Lidocaine does not modify GFAP and NF expression in an excitotoxic spinal cord injury model

SISTI MS, NISHIDA F, ZANUZZI CN, CAMIÑA AE, VON WERNICH M, PORTIANSKY EL

Congreso; XXXII Congreso Anual Sociedad Argentina de Investigación en Neurociencias; 2017

Lidocaine has some neuroprotective and anti-neuroinflammatory effects when administered at certain concentrations. After a spinal cord injury (SCI), astrocytes may contribute either to the formation of an inhibitory glial scar or can participate in neural repair. Increased expression of GFAP is one of the hallmarks of their activation while neurofilament (NF) expression is an indicator of neuronal integrity. The goal of the present work was to determine the effect of an intraparenchymal injection of lidocaine on GFAP and NF expression in a rat spinal cord kainic acid (KA) excitotoxic model. Male Sprague-Dawley rats were injected either with 1mM KA (KA1), 0.5% lidocaine (L05), 1 mM KA + 0.5% lidocaine (KA1-L05) or saline (sham) at the C5 segment. Intact rats were used as controls. Rats were euthanized either at 1, 2, 3, 7 or 14 post-injection days and their spinal cord was extracted, segmented and immunohistochemically processed. Besides KA1-L05 protocol has previously shown that neuronal cell counting was not significantly reduced as it occurs with the KA1 group, in this work we showed that lidocaine alone or simultaneously injected with KA significantly avoids the GFAP+ astrocytes increase observed for the KA1 and the sham groups. In addition, KA1-L05 did not reduced NF expression as observed for the KA1 group, along the experiment. These results suggest that lidocaine might be preventing neuronal damage and astrocytes reactivity in the KA-excitotoxic SCI process.