The role of synaptic plasticity on rats with visceral hypersensitivity induced by transient intestinal infection / 中华消化杂志

ABSTRACT

Objective To investigate the role of synaptic plasticity on the formation of visceral hypersensitivity induced by transient intestinal infection in rats. Methods Thirty male Sprague-Dawley rats were divided into normal control, acute infection and chronic infection groups with 10 each. The area under curve (AUC) of electromyography (EMG) in 10 s was used to evaluate the visceral sensitivity induced by different eolorectal distention (20,40,60 and 80 mmHg). Histological change of the colon was evaluated by H-E staining. Synaptic uhrastrueture such as synaptic cleft and synaptic vesicles was observed using transmission electron mieroseope. The mRNA and protein expressions of synaptophysin and postsynaptic density protein-95 (PSD-95) were examined by RT-PCR and Western blot, respectively. significantly higher than those of normal controls(P=0. 012, 0. 005, respectively ). In contrast, AUC of acute infection were significantly lower than those of normal controls ( P = 0. 018,0. 012, respectively ). Under the distention of 20 and 80 mmHg, no significant difference was observed among three groups (P= rats compared to normal controls(23.45±4.10 vs. 9.10±2.42, P=0. 027),but there was no statistical difference between chronic infection rats and normal controls (13. 95±7.96 vs. 9.15±2.42, P=0.78). increased. In acute infection rats, mitochondria cristae disappeared, synaptic vesicles and the length of controls, mRNA and protein of synaptophysin in ileocecum, proximal colon and distal colon were significantly increased in chronic infection rats (P＜0. 05 ), but decreased in acute infection rats with no significant difference. Compared with controls, no significant downregulation was noted in the expression protein expressions of PSD-95 were both increased in chronic infection rats (P＜0.05), and decreased in acute infection rats (P＜0.05). Conclusion Synaptic plasticity plays an important role in the formation of visceral hypersensitivity induced by transient intestinal infection in rats.