| Pain is a common clinical symptom. There is a pain-convection system in nervous system as well as a complex pain-modulation network. It's believed that periaqueductal gray , rostral ventromedial medulla (NRM, Rpg, Rpgl and Rgcα) and lateral reticular formation of dorsal pons (LC and KF) all take part in the process of pain sensation and pain modulation. Recently investigations indicated that pain information could be transmitted to limbic forebrain formation through reticular formation of brain stem, central gray substance of midbrain and hypothalamus, which constituted complex circuits. The circuits played an important role in pain affection, pain experience and pain behavior.Hippocampus is an important conformation of limbic system. Hippocampus formation is related with pain sensation and pain modulation besides learning, memory and emotion. Subcutaneous injection of formalin could change the discharge frequency of pain exciting neuron and pain inhibitory neuron in hippocampus. The content 5-HT, c-fos and IL-2mRNA expression in hippocampus could be up-regulated by peripheral subcutaneous injection of formalin, which indicated that hippocampus neuron took part in the sensation of nociceptive information, and its function and metabolism were changed. Other investigations confirmed that electric stimulation of hippocampus could induce the elevation of pain threshold in rat; the injection of sodium glutamate into hippocampus could induce the elevation of the content of 5-HT in endogenous pain modulation system and produce the analgesia effect. And pain behaviors in both acute and tonic phases of the formalin test in rat were significantly reduced by intrahippocampal administration of AP5,a competitive NMDA receptor antagonist. These results showed that hippocampus participated in pain modulation besides the sensation of nociceptive information.Nitric oxide is a kind of important information molecule in central nervous system. Some investigations have shown that NO contributes to pain modulation. For example, the intracerebroventricular microinjection of L-NAME appeared obviously analgesia effect, which could be inversed by the intravenous injection of L-arginine; some researchers also reported that the intracerebroventricular injection of L- arginine could produce the obviously analgesia effect too, which could be effectively antagonized by nitric oxide synthase inhibitor. The research results indicated that the action of NO was not coincident. Many nuclues labeled with NOS-positive neurons in central nervous system displayed different roles in pain modulation. NOS-positive neurons are also located in hippocampus, whether the NOS–positive neurons change or not has not been reported during the peripheral nociceptive information is input to hippocampus.Thereby, our present study was undertaken to observe the changes of NOS expression including its region distribution character and time course in the rat hippocampus during formalin-induced inflammatory pain, and further to examine the effect of intrathecal injection of NMDA receptor antagonist MK-801 on the NOS expression and NO content in the hippocampus during this process.1. The changes of NOS expression and NO content in the hippocampus of rats during formalin-induced inflammatory pain.Eighty-four male SD rats (260-280g in weight) were divided randomly into 6 groups: Control group and formalin 6h, 12h, 24h, 48h, 72h groups. There were fourteen rats in each group, seven of which were used for observing NOS expression, and other seven were used for measurement of NO content. Rats in Control group were directly perfused, fixed and sacrificed or directly sacrificed without other treatments. Rats in other five groups were perfused, fixed and sacrificed or sacrificed at corresponding time following the formalin injection. NADPH-d histochemistry was used to investigate the changes of NOS expression, nitrate/nitrite (NO3-/NO2-) was assayed to represent NO content in hippocampus.Ten brain sections were drawn to evaluate the NADPH-d |
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