The effect of 1,3-dinitrobenzene on the functioning of the auditory pathway in the rat

1, 3-dinitrobenzene (DNB) has previously been shown to be neuropathic, caus ing gliovascular lesioning in the rat brainstem, with the nuclei of the aud itory pathway being particularly affected. Lesion severity was shown to be dependent on functional activity, which could be markedly decreased within one pathway by monaurally reducing sensory input. The aim of this study was to characterise the changes in electrophysiological and vascular function associated with this asymmetric lesioning. Depth electrodes located in the inferior colliculi were used to measure wave II and IV of the auditory evok ed response (AER) and collicular blood flow. These were measured up to eigh t days after DNB exposure in rats, in which preexisting reduction in sensor y input in one ear was achieved by tympanic membrane rupture. Significant i ncreases of between 14-27 dB were seen in the mean stimulus level required to generate a 50% isoamplitude response for wave IV in the intact (ie vulne rable) pathway over days 1-8 post DNB. No significant changes in this respo nse for the other AER waves were seen over the same recording period. Signi ficant increases in blood flow were seen in the inferior colliculi up to 24 hours after the final dose of DNB. Differences in increased flow between t he colliculi were also highly significant, with peak increases of 200% and 80% seen in the intact and protected sides respectively. This difference sh ows that DNB enhanced blood flow appears to reflect the severity of the DNB induced functional deficit. In both cases, disturbance to normal glial fun ction in maintaining K+ homeostasis, may underlie the neurophysiological de ficit and the increase in blood flow seen at the level of the inferior coll iculi. These asymmetric functional changes were also parallelled by the dif ferential lesion severity between the protected and unprotected pathways. H ence, protection against DNB glial lesion severity by reduction in sensory input, and consequently metabolic demand, is paralleled by the early vascul ar response and functional neuronal deficit seen over the eight day post DN B recording period. (C) 1999 Intox Press, inc.