针刺对同时在丘脑束旁核和尾核记录的痛兴奋与痛抑制神经元单位放电的影响

在44只大白鼠上,通过两根玻璃微电极同时引导丘脑束旁核和尾核神经元的放电,观察伤害性刺激作用于坐骨神经和电针“足三里”对两个神经元放电的影响。实验共记录到81对两个神经元的同时放电,其中包括26对痛兴奋、3对痛抑制、28对痛兴奋和痛抑制、24对其他组合类型的神经元放电。实验结果表明:1.从大白鼠尾核可同时记录到痛兴奋和痛抑制两种神经元的电活动,未见痛兴奋和痛抑制神经元的放电型式相互转换。2.同一伤害性刺激可同时引起丘脑束旁核和尾核中的两个痛兴奋神经元兴奋、两个痛抑制神经元抑制、或一个痛兴奋神经元兴奋和另一个痛抑制神经元的抑制。3.电针“足三里”可同时使丘脑束旁核和尾核的痛兴奋神经元兴奋减弱或痛抑制神经元抑制反应减弱(抑制解除)。本工作证明,伤害性刺激可同时影响丘脑束旁核和尾核中痛兴奋和痛抑制神经元的单位放电变化,而电针“足三里”又同时对两核团中痛兴奋和痛抑制神经元的活动具有调整作用。     

去甲肾上腺素对大鼠丘脑束旁核痛反应神经元电活动的影响

本文观察了41只大鼠脑室注射去甲肾上腺素(NE)后对两侧束旁核痛反应神经元同时由活动的影响。结果表明:1.两个痛兴奋神经元(PEN)的电活动同时受至抑制,表现为诱发放电数目减少,潜伏期延长。2.两个痛抑制神经元(PIN)的抑制效应同时被解除,即诱发放电数目增加,抑制时程箱短。3.一个PEN的电活动受到抑制的同时,另一个PIN的电活动加强。上述结果证明NE能够同时影响丘脑束旁核PEN和PIN的电活动。     

乙酰胆碱对大鼠丘脑束旁核和中脑网状结构痛反应神经元电活动的影响

在54只大鼠上,用两支微电极同时记录神经元放电的方法,研究了脑室注射乙酰胆碱(ACh)对丘脑束旁核(Pf)和中脑网状结构(RF)痛反应神经元电活动的影响。结果表明,当脑内ACh含量增加时,Pf和RF中两个痛兴奋神经元(PEN)的电活动同时减弱,两个痛抑制神经元(PIN)的电活动同时加强,Pf中一个PEN电活动减弱的同时RF中一个PIN电活动加强,或者相反。阿托品可以阻断ACh的上述作用。这提示,ACh对不同中枢痛反应神经元的电活动的影响是通过M胆碱能受体而实现的。     

丘脑束旁核痛兴奋神经元和痛抑制神经元电活动的研究

张香桐(1978)指出,丘脑内接受痛觉信号的结构在丘脑的内侧部分,特别是束旁核和中央外侧核。丘脑束旁核基本上是一个接受痛觉冲动的结构(1979)。我们曾报道(孙明智等,1980),丘脑束旁核存在着痛兴奋和痛抑制两种神经元。当伤害性痛刺激作用于机体时可引起痛兴奋神经元放电数目的增加和痛抑制神经元放电数目的减少,并认为两种神经元的电活动都与痛觉的产生有直接关系。     

视前区微量注射吗啡对大鼠丘脑束旁核痛反应神经元电活动的影响

本实验观察了视前区(POA)内微量注入阿片样物质对丘脑束旁核(Pf)痛反应神经元电活动影响。结果如下:(1)POA 内微量注射高浓度吗啡(10μg/μl)能显著抑制 Pf 内大部分(20/26)痛兴奋神经元(PEN)的痛诱发放电,其中3个神经元注药后对伤害性刺激转变成抑制反应;POA 内微量注射低浓度吗啡(1μg/μl)也显著抑制 Pf 内大部分(19/23)PEN 的痛诱发放电。(2) POA 内微量注射两种浓度的吗啡,均使大多数痛抑制神经元(PIN,共27/33)的完全抑制时程缩短。上述结果提示,POA 内阿片样物质对 Pf 内痛反应神经元的电活动可能具有抑制作用。     

刺激大鼠尾核对丘脑束旁核躯体-内脏会聚神经元放电的影响

实验记录大鼠丘脑束旁核躯体-内脏会聚(PfSV)神经元伤害性放电。观察刺激尾核(Cd)对 PfSV 神经元放电的影响。(1)Cd 对刺激内脏大神经诱发 PfSV 神经元伤害性放电有抑制作用(n=19)。(2)Cd 对刺激腓浅神经和内脏大神经诱发同一 PfSV 神经元伤害性放电均有抑制作用(n=11)。结果提示,躯体和内脏痛觉信息可会聚到丘脑束旁核同一神经元,Cd 可能不仅能抑制躯体痛也能抑制内脏痛。     

大鼠杏仁核簇与痛觉调制的关系

目的：研究伤害性刺激对大鼠杏仁核簇中各亚核痛反应神经元电活动的影响。方法：用串电脉冲刺激坐骨神经作为伤害性刺激,用玻璃微电极引导神经元放电。结果：杏仁核簇中多个亚核均存在痛反应神经元。伤害性刺激使痛兴奋神经元(PEN)诱发放电频率增加;使痛抑制神经元(PIN)诱发放电频率降低,并出现放电频率极低现象;两类神经元电活动相互配合。腹腔注射吗啡(10mg／kg)可以对抗伤害性刺激对痛反应神经元的作用。结论：杏仁核簇中的部分亚核在感受、整合和传递痛觉信息方面起一定作用,是中枢神经系统控制和处理痛觉信息的一个组成部分。     

刺激大鼠下丘脑背内侧核对丘脑束旁核痛相关神经元放电的影响

本文在 79只清醒麻痹大鼠身上,用玻璃微电极记录丘脑束旁核痛兴奋(PfPE)和痛抑制(PfPI)单位的放电及其对刺激下丘脑背内侧核(DMH)的反应,并观察切割脊髓背外侧束的效应。主要结果如下:(1)刺激DMH使PfPE 单位的自发放电及痛放电有明显的抑制作用,而使PfPI 单位的自发放电增多,并解除伤害性刺激引起的抑制效应;(2)刺激DMH引起PfPE 单位的抑制效应,在切割脊髓背外侧束后仍然出现。上述结果提示:DMH 对丘脑束旁核在处理痛觉信息上具有调制作用,这种调制作用可能不通过脑干下行性抑制系统完成,而主要是通过脊髓上联系抑制丘脑束旁核神经元对痛传入的反应。     

电刺激兔尾核对丘脑束旁核神经元痛放电的影响

实验在75只家兔上进行。以玻璃微电极记录丘脑束旁核痛放电,以电脉冲(5次/s、0.2ms、8—10V)通过双极同心电极刺激尾核头部,结果表明刺激尾核对束旁核痛放电既产生抑制效应(34/38),也产生易化效应(4/38)。抑制有两种表现方式:1.改变诱发放电的型式,2.跟随着单个刺激脉冲出现对痛放电的短暂压抑。静脉注射纳洛酮或阿托品可以阻断尾核刺激所引起的第一种抑制效应,提示尾核内阿片肽能系统和胆碱能系统活动参与对束旁核痛觉信号活动的调制。本文也观察到尾核刺激可诱发束旁核神经元出现每分钟约6次的周期性锋形电位串。     

八肽胆囊收缩素对抗吗啡对丘脑束旁核痛反应神经元放电的影响

已知脑室注射硫化八肽胆囊收缩素(CCK-8)对吗啡镇痛效应(用辐射热甩尾反应的潜伏期作测痛指标)有对抗作用。本工作研究了脑室注射CCK-8对吗啡引起的大鼠丘脑两侧束旁核痛反应神经元同时电变化的影响。结果如下:(1)腹腔注射吗啡(10mg/kg)可抑制痛兴奋神经元(PEN)和加强痛抑制神经元(PIN)的电活动。(2)脑室注射CCK-8(15ng/15μl)能对抗吗啡引起PEN放电的抑制作用和PIN电活动的加强作用。无硫CCK-8对吗啡的效应没有对抗作用。(3)注射CCK-8可同时对抗吗啡对束旁核中一个PEN的抑制作用和一个PIN的加强作用。上述结果与甩尾阈测痛的结果一致,即CCK-8对吗啡引起的镇痛效应有明显的对抗作用。     

乙酰胆碱对大鼠丘脑束旁核痛兴奋和痛抑制神经元放电的影响

本实验观察了脑室注射乙酰胆碱(ACh)对丘脑束旁核(Pf)痛兴奋神经元(PEN)和痛抑制神经元(PIN)电活动的影响,并与吗啡的作用进行了比较。结果表明,脑内ACh增加可使PEN放电潜伏期延长,频率降低,持续时程缩短;可使PIN的完全抑制时程缩短。腹腔注射吗啡与ACh的作用相似。M胆碱受体阻断剂阿托品能阻断ACh对PEN和PIN的作用,但不影响吗啡对PEN和PIN的作用。说明吗啡镇痛不是通过胆碱能转递而实现的。     

Dopamine Involved in the Nociceptive Modulation in the Parafascicular Nucleus of Morphine-Dependent Rat

Dopamine regulates pain perception in some areas of the central nervous system. Previously, we have confirmed that dopamine potentiated the electric activities of the evoked discharges of pain-excited neurons (PENs) and inhibited those of pain-inhibited neurons (PINs) in the parafascicular nucleus (Pfn) of normal rats. The mechanism of action of dopamine on pain-related neurons in the Pfn of morphine-dependent rat is still unknown. The present study aimed to determine the effects of dopamine and its receptor antagonist droperidol on the pain-evoked responses of the PEN and PIN in the Pfn of morphine-dependent rats, and to compare the effects between the morphine-dependent rat and the normal rat. The trains of electric impulses applied to the sciatic nerve were used as noxious stimulation. The discharges of PEN or PIN in the Pfn were recorded by using a glass microelectrode. The results showed that intra-Pfn microinjection of dopamine decreased the frequency of noxious stimulation-induced discharges of PEN and increased the frequency of PIN. The intra-Pfn administration of droperidol produced an opposite effect. These results demonstrated that dopamine is involved in nociceptive modulation in the morphine-dependent rat, the responses to noxious stimulation between normal rat and morphine-dependent rat are completely opposite. The effect of dopamine is through the dopamine D₂ receptor of PENs and PINs in Pfn. The results suggest that the dopamine system of the Pfn may become a therapeutic target for analgesia and the treatment of morphine dependence.     

Dopamine Affects the Change of Pain-Related Electrical Activity Induced by Morphine Dependence

Morphine is among the most effective analgesics. However, many evidences suggest that, besides the well-know analgesic activity, repeated opioids treatment can induce some side effects such as dependence, hyperalgesia and tolerance. The mechanism of noxious information transmission in the central nervous system after dependence is not clear. An important neurotransmitter, dopamine (DA) participates not only in the process of opioid dependence but also in pain modulation in the central nervous system. In the present study we observed changes of electrical activities of pain-excitation neurons (PENs) and pain-inhibition neurons (PINs) in the caudate nucleus (Cd) following the development of morphine dependence. We also observed the role of DA on these changes. Our results revealed that both the latency of PEN discharges and the inhibitory duration of PIN discharges decreased, and the net increased values of PEN and PIN discharges increased in the Cd of morphine dependent rats. Those demonstrated that electrical activities of both PENs and PINs increased in morphine dependent rats. DA inhibited the electrical activities of PENs and enhanced those of PINs in morphine dependent rats.     

Cholinergic mechanism involved in the nociceptive modulation of dentate gyrus

Acetylcholine (ACh) causes a wide variety of anti-nociceptive effects. The dentate gyrus (DG) region of the hippocampal formation (HF) has been demonstrated to be involved in nociceptive perception. However, the mechanisms underlying this anti-nociceptive role have not yet been elucidated in the cholinergic pain-related neurons of DG. The electrical activities of pain-related neurons of DG were recorded by a glass microelectrode. Two kinds of pain-related neurons were found: pain-excited neurons (PEN) and pain-inhibited neurons (PIN). The experimental protocol involved intra-DG administration of muscarinic cholinergic receptor (mAChR) agonist or antagonist. Intra-DG microinjection of 1 μl of ACh (0.2 μg/μl) or 1 μl of pilocarpine (0.4 μg/μl) decreased the discharge frequency of PEN and prolonged firing latency, but increased the discharge frequency of PIN and shortened PIN inhibitory duration (ID). Intra-DG administration of 1 μl of atropine (1.0 μg/μl) showed exactly the opposite effects. According to the above experimental results, we can presume that cholinergic pain-related neurons in DG are involved in the modulation of the nociceptive response by affecting the discharge of PEN and PIN.     

谷氨酸及NMDA受体拮抗剂MK-801对大鼠伏核痛兴奋神经元电活动的影响

本文研究了谷氨酸(glutamic acid,Glu)及其NMDA受体拮抗剂5-甲基二氢丙环庚烯亚胺马来酸(MK-801)对人鼠伏核(nucleus accumbens,NAc)痛兴奋神经元(pain-excitation neurons,PEN)痛诱发反应的影响。电刺激坐骨神经作为伤害性刺激,用玻璃微电极记录NAc的PEN放电,观察脑室内注射Glu和NAc内注射MK-801对大鼠NAc中PEN伤害性诱发活动的影响。结果显示,伤害性刺激可使NAc的PEN电活动增强;脑室内注射Glu(10nmol／10μl)可使NAc的PEN伤害性诱发放电频率增加;NAc内注射MK-801(1．0nmol／0．5μl)可阻断这种作用;MK-801本身也可部分抑制PEN伤害性诱发反应。上述结果表明,Glu对PEN伤害性反应的易化作用是通过NMDA受体介导的：Glu和NMDA受体参与NAc伤害性信息传递的调制。