| Pain, an unpleasant sensory and emotional experience, is associated with actual or potential tissue damage, which includes a sensory-discriminative and an affective-motivational component. Meanwhile, it is usually a common symptom of many diseases. Especially, chronic pain has an severe effect on people physically and psychologically, and impairs quality of life of human being markedly. Therefore, revealling the underlying mechanism of pain and eventually finding a solution to relief of pain seems very important today.As well known, the spinal nociception, primary sense center of pain ,can be modulated by several factors. The research on endogenetic pain modulation from central nerve system have developed rapidly and already become one of the most prominent fields in the late decades. The studies show that supraspinal center biphasically modulate spinal nociceptive transmission: descending inhibition and facilitation. As indicated by recent research, descending facilitatory modulation is probably a key mechanism for occurrence and maintenance of neuropathic and inflammatory pain.Anterior cingulate cortex (ACC) is an important part of the limbic system and the high-level center of brain, which not only receives all kinds of information from subcortex, but also is reliably activated by peripheral noxious stimulus, and has been a hotspot of pain exploration. Though the adequate data has already been collected about the ACC modulation of sensatory and emotional component of pain, the studies were almost confined to the aspect : how the ACC receive nociceptive information. The research on how the ACC transmits nociceptive information and how it regulates spinal nociception has been little conducted so far. So here a question comes out: how the ACC modulate the pain in top-down manner and in which way does the ACC is connected to the subcortex nuclei.The present study was designed to investigate how the ACC modulate the spinal nociception and it affect the activation of the central lateral nuclei of intralaminar nuclear by means of electrophysiology and behavior test. The result is as following:1. C-fiber-evoked potentials were significantly enhanced by 145.77 ± 1.86 % of control following unilaterally electrical stimulation of the ACC (60 μA, 0.2 ms, 100 Hz for 1 sec, interval 5 sec, for 2.5 min), and lasted for more than 2 h. Meanwhile the A-fiber-evoked potentials were not affected by the same stimulation. Two kind of intensity(60 and 600μA) regular electrical stimulation of the ACC didn't long lasting enhanced the C-fiber-evoked potentials.2. One week after surgery, PWLs to noxious heating were measured and compared before and after ACC stimulation. The electrical stimulation of the unilateral ACC significantly reduced bilateral PWLs. Shortened bilaterally PWLs appeared 30 min after ceasing stimulation of the ACC, which reached the peak after 1-4 hours and recovery after 24hours.3. One week after implanting microinjection cannula, NMDA( 1.0μl, 10nM) and homocysteic acid (HCA) (1.0μl, 0.1M) was microinjected into the ACC unilaterally, the PWLs were significantly shortened bilaterally.4. Microinjection of L-Arg (1μl 10mM ) , the donor of NO, the C-fiber-evoked potentials and paw withdrawal response significantly enhanced.5. Following the bilateral dorsal reticular nuclei (DRt) were electrolytically lesioned (anodal DC current 200-500 μA, 10-20s), ACC stimulation-induced facilitation of C-fiber-evoked field potentials and paw withdrawal respond was markedly diminished.6. After electrical stimulation of the ACC (60-100 μA, 0.2 ms, 200 Hz, interval 10 sec, for 2s), the spontateous discharge of nociceptive neuronsin the CL was recorded. The results showed most (50%)of them were excited, the rest of 19.2% and 30.8% showed inhibitory and unchanged respectively. In spite of the spontaneous discharge of some neurons didn't change, they alterate their receptive field, the character of neurons and the pattern of discharge after stimulation of the ACC.7. The evoked discharge of nociceptive neurons in th CL was also changed after stimulation of the ACC. The results showed most (56.2%)of them were excited, the rest of 12.5% and 31.3% showed inhibitory and unchanged respectively. Following increased of their evoked discharge some neurons also changed their pattern of discharge from single to burst after stimulation of the cortex.8. Using fluorogold (FG) and fastblue (FB) retrograde tract-tracing technique, the afferent projection of the CL from ACC was traced. FG and FB (3%, 1.0μl) were injected into unilateral CL. Seven days later, the rats were perfused. Forty-micrometer-thick sections were mounted on slides and observed under microscopy. The results showed that the ACC project strongly to CL bilaterally. Ipsilateral has more neurons than the contralateral of the ACC. In addition to the ACC, the claustrum(CI) and the hypothalamus also project a mall quatity neurons to the CL.In conclusion, the ACC is believed to facilitate the spinal nociception in descending mode; DRt contributes to the ACC-induced descending facilitation; The ACC not only has a lot of neurons project to the CL but also can facilitate the spontaneous and evoked discharge of the nociceptive neurons in the CL. All the above suggest that the ACC modulate the pain at the level of spinal and diencephalons...
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