Objective: To study the bidirectional adjustment effe ct of ele ctroacupuncture (E A) on the electrical activities of neurons in caudate nucleus (CN) and parafasci cular nucleus (PFN) in rats with acute cerebral hemor...Objective: To study the bidirectional adjustment effe ct of ele ctroacupuncture (E A) on the electrical activities of neurons in caudate nucleus (CN) and parafasci cular nucleus (PFN) in rats with acute cerebral hemorrhage (ACH). Methods: ① 32 male Wistar rats were evenly randomize d into normal, EA+normal, model and model +EA groups for observing the effect of EA on pain reaction; ② another 40 male Wi star rats were equally randomized into control, saline, model and EA groups for comparing the effects of EA on discharges of pain-reaction neurons in CN and P FN . ACH model was established by intracerebral injection of the rat’s own arteria l blood sample (30μL) into CN and PFN. Pain reaction was tested by using tail -flicking (TF) reflex induced by radiation-heat irradiation. Extra-cellular d ischarges of neurons of CN and PFN were recorded by using glass micropipettes. E A (1 V, 15 Hz and duration of 10 min) was applied to "Baihui"(百会 GV 20) and "Taiyang" (太阳 EX-HN 5). Frequency of discharges of CN and PFN neurons was calculated be fore and after intracerebral injection of blood sample, heat nociceptive stimula tion and EA respectively. Results: Compared with con trol group and pre-EA in the same group, TF latency (TFL) values of normal rats increased significantly; compared w ith pre-injection of blood, TFL of model group also increased pronouncedly ( P<0.0 1). In comparison with model group, TFL values of EA group decreased significant ly (P<0.01), indicating that EA of GV 20 and EX-HN 5 could suppress ACH induced increase of TFL. In ACH rats, the latency of pain-excitement response of disch ar ges of CN and PFN neurons increased significantly, while the net increase values of pain-excitement response decreased significantly in model group (P< 0.05～0.01 ), the duration of pain-inhibitory response and the net decrease values of dis ch arges of CN and PFN neurons increased clearly. Comparison between model and EA groups showed that the latency values of the pain-excitement reaction of disch ar ges of CN and PFN neurons in EA group were significantly lower than those in mod el group (P<0.01), while the net increase values of discharges of CN and PFN neu rons in EA group were considerable higher than those in model group (P< 0.01); th e latency and net decrease values of pain-inhibitory CN and PFN neurons in EA gr oup were clearly lower than those in model group. It indicated that EA could pro l ong the latency of pain-excitatory reaction and shorten the duration of pain-i nhi bitory reactions of the neurons induced by cerebral hemorrhage and raise the exc itement degree of CN and PFN neurons. Conclusion: EA can reduce the excitability of pain-excitement neurons (PEN) and lower the inhibitory degree of pain -inhibitory neurons (PIN) in both CN and PFN, an d thus possesses a bidirectional regulation effect on cerebral hemorrhage-induced c hanges of the electrical activities of neurons in both CN and PFN.展开更多
基金This work was subsidized by National Natural Science Foundation of China (No .39670902)
文摘Objective: To study the bidirectional adjustment effe ct of ele ctroacupuncture (E A) on the electrical activities of neurons in caudate nucleus (CN) and parafasci cular nucleus (PFN) in rats with acute cerebral hemorrhage (ACH). Methods: ① 32 male Wistar rats were evenly randomize d into normal, EA+normal, model and model +EA groups for observing the effect of EA on pain reaction; ② another 40 male Wi star rats were equally randomized into control, saline, model and EA groups for comparing the effects of EA on discharges of pain-reaction neurons in CN and P FN . ACH model was established by intracerebral injection of the rat’s own arteria l blood sample (30μL) into CN and PFN. Pain reaction was tested by using tail -flicking (TF) reflex induced by radiation-heat irradiation. Extra-cellular d ischarges of neurons of CN and PFN were recorded by using glass micropipettes. E A (1 V, 15 Hz and duration of 10 min) was applied to "Baihui"(百会 GV 20) and "Taiyang" (太阳 EX-HN 5). Frequency of discharges of CN and PFN neurons was calculated be fore and after intracerebral injection of blood sample, heat nociceptive stimula tion and EA respectively. Results: Compared with con trol group and pre-EA in the same group, TF latency (TFL) values of normal rats increased significantly; compared w ith pre-injection of blood, TFL of model group also increased pronouncedly ( P<0.0 1). In comparison with model group, TFL values of EA group decreased significant ly (P<0.01), indicating that EA of GV 20 and EX-HN 5 could suppress ACH induced increase of TFL. In ACH rats, the latency of pain-excitement response of disch ar ges of CN and PFN neurons increased significantly, while the net increase values of pain-excitement response decreased significantly in model group (P< 0.05～0.01 ), the duration of pain-inhibitory response and the net decrease values of dis ch arges of CN and PFN neurons increased clearly. Comparison between model and EA groups showed that the latency values of the pain-excitement reaction of disch ar ges of CN and PFN neurons in EA group were significantly lower than those in mod el group (P<0.01), while the net increase values of discharges of CN and PFN neu rons in EA group were considerable higher than those in model group (P< 0.01); th e latency and net decrease values of pain-inhibitory CN and PFN neurons in EA gr oup were clearly lower than those in model group. It indicated that EA could pro l ong the latency of pain-excitatory reaction and shorten the duration of pain-i nhi bitory reactions of the neurons induced by cerebral hemorrhage and raise the exc itement degree of CN and PFN neurons. Conclusion: EA can reduce the excitability of pain-excitement neurons (PEN) and lower the inhibitory degree of pain -inhibitory neurons (PIN) in both CN and PFN, an d thus possesses a bidirectional regulation effect on cerebral hemorrhage-induced c hanges of the electrical activities of neurons in both CN and PFN.
