The Influence of Noise Stress-Induced Pain-Threshold Increase on Central Monoaminergic Neurons

Abstract

Background. In our preliminary experiment, we elicited dose-dependent increases in pain threshold in mice exposed to noises of different intensities. In this study, we investigated the mechanisms by which noise induces an increase in pain-threshold. Methods. ICR male mice weighing 18 to25g were used. We constructed a square-shaped noise chamber measuring 84 cm ×57cm×57 cm, equipped with a square glass window (14 cm × 27 cm) on the top for observation. The pain threshold was determined by the formalin test. Results. We found that norepinephrine (NE, 3 to 300 μg/kg, i.c.v.), serotonin (5-hydroxytryptamine; 5-HT, 3 to 300μg/kg, i.c.v.), and 5-hydroxy-L-tryptophan (5-HTP, 50 mg/kg, i.p.) enhanced the noise-induced antinociception. NE showed significant enhancement at high doses. Amphetamine potentiated the noise stress-induced antinociception at low doses (0.5 mg/kg, s.c.) in the early phase of the formalin test, but at higher doses (1 to5mg/kg, s.c.) in the late phase of the forma-Jin test. Antinociception induced by noise stress was reversed by pchlorophenylalanine (PCPA, 200 mg/kg, i.p.), a5-HT biosynthesis inhibitor, but not reversed by α-methyl-p-tyrosine (α-MT, 100 mg/kg, i.p.), a NE biosynthesis inhibitor. Prazosin (1 mg/kg, i.p.), an α1-adrenergic receptor antagonist and clonidine (0.01 to 0.5 mg/kg, i.p.), an α2 adrenergic receptor agonist, increased the pain threshold. Pargyline (1mg/kg, i.p.), a monoamine oxidase inhibitor and yohimbine (1 mg/kg, i.p.), an α2-adrenergic receptor antagonist, had no effect. Conclusions. The results suggest that the increase in pain threshold induced by noise might be related to serotoninergic and postsynaptic noradrenergic neurons.αl and α2 noradrenergic receptors are involved in noise-induced analgesia.