The effects of Zn 2+ on long-term potentiation of C fiber-evoked potentials in the rat spinal dorsal horn

Abstract

Tetanic stimuli of peripheral C fibers produces long-term potentiation (LTP) in the spinal cord, which may contribute to sensitization of spinal pain-sensitive neurons. Zn 2+ is widely distributed in the central nervous system and has blocked (LTP) in the hippocampus. The present study examined the effects of Zn 2+ on the induction and maintenance of C fiber-evoked LTP in the deep dorsal horn of spinalized rats in vivo. The sciatic nerve was stimulated by tetanic stimuli for inducing LTP. (1) Topical administration of Zinc chloride (15 μM) to the spinal cord 15 min before tetanic stimulation completely blocked the induction of LTP, but not the baseline C responses. When Zn 2+ was given 2 h after induction of LTP, no significant effect occurred. (2) Chelation of Zn 2+ by disodium calcium ethylene diaminetelraacetate (CaEDTA) (500 μM) resulted in no effect on LTP. (3) Coadministration of Zn 2+ (15 μM) and N-methyl-D-aspartic acid (NMDA) (5 μM) significantly attenuated C fiber-evoked potentials, which was prevented by the NMDA receptor antagonist AP-5 (100 μM). The present results showed that Zn 2+ may contribute to the modulation of the formation, but not the maintenance, of spinal LTP. NMDA receptors may be involved in Zn 2+-induced modulation.