Enhanced Intracranial Microdialysis by Reduction of Traumatic Penetration Injury at the Probe Track.

Abstract

Microdialysis provides deep insight into chemical neuroscience by enabling in vivo intracranial chemical monitoring. Nevertheless, implanting a microdialysis probe causes a traumatic penetration injury (TPI) of brain tissue at the probe track. The TPI, which is clearly documented by voltammetry and histochemical imaging, is a drawback because it perturbs the exact tissue from which the brain dialysate samples are derived. Our goal is to reduce, if not eventually eliminate, the TPI and its detrimental effects on neurochemical monitoring. Here, we demonstrate that combining a 5-day wait period after probe implantation with the continuous retrodialysis of a low-micromolar concentration of dexamethasone vastly reduces the TPI. Our approach to reducing the TPI reinstates normal evoked dopamine release activity in the tissue adjacent to the microdialysis probe, brings evoked dopamine release at the probe outlet into quantitative agreement with evoked dopamine release next to the probe, reinstates normal immunoreactivity for tyrosine hydroxylase and the dopamine transporter near the probe track, and greatly suppresses glial activation and scaring near the probe track. This reduction of the TPI and reinstatement of normal evoked dopamine release activity adjacent to the probe track appears to be due to dexamethasone's anti-inflammatory actions.