TY - JOUR

T1 - Effects of Alpha-2 adrenergic agonist mafedine on brain electrical activity in rats after traumatic brain injury

AU - Sysoev, Yuriy I.

AU - Prikhodko, Veronika A.

AU - Chernyakov, Roman T.

AU - Idiyatullin, Ruslan D.

AU - Musienko, Pavel E.

AU - Okovityi, Sergey V.

N1 - Sysoev, Y.I.; Prikhodko, V.A.; Chernyakov, R.T.; Idiyatullin, R.D.; Musienko, P.E.; Okovityi, S.V. Effects of Alpha-2 Adrenergic Agonist Mafedine on Brain Electrical Activity in Rats after Traumatic Brain Injury. Brain Sci. 2021, 11, 981. https://doi.org/10.3390/brainsci11080981

PY - 2021/7/25

Y1 - 2021/7/25

N2 - 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.

AB - 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.

KW - Dexmedetomidine

KW - Electrocorticography

KW - Mafedine

KW - Neuroprotection

KW - Rat

KW - Traumatic brain injury

KW - dexmedetomidine

KW - rat

KW - mafedine

KW - traumatic brain injury

KW - MODEL

KW - electrocorticography

KW - CORTEX

KW - neuroprotection

KW - DEXMEDETOMIDINE

UR - http://www.scopus.com/inward/record.url?scp=85112241217&partnerID=8YFLogxK

UR - https://www.mendeley.com/catalogue/d27d7607-4ea1-3580-b783-492811902a7f/

U2 - 10.3390/brainsci11080981

DO - 10.3390/brainsci11080981

M3 - Article

AN - SCOPUS:85112241217

VL - 11

JO - Brain Sciences

JF - Brain Sciences

SN - 2076-3425

IS - 8

M1 - 981

ER -