MOTOR END PLATE REACTIVITY TO DIVALENT METAL IONS HISTOCHEMICAL STUDIES

TOSHIO NAKAMURA ¹, TATSUJI NAMBA ¹, and DAVID GROB ¹

¹ Departments of Medicine, Maimonides Medical Center and State University of New York, Downstate Medical Center, Brooklyn, New York

Motor end plates in the tibialis anterior muscle of the rat were demonstrated by metal sulfide deposits following injection of aqueous solutions of lead, stannous, cadmium, zinc or cupric ions into the muscle in vivo or in vitro. The appearance of the end plates was similar to the structure demonstrated by cholinesterase staining, with visualization of the subneural apparatus. Neither metal binding nor cholinesterase activity was affected 4 weeks after dissection of the sciatic nerve, indicating that the metal binding site is postsynaptic. Freezing or formalin fixation of muscle prevented binding of all metal ions to the end plate without greatly affecting cholinesterase activity, indicating that these two activities of the end plate are distinct. Prior administration of acetylcholine, d-tubocurarine, neostigmine or diisopropyl fluorophosphate inhibited binding to the end plate of cadmium and zinc ions but did not alter binding of lead and stannous ions. By formation of a lake with alizarin red S previously injected in vivo intramuscularly, the release of calcium ions at the motor end plate following stimulation of the muscle through the nerve or administration of neostigmine was demonstrated. These results suggest a close relationship of the site of binding of divalent metal ions in the motor end plate to the site of calcium release, and a close but not identical relationship to the site of cholinesterase activity and the acetylcholine receptor.

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