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Gen Physiol Biophys ; 38(5): 399-406, 2019 Sep.
Article in English | MEDLINE | ID: mdl-31411570

ABSTRACT

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.


Subject(s)
Neurons/drug effects , Substantia Gelatinosa/cytology , Synaptic Transmission/drug effects , Zinc/pharmacology , Animals , Glutamic Acid/metabolism , Glycine/metabolism , Mice , Neurotransmitter Agents/metabolism , Patch-Clamp Techniques , Rats, Sprague-Dawley , Receptors, Glycine/metabolism , gamma-Aminobutyric Acid/metabolism
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