Functional Imbalance of Glutamate- and GABAergic Neuronal Systems in the Pathogenesis of Focal Drug-Resistant Epilepsy in Humans
Bulletin of Experimental Biology and Medicine, ISSN: 1573-8221, Vol: 168, Issue: 4, Page: 529-532
2020
- 15Citations
- 22Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations15
- Citation Indexes15
- 15
- CrossRef1
- Captures22
- Readers22
- 22
Article Description
The mechanisms of the formation of pharmacological resistance in temporal focal epilepsy remain poorly understood, and effective treatment strategies that can suppress epileptogenesis do not currently exist. We studied the imbalance between the glutamatergic (stimulating) and GABAergic (inhibitory) neuronal systems, as well as the role of apoptotic processes in the pathogenesis of drug-resistant epilepsy. To this end, the expression of Gad65, Vglut2, NR2B, Bcl-2, and caspase-8 proteins was analyzed in the gray and white matter of the temporal cortex of human brain. It was shown that pathological processes in the glutamatergic and GABAergic systems related to drug-resistant epilepsy are accompanied by changes in the content of apoptotic proteins, which can be the cause of neuronal death.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85081691807&origin=inward; http://dx.doi.org/10.1007/s10517-020-04747-3; http://www.ncbi.nlm.nih.gov/pubmed/32147766; http://link.springer.com/10.1007/s10517-020-04747-3; https://dx.doi.org/10.1007/s10517-020-04747-3; https://link.springer.com/article/10.1007/s10517-020-04747-3
Springer Science and Business Media LLC
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