Sodium Cromoglycate Decreases Hippocampal Hyperexcitability and Somatomotor Deficit Subsequent to Severe Traumatic Brain Injury in Rats
Abstract number :
3.045
Submission category :
1. Basic Mechanisms / 1D. Mechanisms of Therapeutic Interventions
Year :
2018
Submission ID :
501114
Source :
www.aesnet.org
Presentation date :
12/3/2018 1:55:12 PM
Published date :
Nov 5, 2018, 18:00 PM
Authors :
Luisa Rocha, Center for Research and Advanced Studies; Marysol Segovia-Oropeza, Center for Research and Advanced Studies; Cindy Santiago-Castañeda, Center for Research and Advanced Studies; Sandra Orozco-Suarez, National Medical Center; and Luis Conc
Rationale: It is known that cromoglycate (CG) induces neuroprotective effects. The present study focused to evaluate the effect of the subchronic administration of CG on hippocampal hyperexcitability and motor deficit induced by a severe traumatic brain injury (TBI) in rats. Methods: Male Wistar rats (250-300 g) were used. Two groups (TBI and TBI-CG) were subjected to a severe TBI (2.7-3.3 atm) using the Lateral Fluid Percussion model. Thereafter, they received the daily administration of CG (50 mg/kg, i.p., TBI-CG group) or vehicle (saline solution, 1 ml/kg, i.p., TBI group), for 10 days. The SHAM group was manipulated as described for the TBI group, except that animals did not receive the TBI. Neuroscore test was applied before and 30 day after TBI to assess the somatomotor performance. On day 23 after the TBI, a bipolar electrode was implanted in the ventral hippocampus ipsilateral to the trauma for the evaluation of hippocampal excitability (afterdischarge threshold, ADT) 30 days after TBI. Results: The SHAM group showed a good somatomotor performance (28 points with the Neuroscore test) during the experimental procedure. At day 30 after manipulation, its ADT was achieved at 365 ± 19 µA. The TBI group had 18 ± 0.5 points in the Neuroscore test (35% less vs basal conditions; p <0.001), indicating a significant impairment in the somatomotor performance. TBI group achieved lower ADT values (163 ± 15 µA; 52% lower vs SHAM group, p<0.001), suggesting hippocampal hyperexcitability. Concerning the TBI-CG group, the somatomotor estimation after trauma (25 ± 0.6 points) was similar to basal conditions (p=0.29). Its ADT values (311 ± 39 µA) were analogous to those of the SHAM group (p=0.345). Conclusions: The results of the present study indicate that the subchronic administration of CG after TBI avoids the long-term hippocampal hyperexcitability and motor impairment. We conclude that CG represents a good therapeutic strategy for a favorable outcome after TBI. Funding: The study was carried out with the support of the National Council of Science and Technology (CONACyT) through scholarship number 458195 and grant 220365.