MOTOR AND EXPLORATORY BEHAVIORAL CONSEQUENCES IN A NEONATAL ANOXIA MODEL

Neonatal anoxia is a major public health problem associated with long-term neurological impairments, as it triggers biochemical cascades that lead to cell death and neurodevelopmental disruption, including reduced ATP production, increased reactive oxygen species, activation of nitric oxide synthase and glial cells, and a neuroinflammatory response characterized by reactive gliosis. Astrocytes also regulate extracellular matrix proteins such as Neuroligin-2, a synaptic adhesion molecule involved in inhibitory synapse maturation and excitatory–inhibitory balance, whose dysregulation has been associated with neuropsychiatric disorders. This study aimed to evaluate behavioral outcomes related to limbic, cortico-striatal and nigrostriatal circuits following neonatal anoxia. Male and female C57BL/6 mice (n = 9-11/group) were subjected to anoxia at postnatal days 3–4 by exposure to 100% nitrogen for 12 min. Behavioral assessments were conducted at postnatal days 30 and 70 using open field, pole test, catalepsy, rotarod, and prepulse inhibition. Data were analyzed using Welch’s t-test or Mann–Whitney test. No significant differences were observed between groups in the pole test, rotarod performance or prepulse inhibition, and no sex differences were detected. However, the anoxia group showed increased locomotor activity in the open field, with higher total distance traveled, reduced time at the borders at both ages (p<.01), and increased time spent in the center at postnatal day 30 (p<.001). A small but significant effect was also observed in the catalepsy test and in the number of falls during rotarod training. These findings indicate that neonatal anoxia induces persistent behavioral alterations, mainly affecting motor and exploratory activity.