EFFECTS OF THE EARLY GLUCOCORTICOIDS-LOADED NANOSYSTEMS IN MOTOR SEQUALAE AND NEUROINFLAMMATORY PROCESSES INDUCED BY MILD TRAUMATIC BRAIN INJURY.

Mar del Plata

Congreso; REUNIÓN DE SOCIEDADES DE BIOCIENCIAS 2023; 2023

Mild traumatic brain injury (mTBI) causes a variety of neuropathological manifestations including cognitive, emotional, and physiological deficits, probably related to early neuroinflammatory processes. Despite the efforts to develop neuroprotective treatments, most preclinical studies did not report significant effects. We have previously shown that nanocarriers loaded with the synthetic glucocorticoid triamcinolone (NT) prevent oxidative stress processes and reduce cognitive and emotional sequelae induced by mTBI. Nevertheless, little is known about NT effects in mTBI-induced motor impairments nor neuroinflammation processes in deficits-related brain structures. The aim of the present work was to characterize mTBI-induced motor deficits and the underlying neuroinflammatory processes, and the impact of early NT treatment in behavioral nor biochemical alterations. mTBI was induced in anesthetized adult male Wistar rats, which 15 min and 24 h later received a dose of NT ( mg/Kg). Seven days after, they were tested for amphetamine (0.5 mg/kg)-induced locomotor activity (LA) or grip strength, and then sacrificed to assess pro-inflammatory cytokines (by RT-PCR) levels in dorsal and ventral striatum. Additional groups were sacrificed at 24 h to assess pro-inflammatory cytokines or 7 d post-mTBI to ascertain TBARS in the same brain structures. Preliminary results indicate that mTBI induced significant increase in LA (RM-ANOVA) and IL-6 and IL-1B (one way ANOVA) in dorsal striatum. We concluded that mTBI induced increases in neuroinflammatory mediators that could have detrimental actions on motor activity. More experiments are in process, to confirm alterations in TBARS levels and NT effects in behavioral and neurochemical alterations induced by mTBI.