| Objective The purpose of this study was to investigate the expression of μ1-opioid receptor (MOR1) mRNA and 5-HT1A receptor (5-HT1A) mRNA in rat thalamic parafascicular nucleus (Pf) induced by coronary artery occlusion (CAO) and to investigate the intervention effects of morphine and tramadol on the expression. Methods Adult male SD rats, weighting between 260g -280g,were randomly divided into group MOR1 and group 5-HT1A receptor. MOR1 was then divided into four groups: group A (n=18), the control group, with non-CAO; group B (n=18), with CAO only; group C (n=18), with Morphine + CAO; and group D (n=18), with Tramadol + CAO. Each group was divided into three different sub-groups which were observed at T 1(1h),T2(3h),T3(6h) respectively (n=6). And 5-HT1A receptor was divided into four groups: Group C, the control group, with non-CAO; Group CAO 1h, with CAO for 1 hour; Group CAO 3h, with CAO for 3 hours; and Group CAO 6h, with CAO for 6 hours; in order to find a time point at which the expression of 5-HT1A receptor mRNA increased significantly. Then rats were divided into three groups: Group CAO 6h; Group M, with Morphine+CAO 6h; and Group T, with Tramadol + CAO 6h. Coronary artery wasn't occluded in group non-CAO, rats were respectively pre-administrated 1.25mg/kg morphine in group M and 12.5mg/kg tramadol in group T through caudal vein before CAO 15 minutes the rest procedures were same as group CAO. Rats were killed at different time points, and then their brains were dissected in order to perform in situ hybridization (ISH) of brain tissue cryo-section. Brain slides of Pf were examined and analyzed semi-quantitively for expression of μMOR1 mRNA and 5-HT1A receptor mRNA using ISH technique with IDA-2000 digital micro-image analysis systems. All experiments were done at same labotoray and under same condition. Results The expression of MOR1 mRNA and 5-HT1A receptor mRNA in rat Pf increased significantly at 1h, 3h, 6h after CAO as compared with that in group non-CAO, and there was an increasing trend with the development of myocardial ischemia in group CAO, the value was the highest at 6h in group CAO. The expression of MOR1 mRNA and 5-HT1A receptor mRNA decreased significantly in group M and group T, but there were no significant differences between group Morphine and group Tramadol. Conclusions Myocardial ischemia alone could increase the expression of MOR1 mRNA and 5-HT1A receptor mRNA in rat Pf, and MOR1 and 5-HT1A receptor in Pf were involved in centeral modulation of nocuous input evoked by acute myocardial ischemia; Morphine and Tramadol decreased the expression of MOR1 mRNA and 5-HT1A receptor mRNA in rat Pf, this effects may derive from suppression of nociceptive inferent signals induced by CAO at different levels. |
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