| Soreness is one of the most common disorders of patients, which is difficult to tolerate sometimes. At present, there is not an ideal effective method to treat pain in clinic. Therefore, study of algesia has important theoretical and practical significance.Anterior cingulate gyrus (ACG) is an important component of limbic system and one of main centers of algesia. ACG is involved in nociceptive signal reception and modulation of algesia. Our previous study has discovered that there are somatic nociceptive neurons and the representative area of saphenous nerve (SN) in ACG. Our laboratory shows that noxious electric stimulation of SN induces evoked responses and significant increases in Fos protein expression of ACG neurons. But no study has been done to clarify which neurotransmitter is involved in the process of ACG somatic nociception.Studies have discovered that the main excitatory neurotransmitter in central nervous system is glutamic acid. Noxious afferent signals cause increase in glutamic acid release of nerve centers and abnormal activation of glutamic acid receptors. Different glutamic acid receptors play different important roles by different mechanisms in formation of algesia. Some reports show that dopamine(DA) is involved in reception and modulation of algesia. Pathway of dopaminergic neuron projects to ACG. But whether DA takes part in the process of ACG somatic nociception is not clear. Therefore, in the present study, high performance liquid chromatography-electrochemical detection(HPLC-ECD) was used to study influence of strong noxious electric stimulation of SN to DA content in rat ACG, and effects of morphine and MK-801 and CNQX on change of DA content in rat ACG induced by the noxious electric stimulation of SN, to elucidate whether SN somatic noxious inputs cause change of DA content in ACG and its mechanism. The experiment could confirm whether SN somatic noxious inputs activate dopaminergic nervous system in ACG to take part in reception and modulation of algesia, and provide new scientific experimental data for exploitation of new pain-killer and analgesia.In the present study, male 66 Wistar rats with body mass 200g to 270g were randomly classified into control groups (included blank control group, sham stimulation control group, 10min after normal saline hypodermic injection and then 30min after noxious electrical stimulation SN with 1.0mA, 10min after normal saline injection via caudal veins and then 30min after noxious electrical stimulation SN with 1.0mA) and experimental groups (included 15 min, 30 min, 1 h, 2 h after noxious electric stimulation SN with 1.0mA, 10min after morphine hypodermic injection and then 30min after 1.0mA noxious electric stimulations on SN, 10min after MK-801 or CNQX injection via caudal veins and then 30min after 1.0mA noxious electric stimulations on SN). The experimental rats were decapitated respectively. The samples of ACG were taken from the brains on an ice box, then weighed, homogenated, centrifugated with high speed. The DA content in 20μl clear supernatant liquid of the samples of ACG was examined by using HPLC-ECD.The experimental results displayed that compared with control groups, DA content of ACG at 15min group after noxious electric stimulation of SN increased significantly (P<0.01). At 30min after noxious electric stimulation SN, DA content in ACG increased to its peak(P<0.01). DA content in ACG was still higher than that of control groups, but started to decrease 1h after stimulating SN(P<0.05). DA content in ACG recovered gradually 2h after stimulating SN(P>0.05). These results suggested that ACG can receive the nociceptive information inputs of SN, and then enhances activity of dopaminergic neurons in ACG, which causes time-dependent increase in DA content of ACG.Moreover,the study discovered that compared with that of control groups, DA content in ACG increased lightly at 10min after hypodermic injection of morphine followed by 30min after 1.0mA stimulation on SN, but there was no significant difference(P>0.05). Compared with that of control groups, DA content in ACG increased significantly at 10min after normal saline hypodermic injection and then 30min after 1.0mA noxious stimulation on SN(P<0.01). The results displayed that morphine inhibited the increase in DA content in ACG induced by noxious electric stimulation of SN.Our experimental data showed that compared with control groups, DA content in ACG had not significant change at 10min after injection of MK-801 or CNQX (1mg/kg body mass) via caudal vena and then 30min after noxious electric stimulation of SN (P>0.05). Compared with control groups, DA content in ACG increased obviously at 10min after injection of normal saline via caudal vena and then 30min after noxious electric stimulation of SN (P<0.01). These results displayed that the significant increase in DA content in ACG caused by noxious electric stimulation of SN was inhibited by MK-801 or CNQX, which suggested that both NMDA and AMPA/Kainate receptors are involved in the course of increase in DA content of ACG induced by noxious electric stimulation on SN. |
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