Modulation of inhibitory and excitatory neurotransmissions by Zn²⁺ on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice

The substantia gelatinosa of the trigeminal subnucleus caudalis has been considered to be an essential location for the transference of orofacial sensory signals. The co-localization of inhibitory and excitatory neurotransmitters in the same substantia gelatinosa (SG) neurons has demonstrated their essential part in the modification of nociceptive transmission. Zn²⁺ is particularly numerous in the mammalian central nervous system. There are proofs demonstrating the role of Zn²⁺ in the modulation of voltage-and ligand-gated ion channels. However, little is known about what roles Zn²⁺ may play in the modulation of signal transmission in the SG neurons of the trigeminal subnucleus caudalis (Vc). Therefore, in this study, we used the whole-cell patch clamp technique to find out the effect of Zn²⁺ on the responses of three main neurotransmitters (glycine, GABA, and glutamate) on SG neurons of the Vc in mice. We have proved that Zn²⁺ induces a big potentiation of glycine receptor-mediated response but attenuates GABA-and glutamate-induced responses at micromolar concentrations, however, enhances glutamate-induced response at nanomolar concentration. Taken together, these data demonstrated that Zn²⁺ can modulate glycine, GABA and glutamate-mediated actions on the SG neurons of the Vc and support an important mechanism in spinal sensory information signaling.