Neurotoxic effects of mercury on auditory cortex networks growing on microelectrode arrays: a preliminary analysis

Mercury is known to cause sensorineural hearing loss and impaired speech perception. However, there is still a lack of a quantitative description of mercury toxicity on central auditory structures. This is a preliminary study using the novel technique of microelectrode array (MEA) recordings to evaluate acute and chronic neurotoxic effects of mercury on auditory cortex networks (ACNs) in vitro. Morphological and electrophysiological effects of mercuric chloride (HgCl2) were studied. Neurons dissociated from auditory cortices of 14-day-old mouse embryos were grown on photoetched MEAs containing 64 transparent indium-tin oxide (ITO) electrodes. For acute electrophysiological experiments, the spontaneous spiking and bursting activity from ACNs were compared before and after application of HgCl2. For chronic electrophysiological experiments, auditory cortex cultures were treated with various concentrations of HgCl2 from the day of seeding, and were tested 4 weeks later for the presence of spontaneous activity. Morphological analysis was conducted on 8-day-old ACNs treated with HgCl2 for 3 days. Results of acute experiments indicated that <75 mM of HgCl2 had an excitatory effect of variable magnitude on the spontaneous activity of ACNs; however, concentrations above 100 μM completely and irreversibly inhibited spike and burst activity. Chronic exposure of ACNs to 10 μM HgCl2 completely blocked the spontaneous activity. Morphological analysis indicated that 10 μM HgCl2 caused neuronal cell death in 3 days. It is concluded that HgCl2 has a more toxic effect on auditory networks when exposed chronically, and the levels of mercury showing toxic effects on ACNs are within the dose range shown to cause neurologic symptoms in humans. (C) 2002 Elsevier Science Inc. All rights reserved.