Sodium Cromoglycate Decreases Sensorimotor Impairment and Hippocampal Alterations Induced by Severe Traumatic Brain Injury in Rats
Por:
Segovia-Oropeza, Marysol, Santiago-Castaneda, Cindy, Orozco-Suarez, Sandra Adela, Concha, Luis, Rocha, Luisa
Publicada:
1 dic 2020
Categoría:
Neurology (clinical)
Resumen:
Severe traumatic brain injury (TBI) results in significant functional
disturbances in the hippocampus. Studies support that sodium
cromoglycate (CG) induces neuroprotective effects. This study focused on
investigating the effects of post-TBI subchronic administration of CG on
hippocampal hyperexcitability and damage as well as on sensorimotor
impairment in rats. In contrast to the control group (Sham+SS group),
animals undergoing severe TBI (TBI+SS group) showed sensorimotor
dysfunction over the experimental post-TBI period (day 2, 55%,p <
0.001; day 23, 39.5%,p < 0.001; day 30, 38.6%,p < 0.01). On day 30
post-TBI, TBI+SS group showed neuronal hyperexcitability (63.3%,p <
0.01). The hippocampus ipsilateral to the injury showed volume reduction
(14.4%, p < 0.001) with a volume of damage of 0.15 +/- 0.09 mm(3).
These changes were associated with neuronal loss in the dentate gyrus
(ipsilateral, 33%,p < 0.05); hilus (ipsilateral, 77%,p < 0.001;
contralateral, 51%,p < 0.001); Cornu Ammonis (CA)1 (ipsilateral, 40%,p
< 0.01), and CA3 (ipsilateral, 52%,p < 0.001; contralateral, 34%,p <
0.01). Animals receiving subchronic treatment with CG (50 mg/kg, s.c.
daily for 10 days) after TBI (TBI+CG group) displayed a sensorimotor
dysfunction less evident than that of the TBI+SS group (p < 0.001).
Their hippocampal excitability was similar to that of the Sham+SS group
(p = 0.21). The TBI+CG group presented hippocampal volume reduction
(12.7%,p = 0.94) and damage (0.10 +/- 0.03 mm(3),p > 0.99) similar to
the TBI+SS group. However, their hippocampal neuronal preservation was
similar to that of the Sham+SS group. These results indicate that CG
represents an appropriate and novel pharmacological strategy to reduce
the long-term sensorimotor impairment and hippocampal damage and
hyperexcitability that result as consequences of severe TBI.
Filiaciones:
Segovia-Oropeza, Marysol:
Ctr Res & Adv Studies, Dept Pharmacobiol, Mexico City, DF, Mexico
Santiago-Castaneda, Cindy:
Ctr Res & Adv Studies, Dept Pharmacobiol, Mexico City, DF, Mexico
Orozco-Suarez, Sandra Adela:
Natl Med Ctr, Unit Med Res Neurol Dis, Mexico City, DF, Mexico
Concha, Luis:
Univ Nacl Autonoma Mexico, Inst Neurobiol, Campus Juriquilla, Queretaro, Mexico
Rocha, Luisa:
Ctr Res & Adv Studies, Dept Pharmacobiol, Mexico City, DF, Mexico
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