Equine grass sickness, but not botulism, causes autonomic and enteric neurodegeneration and increases soluble N-ethylmaleimide-sensitive factor attachment receptor protein expression within neuronal perikarya.
Abstract: Equine grass sickness (EGS) is of unknown aetiology. Despite some evidence suggesting that it represents a toxico-infection with Clostridium botulinum types C and/or D, the effect of EGS on the functional targets of botulinum neurotoxins, namely the soluble N-ethylmaleimide-sensitive factor attachment receptor (SNARE) proteins, is unknown. Further, while it is commonly stated that, unlike EGS, equine botulism is not associated with autonomic and enteric neurodegeneration, this has not been definitively assessed. Objective: To determine: 1) whether botulism causes autonomic and enteric neurodegeneration; and 2) the effect of EGS on the expression of SNARE proteins within cranial cervical ganglion (CCG) and enteric neuronal perikarya. Methods: Descriptive study. Methods: Light microscopy was used to compare the morphology of neurons in haematoxylin-eosin stained sections of CCG and ileum from 6 EGS horses, 5 botulism horses and 6 control horses. Immunohistochemistry was used to compare the expression of synaptosomal-associated protein-25, synaptobrevin (Syb) and syntaxin within CCG neurons, and of Syb in enteric neurons, from horses with EGS, horses with botulism and control horses. The concentrations of these SNARE proteins in extracts of CCG from EGS and control horses were compared using quantitative fluorescent western blotting. Results: EGS, but not botulism, was associated with autonomic and enteric neurodegeneration and with increased immunoreactivity for SNARE proteins within neuronal perikarya. Quantitative fluorescent western blotting confirmed increased concentrations of synaptosomal-associated protein-25, Syb and syntaxin within CCG extracts from EGS vs. control horses, with the increases in the latter 2 proteins being statistically significant. Conclusions: The occurrence of autonomic and enteric neurodegeneration, and increased expression of SNARE proteins within neuronal perikarya, in EGS but not botulism, suggests that EGS may not be caused by botulinum neurotoxins. Further investigation of the aetiology of EGS is therefore warranted.
© 2015 EVJ Ltd.
Publication Date: 2016-01-11 PubMed ID: 26640078DOI: 10.1111/evj.12543Google Scholar: Lookup
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- Journal Article
Summary
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This research explores the effects of Equine Grass Sickness and Botulism in horses, specifically focusing on neurodegeneration and the expression of certain proteins called SNARE. The study found that Equine Grass Sickness, but not Botulism, causes neurodegeneration and increases the expression of SNARE proteins. This helps to uncover new insights about the possible causes of Equine Grass Sickness, indicating that it may not be caused by botulinum neurotoxins as previously thought.
Study Objective
- The research aims to determine whether botulism causes autonomic and enteric neurodegeneration (the progressive loss of structure or function of neurons, including death of neurons).
- Another goal is to investigate the effects of Equine Grass Sickness (EGS) on the expression of SNARE proteins within specific areas of the nervous system.
Method
- The study utilised light microscopy to compare the morphology of neurons in stained sections from horses affected by EGS, botulism, and control horses.
- Immunohistochemistry was used to compare the expression of certain proteins (synaptosomal-associated protein-25, synaptobrevin, and syntaxin) within the neurons of these horses.
- Additionally, the concentrations of these SNARE proteins were compared using quantitative fluorescent western blotting, a widely used analytical technique to detect specific proteins in a sample of tissue homogenate or extract.
Findings
- The study found that EGS, but not botulism, was associated with autonomic and enteric neurodegeneration. This means that horses suffering from EGS showed progressive degeneration of their neurons, unlike those affected by botulism.
- EGS was also linked to increased immunoreactivity for SNARE proteins within neuronal perikarya, indicating that EGS affects the expression of these proteins.
- Quantitative fluorescent western blotting confirmed increased concentrations of the studied proteins within extracts from EGS affected horses, supporting the earlier findings.
Conclusion
- The research concludes that the occurrence of autonomic and enteric neurodegeneration, and increased expression of SNARE proteins within neuronal perikarya, in EGS but not botulism, suggests that EGS may not be caused by botulinum neurotoxins.
- This insight disrupts the previous understanding of EGS, and suggests the need for further investigation into its cause.
Cite This Article
APA
McGorum BC, Scholes S, Milne EM, Eaton SL, Wishart TM, Poxton IR, Moss S, Wernery U, Davey T, Harris JB, Pirie RS.
(2016).
Equine grass sickness, but not botulism, causes autonomic and enteric neurodegeneration and increases soluble N-ethylmaleimide-sensitive factor attachment receptor protein expression within neuronal perikarya.
Equine Vet J, 48(6), 786-791.
https://doi.org/10.1111/evj.12543 Publication
Researcher Affiliations
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, University of Edinburgh, Roslin, UK. bruce.mcgorum@ed.ac.uk.
- SAC Consulting Veterinary Services, Penicuik, Midlothian, UK.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, University of Edinburgh, Roslin, UK.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, University of Edinburgh, Roslin, UK.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, University of Edinburgh, Roslin, UK.
- Euan MacDonald Centre for Motor Neuron Disease Research, University of Edinburgh, Midlothian, UK.
- Edinburgh Infectious Diseases, University of Edinburgh, Midlothian, UK.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, University of Edinburgh, Roslin, UK.
- Central Veterinary Research Laboratory, Dubai, United Arab Emirates.
- Electron Microscopy Research Services, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
- Medical Toxicology Centre and Institute of Neuroscience, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, University of Edinburgh, Roslin, UK.
MeSH Terms
- Animals
- Autonomic Nervous System Diseases / veterinary
- Botulism / veterinary
- Gene Expression Regulation
- Horse Diseases / physiopathology
- Horses
- N-Ethylmaleimide-Sensitive Proteins / genetics
- N-Ethylmaleimide-Sensitive Proteins / metabolism
- Neurons / metabolism
- SNARE Proteins / genetics
- SNARE Proteins / metabolism
Citations
This article has been cited 2 times.- Lindberg I, Shu Z, Lam H, Helwig M, Yucer N, Laperle A, Svendsen CN, Di Monte DA, Maidment NT. The proSAAS Chaperone Provides Neuroprotection and Attenuates Transsynaptic α-Synuclein Spread in Rodent Models of Parkinson's Disease.. J Parkinsons Dis 2022;12(5):1463-1478.
- Chaplot K, Jarvela TS, Lindberg I. Secreted Chaperones in Neurodegeneration.. Front Aging Neurosci 2020;12:268.
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