CHARACTERIZATION OF NON-DISABLING SENSORIMOTOR DEFICITS INDUCED BY MILD TRAUMATIC BRAIN INJURY IN RATS.

SOFÍA DE LA FUENTE; MARIELA F. PÉREZ.

Mar del Plata

Congreso; Reunión conjunta de sociedades de biociencias 2022; 2022

Traumatic brain injury (TBI) causes a many neuropathological manifestations including cognitive, emotional, motor and psychological deficits, probably related to early neuroinflamatory processes. At cellular level, axons of catecolaminergic neurons are particularly vulnerable to primary and secondary injury mechanisms. Then, alterations in dopaminergic neurotransmission, mainly at striatum and the limbic system, could be involved in the mechanisms that underlie sensorimotor deficits induced by TBI. In fact, administration of dopamine-acting drugs in TBI patients improved symptoms related to the executive and cognitive function. We have previously shown that mild TBI (mTBI) generates cognitive deficits coincidently with increased levels of oxidative stress (OS) biomarkers (protein-AOPP and lipid-MDA peroxidation), right after mTBI that lasted over a 7 days (d) in brain areas mainly related to these functions. However, little is known about mTBI-induced sensorimotor consequences nor OS in brain structures related to these effects. Objective: to characterize motor and sensory deficits as well as AOPP and MDA levels in striatum after mTBI. Materials and methods: mTBI was induced in anesthetized adult male Wistar rats and 7 d after were tested in grip strength (GS), hot plate (HP) or amphetamine (0.5 mg/kg)-induced locomotor activity (LA). Other groups were sacrificed 60 min, 24 h or 7 d after mTBI to determine AOPP or MDA levels. Results: preliminary results indicate that mTBI induced significant decrease in time to fall in GS, increased in the latency in HP (p<0.05 unpaired t-test) and reduced LA (RM-ANOVA). AOPP and MDA determinations are still in progress. Conclusions: mTBI induced sensorimotor deficits in animals with apparent normal motor performance. These deficits may be related to early neuroinflammatory processes that could alter neuronal functioning in brain structures related to cognitive, sensorimotor and psychiatric disorders described in TBI patients.