Using a 100-point Todd scale, we examined the level of neurological deficiency in male albino rats subjected to dosed experimental traumatic brain injury (TBI). In one of the three experimental groups with TBI, animals were not subjected to additional influences; in another group, the central cholinergic system (CChS) was activated by introduction of a central-action cholinomimetic, choline alfoscerate (Gliatilin); in the third group, the activity of the above system was suppressed by a cholinoblocker, biperiden (Akineton). In rats with TBI, the level of neurological deficiency progressively increased; in this group, the estimates at 3 and 72 h after TBI induction corresponded to 474 and 950% of the respective values in intact animals. Blocking of the cholinergic system additionally aggravated manifestations of neurological deficiency, especially within earlier time intervals after TBI (3 and 24 h). Pharmacological activation of the CChS significantly smoothed manifestations of neurological disorders (several times, as compared with those in the TBI group with no additional influences).
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Zyablitsev, S.V., Khudoley, S.A., Sudilovskaya, Y.L. et al. Effects of Modifications of the Functional State of the Central Cholinergic System on Neurological Deficiency Related to Experimental Traumatic Brain Injury. Neurophysiology 47, 168–170 (2015). https://doi.org/10.1007/s11062-015-9515-0
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DOI: https://doi.org/10.1007/s11062-015-9515-0