Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices

• Published in: Canadian journal of physiology and pharmacology Vol. 64; no. 12; p. 1507
• Main Authors: McKay, S J, Reynolds, J N, Racz, W J
• Format: Journal Article
• Language: English
• Published: Canada 01-12-1986
• Subjects: 4-Chloromercuribenzenesulfonate - toxicity; Animals; Calcium - metabolism; Calcium - pharmacology; Corpus Striatum - drug effects; Corpus Striatum - metabolism; Dopamine - metabolism; In Vitro Techniques; Ion Channels - drug effects; Male; Mercuric Chloride - toxicity; Mercury - toxicity; Methylmercury Compounds - toxicity; Mice; Potassium - pharmacology
• ISSN: 0008-4212
• DOI: 10.1139/y86-254

The effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices have been examined. All mercury compounds examined produced concentration-dependent increases in the spontaneous release of [3H]dopamine, with an order of potency of methylmercury greater than mercuric (Hg2+) mercury greater than p-choloromercuribenzene sulfonic acid. Methylmercury had no effect on the 25 mM potassium evoked release of [3H]dopamine in the presence of 1.3 mM calcium. However, in calcium-free conditions, methylmercury significantly increased the potassium-evoked release of [3H]dopamine. Mercuric mercury significantly reduced the 25 mM potassium evoked release of [3H]dopamine in the presence of 1.3 mM calcium, and this response was not reversible with brief washing of the tissue. In calcium-free conditions, mercuric mercury significantly elevated the evoked release of [3H]dopamine, similar to the result obtained with methylmercury. It is suggested that mercury compounds alter dopaminergic synaptic function, possibly by disrupting calcium homeostasis or calcium-dependent processes, and that methylmercury and mercuric mercury can have differential effects to alter dopaminergic neurotransmission.