The neuromuscular junction (NMJ) is the synapse between a motor neuron and a skeletal muscle fiber. When an action potential reaches the motor nerve terminal, it triggers the release of the neurotransmitter acetylcholine (ACh), which binds to receptors on the muscle fiber endplate. This binding depolarizes the muscle membrane and initiates muscle contraction. Terminal Schwann cells and kranocytes are supporting cells that cap the nerve terminal and endplate region and contribute to the structural integrity, maintenance, and repair of the NMJ.

Neuromuscular Junction (NMJ) | Staining & Analysis

Q: Which diseases and conditions affect the NMJ?

Disruption of the neuromuscular junction has been reported in many motor neuron diseases, peripheral neuropathies, and muscular dystrophies, including but not limited to: Amyotrophic Lateral Sclerosis (ALS) Myasthenia Gravis Congenital myasthenic syndromes and Lambert–Eaton myasthenic syndrome (LEMS) Charcot–Marie–Tooth Disease Spinal Muscular Atrophy (SMA) Duchenne muscular dystrophy (DMD)

Q: How is the NMJ affected in neurodegenerative disorders?

In many neurodegenerative motor neuron disease (MND) models, NMJ degeneration occurs before the onset of overt motor neuron loss and clinical symptoms. Morphological changes in NMJs consistently observed in various animal models of motor neuron disease include: Increased axonal and terminal fragmentation Loss of axonal neuromuscular junction innervation Increased neuromuscular junction denervation Axonal sprouting and incomplete reinnervation Altered endplate morphology Disrupted arrangement and clustering of acetylcholine receptors

Q: How can NMJ morphology be studied?

Multiplex immunofluorescence is a powerful tool to study NMJ morphology because it offers high-sensitivity staining of the various subcomponents of the NMJ. Super-resolution microscopy and electron microscopy (EM) can also be useful to study the mechanisms of synaptic transmission, but these imaging modalities offer a much lower throughput and are generally less suitable for large-scale therapeutic efficacy studies.

Q: Can we study NMJ longitudinally?

Multiple non-invasive methods can be used to assess NMJ function longitudinally, including: Electromyography (EMG) Motor unit number estimation (MUNE) Compound muscle action potential (CMAP) In vivo imaging using fluorescent probes targeting NMJ components However, these methods primarily assess NMJ function and do not directly capture the detailed morphological changes that occur at individual NMJs during disease progression.

Q: What are complementary biomarkers to study NMJ-related diseases?

Motor function and coordination can be monitored using standardized behavioral tests in animal models (hindlimb clasping, hindlimb paralysis scoring, and grid-based agility), while non-invasive imaging modalities, such as DEXA, CT, and MRI, provide quantitative measures of muscle volume and atrophy. Blood and CSF biomarkers can also offer minimally invasive indicators of ongoing pathology.

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What Services does Biospective offer for NMJ Staining & NMJ Analysis?

The neuromuscular junction (NMJ) is affected in a wide variety of neurological and muscle diseases, including:

Amyotrophic lateral sclerosis (ALS) (Verma, 2022)
Myasthenia gravis (Vincent, 2002)
Charcot-Marie-Tooth disease (Cipriani, 2018)
Spinal muscular atrophy (SMA) (Murray, 2010) and
Duchenne muscular dystrophy (DMD) (Pratt, 2015)

Quantitative analysis of NMJ features, such as NMJ innervation and NMJ denervation, is critical to understanding disease progression and response to therapeutic intervention, particularly with respect to ALS pathology and NMJ pathology in other neuromuscular disease models. Our team at Biospective has developed robust methods for multiplex immunofluorescence staining and quantitative image analysis of NMJs from muscle tissue sections, including optimization for ALS neuromuscular junction studies.

What is Biospective's Process for NMJ Staining & Analysis?

Our Process for NMJ Staining & Analysis

At Biospective, we have implemented a standardized, highly reproducible multi-step process for staining and analysis of NMJs from formalin-fixed muscles:

1. Tissue Sectioning

We embed the muscles in OCT before freezing and storage at -80^oC
We generate high-quality, fixed-frozen tissue sections using specially-equipped microtomes
Sections are mounted on high-performance glass slides ensure adherence during the staining process

2. Multiplex Immunofluorescence NMJ Staining of Tissue Sections

We perform multiplex staining for:
- Presynaptic terminal (SV2A)
- Motor endplates (alpha-bungarotoxin)
- Innervating axon (beta-III-tubulin)
Staining is conducted using a high-throughput, automated IHC/IF instrument to ensure consistency and reproducibility

3. Slide Scanning

Whole sections are digitized at ultrahigh spatial resolution using a digital slide scanner
The resulting images are used for both visualization and quantitative analysis

4. Image Segmentation, NMJ Quantification, and NMJ Analysis

Our imaging scientists have developed advanced, fully-automated segmentation methods for presynaptic terminals (SV2A), motor endplates (α-bungarotoxin), and innervating axons (β-III-tubulin)
Our neuromuscular junction analysis tools allow for high-throughput, low bias neuromuscular junction quantification
We derive a range of quantitative metrics from the segmented images to characterize NMJ morphology and functional state

Sample Collection, Preparation, and Shipping Guidelines

We provide comprehensive support to ensure sample integrity and data reliability:

Sample Collection: Animals should be perfused with cold PBS and/or 10% neutral-buffered formalin, and the muscles should be carefully extracted.
Sample Preparation: Muscle tissue must be briefly fixed in 10% neutral-buffered formalin and snap frozen. 
Sample Shipping: Samples must be shipped on dry ice using insulated containers, avoiding repeated freeze-thaw cycles.

Schematic illustrating the key components of the neuromuscular junction (NMJ), including presynaptic motor neuron terminals, postsynaptic motor endplate, terminal Schwann cells, and kranocytes.  Abbreviations: Neuromuscular Junction (NMJ), Acetylcholine (ACh), ACh Receptors (AChR).

What is the Neuromuscular Junction (NMJ)?

The neuromuscular junction (NMJ) is a specialized synapse that enables communication between motor neurons and skeletal muscle fibers, allowing precise muscle contractions. Presynaptic motor neuron terminals release acetylcholine (ACh) in response to electrical signals, which binds to receptors in the motor endplate of the muscle membrane, triggering an action potential and subsequent muscle contraction.

Why Analyze the NMJ?

Early site of pathology: NMJs are affected before motor neuron loss in multiple neurodegenerative diseases (the “dying-back” process).
Quantitative readout: Enables monitoring of denervation, remodeling, and therapeutic response in preclinical models.
Experimentally accessible: The peripheral body location allows robust imaging & analysis, facilitating high-resolution assessment of synaptic integrity.

In this video, we provide an overview of our NMJ staining & analysis. It also includes an illustrative example of NMJ denervation in a mouse model of ALS, demonstrating how our services can be used to measure neurodegeneration, monitor disease progression, and evaluate potential therapies in preclinical studies.

Video Transcript

The neuromuscular junction is the synapse between motor neurons and muscle fibers, which is crucial for voluntary muscle contraction. Early degeneration at neuromuscular junctions is a hallmark of diseases like ALS, often occurring before motor neuron loss. Quantifying NMJ morphology, innervation, and denervation provides critical insights into disease progression and therapeutic effects.

At the neuromuscular junction, a motor neuron releases acetylcholine, which binds to receptors on the muscle fiber and triggers an action potential along its membrane leading to muscle contraction. 

Multiplex Immunofluorescence is used to study the neuromuscular junction in detail. In this study, gastrocnemius muscles of mice were collected, perfused, embedded in OCT and cut into thin sections. Multiplex Immunofluorescence was then performed to visualize presynaptic terminals, motor endplates, and innervating axons.  

Here, we show a low magnification view of the gastrocnemius muscle, along with a high magnification close-up of the neuromuscular junctions. The postsynaptic component is labeled with α-bungarotoxin, the presynaptic terminals with SV2A, and the axons with β-III-tubulin. 

A fully automated segmentation method was used to quantify NMJ morphology from the multiplex immunofluorescent images. In our method, each fluorescent channel is segmented separately using local thresholding, and innervation then is calculated as the overlap between the SV2A and α-bungarotoxin segmentations. A broad set of morphological features from the presynaptic and postsynaptic components is then used to classify each neuromuscular junction. 

We validated this method in the rNLS8 TDP-43 ΔNLS mouse model of ALS, which shows progressive ALS-like pathology, including NMJ degeneration, muscle atrophy, brain atrophy, and neuroinflammation. 

Eight weeks after induction, Biospective’s Low Dox rNLS8 mouse model displays a pronounced reduction in neuromuscular junction innervation relative to tTA control mice. 

At the same time point, Low Dox rNLS8 mice also show fewer axonal projections and less complex presynaptic branching than Control mice. 

Grip strength testing confirmed that rNLS8 mice generate less muscle force than their Control counterparts. 

Serial non-invasive CT imaging demonstrated a clear time-dependent loss of muscle volume in rNLS8 mice relative to Controls. 

Electrophysiological recordings revealed diminished compound muscle action potentials in rNLS8 mice, indicating compromised neuromuscular function. 

In summary, Low Dox rNLS8 mice show clear disruptions in neuromuscular junction innervation and presynaptic architecture. Our quantitative analysis of these changes is consistent with clinically relevant readouts, including muscle weakness, EMG abnormalities, and muscle atrophy. 

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What is the Value of NMJ Analysis in Animal Models?

The NMJ is highly sensitive to innervation changes, morphological alterations, and degeneration across multiple neuromuscular diseases. NMJ analysis in animal models allows researchers to monitor disease progression and evaluate the efficacy of experimental therapeutic agents in preclinical studies.

Leveraging our validated imaging platforms, scientific expertise, and extensive experience, we provide robust, reproducible NMJ quantification across diverse models and species. Here, we highlight NMJ alterations in a mouse model of ALS that we routinely use for testing novel therapeutic interventions.

Amyotrophic Lateral Sclerosis (ALS) Models & ALS NMJ Pathology

An optimal animal model of ALS (or motor neuron disease [MND]) should exhibit the following key features:

Symptom similarity to human ALS / MND, including motor deficits and NMJ vulnerability
Progressive disease course, allowing longitudinal studies of pathology
Disease modification, enabling interventions that alter disease progression
Availability of age-appropriate animals for preclinical studies
Low inter-animal variability, ensuring reproducible results across cohorts

TDP-43ΔNLS (rNLS8) Model

The TDP-43ΔNLS (rNLS8) Model mouse model meets these criteria, making it an attractive system for ALS drug development. This model expresses human TDP-43 with a defective nuclear localization signal (NLS), which impairs nuclear import and leads to cytoplasmic accumulation of TDP-43 in neurons. Over time, this mislocalized protein forms phosphorylated TDP-43 aggregates, recapitulating key pathological features observed in ALS patients.

At Biospective, we utilize both the original and modified versions of the rNLS8 ALS mouse model of TDP-43 proteinopathy:

Original mouse model ("Off Dox"): rapid disease progression over weeks
Biospective mouse model ("Low Dox"): slower, progressive disease over months

Both models exhibit progressive pathology, including: 

Motor neuron degeneration & regional brain atrophy
Cytoplasmic TDP-43 accumulation and phosphorylated TDP-43 aggregates
Motor deficits
Brain, spinal cord, and neuromuscular junction (NMJ) pathology

For more information, see our Resources:

How is the NMJ Affected in the TDP-43ΔNLS (rNLS8) Mouse Model of ALS?

Biospective’s research scientists have conducted a rigorous evaluation of NMJ integrity and denervation in TDP-43 transgenic mouse models. This study compared tTA control mice with "Low Dox" rNLS8 mice at 8 weeks post-model induction.

Our study demonstrated:

Marked reductions in SV2A/α-bungarotoxin co-localization, indicating NMJ denervation
Decreased total axonal projections
Simplified presynaptic architecture, reflecting ALS-like synaptic pathology

These findings highlight the progressive synaptic dysfunction at the NMJ and support this mouse model’s use for preclinical evaluation of therapeutic interventions targeting NMJ preservation in ALS.

In the "Image Interactive" below, you can find results from our NMJ analysis, including high-resolution Multiplex Immunofluorescence tissue sections of muscle from Biospective's “Low Dox” TDP-43ΔNLS (rNLS8) mouse model and control mice.

You can pan around the image using the left mouse button. You can zoom in and out using the mouse/trackpad (up/down) or the + and - buttons in the upper left corner. You can toggle (on/off), change color, and adjust image settings for the channels in the Control Panel in the upper right corner.

We suggest using Full Screen Mode for the best interactive experience.

Neuromuscular Junction (NMJ) Denervation in the TDP-43ΔNLS (rNLS8) Mouse Model of ALS

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Authors: Pasquale Esposito, Robin Guay-Lord, Lionel Breuillaud, Kristina DeDuck, and Barry J. Bedell

Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease characterized by motor neuron degeneration, leading to muscle weakness, paralysis, and ultimately respiratory failure. Early in disease progression, neuromuscular junctions (NMJs) — the synaptic connections between motor neurons and skeletal muscles — undergo structural and functional alterations that precede overt neuron loss, hypothesized to reflect a “dying-back” process and progressive denervation.

Biospective has implemented a low doxycycline (“Low Dox”) version of the well-established TDP-43ΔNLS (rNLS8) mouse model, enabling controlled and progressive induction of TDP-43 pathology and early NMJ impairment. In this model:

rNLS8 mice express human TDP-43ΔNLS under doxycycline control of the neurofilament heavy (NEFH) promoter
The Low Dox protocol induces gradual TDP-43 mislocalization and aggregation (including phosphorylated cytoplasmic inclusions) over several weeks/months, modeling progressive NMJ pathology
Early NMJ pathology mirrors the initial synaptic vulnerability hypothesized in human ALS

This Interactive Presentation highlights NMJ structural alterations in the Low Dox rNLS8 model, including:

Reduced presynaptic terminals
Loss of synaptic alignment
Simplified axonal arborization

The rNLS8 mouse is a bigenic, doxycycline-regulated model generated by crossing the tetO-hTDP-43ΔNLS responder line with the NEFH-tTA driver line, with tTA-only littermates serving as controls. For this study, 40 µm-thick fixed-frozen gastrocnemius muscle tissue sections from N=13 Low Dox rNLS8 mice and N=13 tTA control mice were labeled for presynaptic (SV2A, βIII-tubulin) and postsynaptic (alpha-bungarotoxin) NMJ components, with nuclei counterstained using DAPI. This multiplex immunofluorescence approach enabled quantitative and spatial analysis of denervation, synaptic alignment, and axonal arborization, capturing subtle NMJ alterations that precede motor neuron loss.

To navigate though this Image Story, you can use the arrows and/or the Table of Contents icon in the upper right corner of this panel.

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You can also interact with the microscopy image in the Image Viewer on the right at any time to further explore this high-resolution data.

Overview of NMJ Architecture in the Mouse Gastrocnemius Muscle

This high-resolution microscopy image shows α-bungarotoxin (α-BTX) labeling of postsynaptic acetylcholine receptors (AChRs) in 40 µm-thick tissue sections of mouse gastrocnemius muscle. The image highlights the distribution of NMJs across muscle fibers, with each motor endplate appearing as a compact α-BTX-positive region.

Using our PERMITS™ quantitative analysis, we quantified the density of α-BTX in the gastrocnemius muscle. The plot below shows no significant difference between rNLS8 Low Dox mice and tTA control mice, indicating that the overall NMJ density and spatial organization remain preserved at this stage of disease progression.

A graph showing the difference in alpha-bungarotoxin staining density between Low Dox and Control mice

α-BTX signal density for tTA mice (control) compared to Low Dox rNLS8 mice; mean ± SEM. There is no significant difference between groups.

Multiplex Labeling of Presynaptic and Postsynaptic NMJ Components

This multiplex immunofluorescence (mIF) image shows α-BTX (postsynaptic AChRs), SV2A (presynaptic vesicles), and βIII-tubulin (axonal projections) from a tTA control mouse. In tTA controls, strong SV2A–α-BTX co-localization (which appear in yellow) indicates intact innervation and proper synaptic alignment. In Low Dox rNLS8 mice, SV2A signal is reduced or absent at α-BTX-positive endplates, indicating denervation. βIII-tubulin labeling demonstrates decreased axonal signal at NMJ sites, reflecting early compromise of axonal integrity at the junction.

Using our PERMITS™ quantitative analysis, we measured both the degree of SV2A–α-BTX overlap and the complexity of presynaptic branching. The plots below show that Low Dox mice exhibit a significant reduction in presynaptic branching complexity and decreased overlap between α-BTX and SV2A compared to tTA controls, reflecting impaired synaptic integrity and progressive denervation.

A graph showing differences in NMJ innervation between Low Dox and control mice

SV2A/α-BTX overlap (%) in tTA mice (control) vs. Low Dox rNLS8 mice; mean ± SEM, t-test, **** p < 0.0001.

A graph showing the difference in presynaptic branching complexity between Low Dox and control mice

Presynaptic branching complexity in tTA mice (control) vs. Low Dox rNLS8 mice; mean ± SEM, t-test, **** p < 0.0001.

Classification of NMJs was performed based on the percentage of SV2A signal overlapping α-BTX labeling, and these categories can be visualized directly as colored boxes in the microscopy images. Fully denervated NMJs were defined as having 0-20% SV2A/α-BTX overlap, indicating minimal or absent presynaptic contact. Partially innervated NMJs were defined as having 20-80% overlap, reflecting reduced or incomplete presynaptic coverage. Fully innervated NMJs were classified as 80-100% overlap, representing intact synaptic alignment and preserved presynaptic connectivity.

Fully Innervated NMJs in a tTA Mouse Gastrocnemius Muscle

This high-magnification microscopy image shows NMJs from a tTA control mouse. Fully innervated NMJs are evident, in which α-BTX and SV2A signals exhibit precise spatial overlap (yellow), indicating full synaptic coverage and an intact neurotransmission architecture.

Using PERMITS™ analysis, we quantified the density of fully innervated NMJs. The plot below shows that Low Dox mice have significantly fewer fully innervated NMJs compared to tTA controls.

A graph showing the difference in NMJs that are fully innervated between Low Dox and control mice

Fully innervated NMJ (defined as 80–100% overlap between α-BTX and SV2A) density for tTA mice (control) compared to Low Dox rNLS8 mice; mean ± SEM, t-test, **** p < 0.0001.

Denervated NMJs in a Low Dox rNLS8 Mouse Gastrocnemius Muscle

This high-magnification microscopy image shows denervated NMJs in a Low Dox rNLS8 mouse. Postsynaptic acetylcholine receptor clusters (α-BTX) remain visible, but presynaptic terminals (SV2A) are markedly reduced or absent, indicating partial and/or complete denervation of NMJs.

Using PERMITS™ analysis, quantitative measurements were performed to examine the density of partially innervated and fully denervated NMJs. The plots below demonstrate that Low Dox mice exhibit significantly more partially innervated and fully denervated NMJs compared to tTA controls.

A graph showing the difference in NMJs that are fully denervated between Low Dox and control mice

Fully denervated NMJs (defined as 0–20% overlap between α-BTX and SV2A) density for tTA mice (control) compared to Low Dox rNLS8 mice; mean ± SEM, t-test, **** p < 0.0001.

A graph showing the difference between NMJs that are partially innervated between Low Dox and control mice

Partially innervated NMJs (defined as 20–80% overlap between α-BTX and SV2A) density for tTA mice (control) compared to Low Dox rNLS8 mice; mean ± SEM, t-test, ** p < 0.01.

Reduced Axonal Density in the Gastrocnemius Muscle from a Low Dox rNLS8 Mouse

This microscopy image shows reduced motor axon density in a Low Dox rNLS8 mouse, an early sign of distal axonal pathology before overt denervation. βIII-tubulin and SV2A labeling reveal fewer axonal branches projecting to postsynaptic endplates, with fragmented presynaptic networks and shortened terminals compared to controls.

Using PERMITS™ analysis, total axonal projections were quantified. The plot below shows that Low Dox mice have significantly fewer axonal projections compared to tTA controls.

A graph showing the difference in total axonal projections between Low Dox and control mice

Total axonal projections for tTA mice (control) compared to Low Dox rNLS8 mice; mean ± SEM, t-test, **** p < 0.0001.

Sample Size Estimates for Detecting NMJ Structural Changes between Low Dox Mice and tTA Control Mice

The table below summarizes our sample size estimates for detecting changes between tTA control and Low Dox mice in SV2A–α-BTX overlap, presynaptic branching complexity, and total axonal projections. The sample sizes were estimated from observed effects change and standard deviations taken from N=13 mice in each of the two groups. Fewer than 15 mice/group are estimated to be required to detect statistical significance for an observed between-group difference of 25% in SV2A–α-BTX overlap, with <10 and <5 mice/group estimated to be required for detection of 33% and 50% between-group differences, respectively.

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Sample size estimates (# of mice/group) for detection of statistically significant differences in SV2A–α-BTX overlap, presynaptic branching complexity, and total axonal projections between tTA mice (control) and Low Dox rNLS8 mice. Green shading indicates that a sample size of 1-15 mice/group is required, light green shading indicates that 15-30 mice/group are required, and yellow shading denotes that 30-45 mice/group are needed to detect the observed between-group differences.

Multi-Modality Assessments of Neuromuscular Junction Structure and Function in the TDP-43ΔNLS Model

In addition to the NMJ innervation and structural changes highlighted here, we have quantified muscle atrophy using non-invasive longitudinal in vivo CT imaging, assessed muscle electrophysiology through EMG (measuring CMAP amplitude and latency), and evaluated muscle weakness via grip strength tests, all of which reflect clinically relevant features of human ALS.

Change in hindlimb muscle volume for Low Dox mice compared to control mice over a period of 10 weeks following model induction; mean ± SEM.

A graph showing the difference in CMAP maximum amplitude in Low Dox mice at 10 weeks following model induction

Maximum amplitude of compound muscle action potential (CMAP) measured in Low Dox mice at baseline (prior to model induction) and 10 weeks following model induction ; mean ± SEM, t-test, **** p < 0.0001

A graph showing the difference in CMAP latency in Low Dox mice at 10 weeks following model induction

Latency of compound muscle action potential (CMAP) measured in Low Dox mice at baseline (prior to model induction) and 10 weeks following model induction ; mean ± SEM, t-test, **** p < 0.0001

A graph showing the difference in grip strength between Low Dox and control mice

Average grip strength for Low Dox mice at 8 weeks post-induction compared to control mice; mean ± SEM, t-test, **** p < 0.0001.

Summary

This doxycycline-regulated TDP-43 mouse model (rNLS8) reproduces key features of early ALS pathology, including progressive NMJ disruption, manifested as partial and full denervation, and reduced axonal projections at NMJ sites, preceding overt motor neuron loss.

Biospective’s Low Dox protocol induces gradual TDP-43 mislocalization and cytoplasmic aggregation over several weeks, producing measurable decreases in presynaptic branching and NMJ innervation relative to tTA controls.

Combined with automated tissue staining and high-throughput imaging and analysis, the inducible rNLS8 TDP-43ΔNLS model enables precise, quantitative assessment of NMJ and axonal pathology, making it an ideal platform for preclinical evaluation of therapeutics targeting early synaptic deficits in ALS.

Please feel free to further explore the microscopy images in the viewer.

We would be happy to discuss this ALS mouse model, its characterization, and our NMJ analysis if you would like to Contact Us.

Table of Contents

Section: tTA Control

Zoom level

Segmentations

Fully Denervated NMJ

Partially Innervated NMJ

Fully Innervated NMJ

Channels

Nuclei (DAPI)

Postsynaptic (α-BTX)

Presynaptic (SV2A + βIII-tubulin)

Image Interactive displaying NMJ analysis results, featuring high-resolution Multiplex Immunofluorescence muscle sections from Biospective’s “Low Dox” TDP-43ΔNLS (rNLS8) mouse model alongside control tissues.

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How does Automation improve Results?

We use automated neuromuscular junction staining and analysis with advanced high-throughput imaging and quantification platforms. This approach ensures accurate and and reproducible assessment of neuromuscular junction structure and integrity across multiple samples and experimental conditions.

Comparison between Manual and Automated Staining & Analysis of the NMJ

Feature	Manual	Automated
Staining Consistency	Variable antibody incubation and uneven reagent distribution	Precisely controlled timing, temperature, and reagent application
Throughput & Efficiency	Time-consuming and limited number of slides analyzed	High-throughput staining, imaging, and data processing
Reproducibility	Operator-dependent variability in staining and analysis	Standardized protocols and algorithm-driven NMJ quantification
Data Accuracy & Analysis Depth	Subjective NMJ assessment; limited quantitative precision	Automated segmentation-localization, and morphological analysis
Morphological Profiling	Manual measurement of NMJ size, shape, and complexity	Automated extraction of NMJ area, perimeter, branching, and complexity metrics
Spatial Mapping	Limited to selected regions-of-interest (ROIs)	Whole-section mapping of NMJ distribution and synaptic coverage

This table compares manual and automated neuromuscular junction (NMJ) staining and analysis across key criteria, including staining consistency, throughput and efficiency, reproducibility, data accuracy and analysis depth, morphological profiling, and spatial mapping.

Example images of NMJs from mouse muscle that have undergone automated staining and image analysis using the processes developed at Biospective.

To discuss your study requirements or request a quote for Neuromuscular Junction (NMJ) staining and quantification services

FAQs

What is an NMJ?

Which diseases and conditions affect the NMJ?

How is the NMJ affected in neurodegenerative disorders?

How can NMJ morphology be studied?

Can we study NMJ longitudinally?

What are complementary biomarkers to study NMJ-related diseases?

References

Keywords

Neuromuscular Junction (NMJ) – Tissue Staining & Image Analysis Services for Muscle Specimens

Biospective provides industry-leading staining of the neuromuscular junction using multiplex immunofluorescence & image analysis of innervation & denervation.

What Services does Biospective offer for NMJ Staining & NMJ Analysis?

What is Biospective's Process for NMJ Staining & Analysis?

Our Process for NMJ Staining & Analysis

Sample Collection, Preparation, and Shipping Guidelines

What is the Neuromuscular Junction (NMJ)?

Why Analyze the NMJ?

What is the Value of NMJ Analysis in Animal Models?

Amyotrophic Lateral Sclerosis (ALS) Models & ALS NMJ Pathology

TDP-43ΔNLS (rNLS8) Model

How is the NMJ Affected in the TDP-43ΔNLS (rNLS8) Mouse Model of ALS?

Our study demonstrated:

How does Automation improve Results?

Comparison between Manual and Automated Staining & Analysis of the NMJ

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Neuromuscular Junction (NMJ) Morphology & ALS Models

ALS Mouse Models for Drug Development

ALS Mouse Models & Spinal Motor Neurons

TDP-43 ΔNLS (rNLS8) Mice for ALS Drug Development

More Information

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