-catenin and, thus, β-catenin participation in T cell factor (TCF)-mediated transcription. Using CD140a/PDGFRα-based fluorescence-activated cell sorting to isolate fetal OPCs from the fetal brain at gestational ages 16–22 weeks, we asked whether pleiotrophin modulated the expansion of OPCs and, if so, whether this was effected through the serial engagement of PTPRZ1 and β-catenin-dependent signals, such as TCF-mediated transcription. Lentiviral shRNAi knockdown of PTPRZ1 induced TCF-mediated transcription and substantially augmented GSK3β inhibition-induced TCF-reporter luciferase expression, suggesting dual regulation of β-catenin and the importance of PTPRZ1 as a tonic brake upon TCF-dependent transcription. Pharmacological inhibition of GSK3β triggered substrate detachment and initiated sphere formation, yet had no effect on either proliferation or net cell number. In contrast, pleiotrophin strongly potentiated the proliferation of CD140a+-sorted OPCs, as did PTPRZ1 knockdown, which significantly increased the total number of population doublings exhibited by OPCs before mitotic senescence. These observations suggest that pleiotrophin inhibition of PTPRZ1 contributes to the homeostatic self-renewal of OPCs and that this process is mediated by the tonic activation of β-catenin/TCF-dependent transcription.

Images: To verify that GSK3β inhibition was effecting TCF activation through altering localization of β-catenin, the Wnt signaling intermediate, β-catenin, was localized by confocal imaging in OPCs, validated as such by their coexpression of Olig2.

Marker Options:

Name	Catalog #	Type	Species	Applications	Size	Price
CNPase	CH23013	Chicken IgY	H; M	ICC; IHC	100 ul	$89
Caspr2	SP15104	Sheep IgG	H; M	IHC; WB; E	100 ug	$365
HSP105	MO20028	Mouse IgG	H; M; R	IHC; WB	100 ul	$155
MAG/Siglec 4a	GT15152	Goat IgG	R	IHC; WB; E	100 ug	$365
MOG	GT15141	Goat IgG	H	IHC; WB; E	100 ug	$365
Mash1	GT15216	Goat IgG	M	IHC; WB; E	100 ug	$365
Mash1	MO15048	Rat IgG	H; M	ICC; WB; E	100 ug	$255
NOGO Receptor	GT15154	Goat IgG	H	IHC; WB; E	100 ug	$365
OMgp	GT15200	Goat IgG	H	WB; E	100 ug	$365
Olig1	RA14141	Rabbit IgG	R	IHC	100 ul 100 ul @ 1mg/ml	$350 $95
Olig1,2,3	MO15059	Mouse IgG	H; R	IHC	100 ug	$305
Olig2	GT15132	Goat IgG	H; M	IHC; WB; E	100 ug	$365
Olig2	RA25081	Rabbit IgG	H; M; R	ICC; IHC; WB; IP	100 ul	$395
Oligodendrocyte Marker O1	MO15001	Mouse IgM	H; M; R	IHC; FC	50 ug	$215
Oligodendrocyte Marker O4	MO15002	Mouse IgM	C; H; M; R	IHC	50 ug	$215
Oligodendrocyte Marker O4-Phycoerythrin Labeled	FC15013	Mouse IgM	H	FC	100 Tests	$305
PDGF R Alpha/CD140A	GT15150	Goat IgG	M	IHC; WB; E	100 ug	$365

ApoTransferrin and the fate of Neural Stem Cell/Progenitors

Implications for De-Myelinating Diseases Like MS and ALS

Dr. Juana María Pasquini and her team at the University of Buenos Aires are ongoing users of our Neural Stem Cell-Progenitor (NSC-NP) Markers. In this study, they use these markers to determine the states and fates of NSCs and NPs as they proliferate and differentiate and the related role of ApoTransferrin (aTF). Here we learn aTf exposure during differentiating conditions favours OL maturation from OPCs by promoting OL morphological development. This evidence supports a key role of Tf on the generation of OL from NSC/NPCs and highlights its potential in demyelinating disorder treatment: Silvestroff L , Franco PG , Pasquini JM (2012) ApoTransferrin: Dual Role on Adult Subventricular Zone-Derived Neurospheres. PLoS ONE 7(3): e33937. doi:10.1371/journal.pone.0033937.

Proliferation rates under different conditions are shown in A–C. BrdU incorporation (red) during proliferation (CTLP, A) or differentiation (CTLPCTLD, B). BrdU+ cells are expressed as a percentage of total nuclei for either condition in C. Free floating NS during proliferation express Nestin (D, green) and GFAP (E, green). After dissociation, NS-derived cells continue to express Nestin (F, green). PDGFRα+ (G, green) and NG2+ cells (H, green). Few MBP+ (I, green) cells were found under proliferative conditions. A large proportion of BrdU incorporating cells (J, red) co-expressed with NG2 (J, green). Some BLBP+ cells (K, green) incorporated BrdU (K, red). After differentiation (L–O), MBP+ cells were found with a highly branched and complex morphology (L, green). Cells expressed GFAP (M, green), as well as the neuronal NF200 marker (N, green). BrdU incorporating (O, red) cells were mostly NG2+ (O, green) during differentiation conditions. BrdU+ cells co-expressing NG2, as a proportion of total BrdU+ cells, are shown in P for either culture condition. A representative Western Blot membrane in Q shows how MBP levels increase in whole cell protein extracts as cells differentiate. The densitometric analysis of the MBP isoforms/GAPDH ratio of 5 independent experiments was semi-quantitated in R. All 4 MBP isoforms were pooled and considered as a single value before normalizing to GAPDH values. Blue colour in images indicates Höechst nuclear dye. Scale bar in A represents 250 µm for A and B. Scale bar in D equals 100 µm in D–I and L–N, scale bar in J equals 250 µm in J and O, and scale bar in K represents 50 µm. Bars in P represent mean values of 2 independent experiments. Bars in C and R represent Mean + SD of 4 and 5 individual cultures, respectively. Student's t Test was used to analyze data in C, while a One Way ANOVA with an SNK Post-test was used to analyze data in R. * p<0.05, ** p<0.01, *** p<0.001

Note:  PDGFRα+ is a marker for oligodendrocytes (OLs).

Here's the pathway model that sumarizes authors' findings

I will keep you posted on research that could implications for the discovery of de-myelinating disorder therapies.

Primary Neuron Assays for Studying Neurodegeneration

Our goal is to provide our customers and collaborators the tools they need to insure success. This is defined by having the specific Primary Neurons, Growth Factor plus the Markers to meet unique research needs.

The proof is in the results. Here are some highlights.

Images/Data: FIGURE 5. Microglial p38α MAPK-dependent TNFα is involved in LPS-induced neurite degeneration. (A) Photomicrographs of MAP-2 immunocytochemistry show the morphology of neurons after 72h of co-culture with microglia. The arrow points to the appearance of neurites that have been damaged by LPS-activated WT microglia. In contrast, the arrowhead points to the morphological appearance of healthy, undamaged neurites. (B) Diagram of the Sholl method for quantifying the total number of healthy neurites that intersect the concentric circles. (C) Quantification of healthy neurites by the Sholl analysis demonstrates that LPS stimulation of p38α WT microglia in co-culture causes neurite degeneration as seen by a significant reduction in the number of intersections by healthy neurites in the LPS-stimulated group compared to the unstimulated group (white bars). This degeneration can be attenuated by the addition of a blocking antibody to TNFα (5μg/ml), while the non-immune IgG control was not protective (gray bars). Microglia from p38α KO mice stimulated with LPS (black bar) also have significantly less neurite degeneration than the LPS-stimulated p38α WT microglia (white bar). However, by adding TNFα back to the p38α KO microglia co-culture, there is a significant decrease in the healthy neurite arborization compared to the p38α KO microglia stimulated with LPS alone (black bars). (***p<0.005; Bonferroni’s multiple comparison test). Data represents 2 independent experiments. Scale bar equals 25μm. Molecular Neurodegeneration 2011, 6:84 doi:10.1186/1750-1326-6-84

hN2 cells grown in culture for 4 days and stained with our chicken polyclonal to Neurofilament light or low molecular weight chain NF-L, a marker of neurons. Many of the differentiating cells show strong cytoplasmic and clearly fibrillar staining for NF-L. Blue stain is DAPI and reveals cell nuclei of some non neuronal cells in this culture.

We will continue to post relevant images and data that demonstrate our capabilities.

PINK1 and Alzheimer's and Multiple Sclerosis

I would like to highlight a recent publication referencing use of our PTEN-induced kinase/PINK1 Antibody.

Jack Van Horssen et al. investigated PINK1 expression in well-characterized brain samples derived from MS and AD individuals using immunohistochemistry.

Micha M.M. Wilhelmus, Susanne M.A. van der Pol, Quentin Jansen, Maarten E. Witte, Paul van der Valk, Annemieke J.M. Rozemuller, Benjamin Drukarch, Helga E. de Vries and Jack Van Horssen. Association of Parkinson disease-related protein PINK1 with Alzheimer disease and multiple sclerosis brain lesions. Free Radical Biology and Medicine. Volume 50, Issue 3, 1 February 2011, Pages 469-476.

Abstract: Mitochondrial dysfunction and oxidative stress are hallmarks of various neurological disorders, including multiple sclerosis (MS), Alzheimer disease (AD), and Parkinson disease (PD). Mutations in PINK1, a mitochondrial kinase, have been linked to the occurrence of early onset parkinsonism. Currently, various studies support the notion of a neuroprotective role for PINK1, as it protects cells from stress-mediated mitochondrial dysfunction, oxidative stress, and apoptosis. Because information about the distribution pattern of PINK1 in neurological diseases other than PD is scarce, we here investigated PINK1 expression in well-characterized brain samples derived from MS and AD individuals using immunohistochemistry. In control gray matter PINK1 immunoreactivity was observed in neurons, particularly neurons in layers IV–VI. Astrocytes were the most prominent cell type decorated by anti-PINK1 antibody in the white matter. In addition, PINK1 staining was observed in the cerebrovasculature. In AD, PINK1 was found to colocalize with classic senile plaques and vascular amyloid depositions, as well as reactive astrocytes associated with the characteristic AD lesions. Interestingly, PINK1 was absent from neurofibrillary tangles. In active demyelinating MS lesions we observed a marked astrocytic PINK1 immunostaining, whereas astrocytes in chronic lesions were weakly stained. Taken together, we observed PINK1 immunostaining in both AD and MS lesions, predominantly in reactive astrocytes associated with these lesions, suggesting that the increase in astrocytic PINK1 protein might be an intrinsic protective mechanism to limit cellular injury.

Immunohistochemistry

Immunohistochemistry was used to detect PINK1 immunostaining in temporal neocortex and white matter in AD, MS, and control subjects. Cryosections (5 μm) were air-dried and fixed in acetone for 10 min. Next, sections were incubated with an affinity-purified rabbit anti-PINK1 antibody (1:100; Neuromics, Edina, MN, USA) for 60 min at room temperature. Then, the slides were incubated with EnVision kit horseradish peroxidase-labeled anti-mouse/rabbit (DAKO, Glostrup, Denmark) for 30 min at room temperature and finally diaminobenzidine tetrachloride. Between incubation steps, sections were thoroughly washed with phosphate-buffered saline (PBS). After a short rinse in tap water sections were incubated with hematoxylin for 1 min and extensively washed with tap water for 10 min. Finally, sections were dehydrated with ethanol followed by xylol and mounted with Entellan (Merck, Darmstadt, Germany). All antibodies were diluted in PBS containing 0.1% bovine serum albumin (Boehringer–Mannheim, Germany), which also served as a negative control. Negative controls were essentially blank.

Image: In active lesions PINK1 immunostaining was intense in reactive astrocytes (arrows). Double labeling of PINK1 (green) with the astrocytic marker GFAP (red) demonstrated PINK1 expression in astrocytes (inset).

Related Reagents:

Neurodegenerative Disease Research
Antibodies

Neurodegenerative Disease Research Proteins

Neurotransmission
-Neurotransmission Research Antibody Categories

Neurotrophins and Growth Factor Antibodies

Neuron-Glial Expressed-Includes
Neurotrophin Proteins

Primary Neurons and Astrocytes
-Primary human, rat and mouse neurons and astrocytes by Category