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.
Highlights
Traumatic brain injury (TBI) is a leading cause of disability and long-term loss of working capacity in working-age and socially active adults worldwide [1]
We examined and described typical alterations of brain electrical activity observed in rats subjected to penetrating TBI [6,7,8,9]
The dose of mafedine was chosen based on our previous results [15], and that of dexmedetomidine was chosen according to literature data [16,17,18]
Summary
Traumatic brain injury (TBI) is a leading cause of disability and long-term loss of working capacity in working-age and socially active adults worldwide [1]. A major problem for the development of new drugs aimed at improving neuronal survival in traumatic and/or ischemic conditions is the limited translational potential of experimental animal studies. Behavioral and functional testing, biochemical, and immunohistochemical methods are the conventional standards for evaluating pharmacological agents aimed at treating neurological impairments which result from brain trauma and other central nervous-system disorders. Other neuroimaging techniques such as magnetic resonance, computed, and positron emission tomography, are much less commonly used, which is explained by their expensiveness and the high spatial resolutions that are required for small animals
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