HOW IT WORKS
Learn how MEA assays work and the innovation behind Axion's products.
Getting started with Maestro couldn't be easier. Culture your neurons in an Axion multiwell MEA plate [A]. Load this MEA plate into the Maestro MEA system and allow the environmental chamber to automatically equilibrate [B]. Analyze the neural activity of the neurons in the MEA plate label-free and in real-time with AxIS Navigator software [C].
WHAT IS MEA?
Axion’s microelectrode array (MEA) plates have a grid of tightly spaced electrodes embedded in the culture surface of each well [A]. Electrically active cells, such as neurons, can be cultured over the electrodes [B]. Over time, as the cultures become established, neurons can form cohesive networks and present an electrophysiological profile. The resulting electrical activity, spontaneous or induced firing of neurons, is captured from each electrode on a microsecond timescale providing both temporally and spatially precise data [C].
NEURAL NETWORK RECORDINGS
Electrical activity is captured from neurons (orange) cultured over electrodes (gray circle). The Maestro MEA system detects key parameters of neural network function, including activity, oscillation, and synchrony.
- Activity – are the neurons functional? Action potentials are the defining feature of neuron function. High values indicate the neurons are firing action potentials frequently. Low values indicate the neurons may have impaired electrophysiological function.
- Synchrony – are the synapses functional? Synapses are functional connections between neurons, such that an action potential from one neuron affects the likelihood of an action potential from another neuron. Synchrony reflects the strength of synaptic connections, and thus how likely neurons are to generate action potentials simultaneously on millisecond time scales. High values (toward 1) indicate highly synchronous activity, and low values (toward 0) indicate the firing of individual neurons has little influence on the activity in other neurons.
- Oscillation – is the network functional? Neural oscillations, defined by alternating periods of high and low activity, are a hallmark of functional networks with excitatory and inhibitory neurons. Oscillation is a measure of how the spikes from all of the neurons in a well are organized in time. High values indicate that the network exhibits bursts of action potentials interspersed with periods of relative quiescence. Low values indicate action potentials are not coordinated across neurons in the network.
YOUR MINI-BRAINS HAVE BIG POTENTIAL
Discover the electrical activity of your neural organoids.
Recent trends in developmental biology and disease-in-a-dish modeling highlight the value of using cell models that more accurately recapitulate the multicellular organization and structure of in vivo tissues, such as 3D iPSC-derived neural models. Assessing the functionality of these 3D models, commonly referred to as neural organoids, or “mini-brains," is vital for their use in disease modeling, drug discovery, and drug safety. Using Maestro microelectrode array (MEA) technology, any scientist can now quickly and easily measure electrical network behavior from live organoids in a multiwell plate at high throughput.
Experts in the field explain how they are using Axion's technology to better understand neural diseases.
The development of disorders such as autism and schizophrenia are thought to have their origins in the developing brain. But studying the development of the human brain is challenging due to the absence of good model. In this webinar, Prof. Alysson Muotri (UC San Diego) demonstrates that the spontaneous development of neural networks in neural organoids, commonly referred to as “mini-brains,” resembles those found during early human brain formation. The research findings covered in this webinar were published recently in the journal, Cell Stem Cell, and were featured in numerous media outlets including the New York Times and NPR.
Epilepsy is a devastating neurological disease caused by an imbalance in the electrical signals between the cells of the brain. It affects 1% of newborns and very young children. In children, 1/3 of all cases fail to respond to currently available medication. The primary challenge in the fight against epilepsy is the lack of model systems that effectively mirror what goes wrong in human patients. In this webinar, Dr. Evangelos Kiskinis (Northwestern University), demonstrates how patient-specific neurons in vitro recapitulate the neural firing patterns observed in patient EEGs in vivo. Using this platform Dr. Kiskinis hopes to be able to predict what drug would work best for each patient, removing the trial-and-error approach to epilepsy therapy.
Fragile X syndrome is the most prevalent genetic form of intellectual disability. There is no cure or treatment due in part to the complexity in the Fragile X syndrome neuronal circuitry. In this webinar, Dr. John Graef (Fulcrum Therapeutics), demonstrates how using CRISPR gene-editing and patient-derived cells Fulcrum can create the Fragile X syndrome phenotype in a dish. Moreover, this approach has enabled an estimate of the level of FMRP protein expression required to correct the observed Fragile X syndrome phenotype.
“Man on Fire” syndrome, also known as Inherited Erythromelalgia (IEM), is a chronic pain syndrome characterized by burning pain in the hands and feet. The chronic pain of most patients with IEM cannot be relieved by common pain killers making this disease a major unmet medical need. In this webinar, Dr. Yang Yang (Purdue University) discusses advances in the treatment of IEM using a pharmacogenomic approach. The drug responsiveness of different genetic mutations associated with IEM were probed in an in vitro Maestro MEA assay, with the results helping to predict the effective treatment of these IEM patients in the clinic.
Neuromuscular disorders include ALS, myasthenia gravis, and the muscular dystrophies such as Duchenne's. Collectively these disorders exceed an incidence of 1 in 3,000. Although there is a strong genetic understanding of many of these disorders, the poor translatability of animal models to humans has hindered the development of treatments for these diseases. Consequently, there is a need for a model that more faithfully recapitulates the physiology of the human neuromuscular junction. In this webinar, Dr. Elliot Swartz (UCLA) discusses how he is building a light controlled hiPSC model of a neuromuscular junction to help better understand neuromuscular disorders.
Autism, also known as autism spectrum disorder, is a range of conditions classified as neurodevelopmental disorders. Individuals diagnosed with autism show challenges with social skills, repetitive behaviors, speech and nonverbal communication. Autism is estimated to affect about 1% of people, or 62.2 million globally. The genetics of autism are complex meaning better methods are required to help understand the genetic risk factors that underlie autism. In this webinar, Dr. Michael Nestor (The Hussman Institute for Autism) discusses how studying the spontaneous firing activity of patient-derived iPSC neurons in an MEA assay is helping to build a model of autism.
In our daily lives we are exposed to thousands of commercially used chemicals. Many of these chemicals are not toxic at typical exposure levels, but for thousands of chemicals, toxicological information is lacking. The National Academy of Sciences report on ‘‘Toxicity testing in the 21st century’’ highlighted the need for efficient methods to screen chemicals (e.g. insecticides) for their potential to cause toxicity. In this webinar, Dr. Lorena Saavedra (NeuCyte) discusses how measuring compound-induced changes to the spontaneous firing activity of human stem cell-derived neural cells in an MEA assay helped detect potentially harmful neurological side effects of compounds such as pyrethroid insecticides.