Abstract
Cadmium is considered one of the most toxic heavy metals which can cause cytotoxicity in multiple organs including the brain. Despite many studies over the past decades, the cellular and molecular mechanisms underlying its neurotoxicity remain unclear. The present study was designed to examine the acute effects of cadmium chloride (CdCl2) on the electrical activity of the Retzius nerve cells of leech Haemopis sanguisuga using electrophysiological techniques. CdCl2, in concentrations of 10–100 μM, produced a dose- and time-dependent depolarization of Retzius neurons, paralleled by an increase in firing frequency and action potential duration. To examine potential mechanisms, we studied the effects of cadmium on the outward potassium current upon depolarization using a point microelectrode voltage-clamp technique. Reduction of the fast, and partial inhibition of the slow outward current were observed after adding 50 and 100 μM CdCl2 in the external fluid. The present results support the view that the effect of cadmium on the outward potassium channel may be a potential contributing mechanism for cadmium-induced neurotoxic damage. The proposed mechanism of cadmium action on the electrical properties of leech Retzius neurons might have broader significance concerning not only the leeches but vertebrate brains as well.
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More From: Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology
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