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Effects of Alpha-2 Adrenergic Agonist Mafedine on Brain Electrical Activity in Rats after Traumatic Brain Injury.
Sysoev, Yuriy I; Prikhodko, Veronika A; Chernyakov, Roman T; Idiyatullin, Ruslan D; Musienko, Pavel E; Okovityi, Sergey V.
Afiliación
  • Sysoev YI; Department of Pharmacology and Clinical Pharmacology, Saint Petersburg State Chemical and Pharmaceutical University, 197022 Saint Petersburg, Russia.
  • Prikhodko VA; Laboratory of Neuroprosthetics, Institute of Translational Biomedicine, Saint Petersburg State University, 199034 Saint Petersburg, Russia.
  • Chernyakov RT; Pavlov Institute of Physiology RAS, 199034 Saint Petersburg, Russia.
  • Idiyatullin RD; Department of Pharmacology and Clinical Pharmacology, Saint Petersburg State Chemical and Pharmaceutical University, 197022 Saint Petersburg, Russia.
  • Musienko PE; N.P. Bechtereva Institute of the Human Brain of the Russian Academy of Sciences, 197376 Saint Petersburg, Russia.
  • Okovityi SV; Department of Pharmacology and Clinical Pharmacology, Saint Petersburg State Chemical and Pharmaceutical University, 197022 Saint Petersburg, Russia.
Brain Sci ; 11(8)2021 Jul 25.
Article en En | MEDLINE | ID: mdl-34439602
ABSTRACT
The search for and development of new neuroprotective (or cerebroprotective) drugs, as well as suitable methods for their preclinical efficacy evaluation, are priorities for current biomedical research. Alpha-2 adrenergic agonists, such as mafedine and dexmedetomidine, are a highly appealing group of drugs capable of reducing neurological deficits which result from brain trauma and vascular events in both experimental animals and human patients. Thus, our aim was to assess the effects of mafedine and dexmedetomidine on the brain's electrical activity in a controlled cortical-impact model of traumatic brain injury (TBI) in rats. The functional status of the animals was assessed by electrocorticography (ECoG), using ECoG electrodes which were chronically implanted in different cortical regions. The administration of intraperitoneal mafedine sodium at 2.5 mg∙kg-1 at 1 h after TBI induction, and daily for the following 6 days, restored interhemispheric connectivity in remote brain regions and intrahemispheric connections within the unaffected hemisphere at post-TBI day 7. Animals that had received mafedine sodium also demonstrated an improvement in cortical responses to photic and somatosensory stimulation. Dexmedetomidine at 25 µg∙kg-1 did not affect the brain's electrical activity in brain-injured rats. Our results confirm the previously described neuroprotective effects of mafedine sodium and suggest that ECoG registration and analysis are a viable method evaluating drug efficacy in experimental animal models of TBI.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Brain Sci Año: 2021 Tipo del documento: Article País de afiliación: Rusia

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Brain Sci Año: 2021 Tipo del documento: Article País de afiliación: Rusia