Neurotoxin Action
Neurotoxin Action - Related Videos
15:05
Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons
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Cited by 9 •
2015
A custom protocol is described to differentiate mouse ES cells into defined populations of highly pure neurons exhibiting functioning synapses and emergent network behavior. Electrophysiological analysis demonstrates the loss of synaptic transmission following exposure to botulinum neurotoxin serotypes /A-/G and tetanus neurotoxin.
12:25
Isolation and Quantification of Botulinum Neurotoxin From Complex Matrices Using the BoTest Matrix Assays
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Cited by 5 •
2014
The BoTest Matrix botulinum neurotoxin (BoNT) detection assays rapidly purify and quantify BoNT from a range of sample matrices. Here, we present a protocol for the detection and quantification of BoNT from both solid and liquid matrices and demonstrate the assay with BOTOX, tomatoes, and milk.
10:30
A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators
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Cited by 4 •
2013
The botulinum neurotoxin type A light chain (BoNT/A LC) is a metalloprotease that enters motor neurons, cleaves its substrate SNAP-25, and disrupts neurotransmission, thereby resulting in flaccid paralysis. Utilizing a high-throughput-compatible FRET-based assay, large libraries of small molecules can be screened for their impact on BoNT/A LC enzymatic activity.
14:10
A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors
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Cited by 3 •
2014
Botulinum neurotoxin is one of the most potent toxins among Category-A biothreat agents, yet a post-exposure therapeutic is not available. The high content imaging approach is a powerful methodology for identifying novel inhibitors as it enables multiparameter screening using biologically relevant motor neurons, the primary target of this toxin.
12:33
Corticospinal Excitability Modulation During Action Observation
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Cited by 22 •
2013
Single-pulse transcranial magnetic stimulation over the primary motor cortex, neuronavigation, and registration of electromyographic activity of hand muscles were used in this study to explore corticospinal excitability while participants were observing action sequences.
FAQs
Receptor blockade prevents a neurotransmitter signal from producing its usual effect, whereas overstimulation drives signaling beyond normal control. These opposing changes can both disrupt neural communication, but they may produce different physiological outcomes depending on the receptor and affected pathway. Comparing them helps connect a toxin’s molecular interaction with effects such as paralysis, seizures, or sensory changes.
Sodium and calcium channels help regulate electrical activity and communication in nervous tissue. Changing sodium-channel activity can alter membrane potentials, while changing calcium-channel activity can affect events linked to neurotransmitter release. Because these channels influence both neuronal excitability and synaptic signaling, their disruption provides a mechanistic route from molecular toxicity to widespread neurological dysfunction.
Neurotransmitter release controls how one neuron communicates with another cell. If a toxin interferes with this process, downstream cells may receive too little or too much signaling, depending on the direction of the disruption. The resulting pattern of communication helps determine whether exposed tissue shows reduced function, excessive activity, or altered sensory processing.
Exposure assessment benefits from identifying which neural targets are affected and how target disruption relates to physiological outcomes. Linking a molecular interaction with changes in nervous-system function can help investigators interpret neurological signs and evaluate the significance of contact with a toxin. This mechanistic approach adds biological context beyond simply recording that exposure occurred.
Mapping the affected receptor, ion channel, or neurotransmitter-release process identifies a potential point for therapeutic intervention. Researchers can use that connection to consider how an antidote might counter the disrupted pathway or how a drug could deliberately modify similar neural signaling. The value lies in relating a defined molecular target to a measurable neurological outcome.
Selected toxins can serve as probes for studying particular components of neural communication because their effects reveal what happens when receptors, ion channels, or neurotransmitter release are altered. Observing the resulting physiological changes helps researchers connect cellular mechanisms with nervous-system function. This makes toxin-based investigation relevant to both basic biology and toxicology research.