Peer-reviewed veterinary case report
Neurotransmitter changes in epileptic Shetland sheepdog brains
By Morita, Takehito et al.·Published in The Journal of veterinary medical science·2005·Department of Veterinary Pathology, Japan·View original on PubMed →
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Original publication title: Changes in extracellular neurotransmitters in the cerebrum of familial idiopathic epileptic shetland sheepdogs using an intracerebral microdialysis technique and immunohistochemical study for glutamate metabolism.
- Species:
- dog
Plain-English summary
A group of Shetland sheepdogs with a family history of epilepsy were studied to understand what causes their seizures. Researchers found that during seizure activity, levels of certain neurotransmitters, specifically glutamate and aspartate, were higher in the dogs' brains. This suggests that these chemicals might be linked to the seizures. Additionally, a decrease in a specific protein that helps regulate glutamate levels was noted in the dogs that experienced severe seizures. These findings could help in developing better treatments for epilepsy in dogs.
People also search for: Shetland sheepdog seizures · dog epilepsy treatment · high glutamate in dogs · managing dog seizures
Abstract
Intracerebral microdialysis combined with electroencephalographic recordings was performed on 4 dogs of a familial idiopathic epileptic Shetland sheepdog colony to identify the kinds of neurotransmitters responsible for seizure activity. Immunohistochemistry using glutamate (Glu), glutamate transporter (GLT-1 and GLAST), and glutamine synthetase (GS) antibodies was also carried out on the cerebrum of four familial dogs that died of status epilepticus (SE). High values for extracellular levels of Glu and aspartate (ASP) were detected in association with an increased number of spikes and sharp waves during hyperventilation in 3 of 4 the familial epileptic dogs. The values of other amino acids analyzed were not altered in any of the familial epileptic dogs. Immunohistochemically, Glu-positive granules were occasionally found in the perineuronal spaces of the cerebral cortex in 3 of the familial epileptic dogs that died of SE. Immunostains for GLT-1 antibody predominantly decreased in the cerebral cortex and lateral nucleus of the thalamus in all the dogs that died of SE, whereas there were no differences detected in immunolabellings for GLAST and GS antibodies between familial epileptic dogs and controls. These results suggest that an extracellular release of both Glu and Asp may play an important role in the occurrence of seizure activity in this epileptic colony, and that a decreased expression of astrocytic GLT-1 may be related to development of SE.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/16327223/