Neurochemistry and Neuropharmacology
Author: Sofía de la Fuente | Email: s.delafuente@unc.edu.ar
Sofía de la Fuente1°, Aida Marcotti1°,Melisa Macizo Fuentes1°, María Lina Formica2°, Santiago D. Palma2°, Mariela F. Pérez1°
1° Departamento de Farmacología Otto Orsingher, IFEC-CONICET, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Ciudad Universitaria, Córdoba 5000, Argentina
2° Departamento de Ciencias Farmacéuticas, UNITEFA-CONICET, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Ciudad Universitaria, Córdoba 5000, Argentina
Traumatic brain injury (TBI) is the leading cause of long-term physical and cognitive impairment, probably related to early neuroinflammatory processes. Alterations in dopaminergic neurotransmission, mainly in the striatum and limbic system, are involved in the mechanisms underlying sensorimotor deficits induced by TBI. Despite efforts to develop neuroprotective treatments, most preclinical studies show limited efficacy. Previously, we showed that mild TBI (mTBI) induces cognitive deficits that are concomitant with increased oxidative stress biomarkers (OSb), which were attenuated by the administration of triamcinolone-loaded lipidic nanocapsules (NT). Aims: To evaluate mTBI-induced motor alterations as evidenced by amphetamine challenge in adult male Wistar rats, along with OSb and proinflammatory cytokines, and the effects of early NT treatment on these alterations. Results: NT treatment prevented the reduced habituation and locomotor activity in response to amphetamine in mTBI, observed 7 days after mTBI, obtaining responses similar to the SHAM group. We also expect modulation of OSb and proinflammatory cytokine levels in motor-related brain areas by NT treatment. These findings, coupled with previously observed cognitive deficits, suggest a possible hyperdopaminergic state in the mTBI model, likely triggered by early TBI-induced neuroinflammation.