NEUROINFLAMMATORY RESPONSE AFTER EXPERIMENTAL TRAUMA TO THE INFANT RODENT BRAIN

Abstract

PURPOSE. Mechanical trauma to the immature rodent brain induces a local primary injury and a distant secondary neuroapoptosis. These lesions are associated with glial cell activation, infiltration of immune cells, increased levels of proinflammatory mediators and proteases as part of neuroinflammation. METHODS. Seven-day-old rats were subjected to cortical trauma with a weight-drop device. Animals were sacrificed at defined time points from 2 hours to 21 days and brain tissues were processed for molecular, biochemical and histological analyses. RESULTS. We studied the expression, distribution pattern, time course and cellular localization of two pro-inflammatory mediators (IL-1ß and IL-18) and two proteases (MMP-2 and MMP-9). Apoptotic cell death affected mostly neuronal populations in the cortex, thalamus and caudate nucleus mainly ipsilateral to the injury 6 hours to 5 days after trauma. The involvement of microglia, astroglia and monocytesmacrophages were investigated at the site of primary and secondary damages. They may contribute to acute or delayed trauma-induced neuronal deficit. CONCLUSIONS. Our findings suggest that the interleukins, proteases and microglia/astrocytes are involved in trauma-induced neuroinflammatory response and might serve as a potential therapeutic target.

Keywords

• traumatic brain injury
• cortex
• thalamus
• neuroapoptosis
• macroglia
• astrocytes
• il-1β/il-18
• mmp-2/mmp-9