首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到13条相似文献,搜索用时 78 毫秒
1.
应用细胞内记录,研究了豚鼠腹腔神经节(CG)细胞非胆碱能迟慢兴奋性突触后电位(LS-EPSP)与5-羟色胺(5-HT)及P物质(SP)的相互关系。当重复电刺激内脏大神经(SN)时,有78.2%的细胞(161/206)在动作电位发放后出现LS-EPSP,灌注或压力注射5-HT或SP,分别在68.5%的细胞(102/149)及52.1%的细胞(98/188)上引起5-HT或SP去极化反应,两者差异非常显著(P<0.01);大部分具有LS-EPSP的细胞对5-HT(73/88,83.0%)或SP(68/11459.6%)敏感,而不出现LS-EPSP的细胞仅有少数对5-HT(10/26,38.5%)或SP(11/36,30.6%)敏感,两类细胞的差异非常显著(5-HT:P<0.0001,SP:P<0.01)。上述结果支持5-HT与SP均作为递质参与LS-EPSP形成的观点。此外,在133个细胞上同时检测了5-HT与SP的作用,其中有66个细胞(49.6%)对5-HT及SP均敏感,提示在CG细胞,5-HT与SP之间可能存在某种机能联系。  相似文献   

2.
裴文芬  祝延 《生理学报》1996,48(3):263-268
应用细胞内记录,研究了豚鼠腹腔神经节细胞非胆碱能迟慢兴奋性突触后电位与5-羟色胺及P物质的相互关系。当重复电刺激内脏大神经时,有78.2%的细胞在动作电位发放后出现LS-EPSP;灌注或压力注射5-HT或SP,分别在68.5%的细胞(102/149)及52.1%的细胞(98/188)上引起5-HT或SP去极化反应,两者差异非常显著(P〈0.01);大部分具有LS-EPSP的细胞对5-HT(73/8  相似文献   

3.
Kong DH  Wang G  Wang HM  Ke DP  Hu JL  Zhu Y  Huang ZX 《生理学报》2003,55(4):388-394
应用细胞内记录技术,对铃蟾肽(bombesin,BOM)在豚鼠离体肠系膜下神经节(inferior mesenteric ganglion,IMG)非胆碱能兴奋性突触传递中的作用进行了研究。重复电刺激突触前结肠神经,有74.3%(52/70)IMG细胞可诱发迟慢兴奋性突触后电位(ls-EPSP)。在可引出ls-EPSP的细胞中,22%(4/18)细胞同时对BOM和SP敏感。用BOM持续灌流IMG,可明显抑制对BOM敏感细胞的ls-EPSP,对BOM不敏感细胞的ls-EPSP则无影响,且BOM受体与SP受体间无交叉脱敏。BOM受体阻断剂tyr^4[D-phe^12]bombesin能明显可逆性地抑制BOM敏感细胞的ls-EPSP和去极化,但对BOM不敏感细胞则无影响。研究结果提示,BOM可能是介导豚鼠IMG细胞ls-EPSP的一种递质。  相似文献   

4.
陆伟萍  鲍红光  徐晨婕  张蕊  谢文娟 《生物磁学》2013,(35):6969-6971,6948
目的:观察颈椎椎旁神经阻滞联合直线偏振光红外线星状神经节照射治疗颈源性头痛的疗效。方法:120例颈源性头痛患者按照随机数字表法分为三组:颈椎椎旁神经阻滞联合偏振光星状神经节照射40例(A组)、颈椎椎旁神经阻滞40例(B组)、氨酚曲马多联合乙哌立松药物治疗组40例(C组),三周为一疗程。治疗前后测定患者的疼痛视觉模拟评分(VAS)、颈椎活动度评分(ROM)、评定临床疗效。结果:三组治疗后疼痛视觉模拟评分(VAS)、颈椎活动度评分(ROM)均优于治疗前(P〈0.05).A、B组治疗后VAS、ROM评分以及治愈率、有效率优于C组(P〈0.5);A组VAS、ROM评分以及治愈率、有效率优于B组(P〈0.05)。结论:颈椎椎旁神经阻滞联合偏振光星状神经节照射和颈椎椎旁神经阻滞治疗治疗颈源性头痛疗效明显优于氨酚曲马多联合乙哌立松药物治疗组;颈椎椎旁神经阻滞联合偏振光星状神经节照射治疗颈源性头痛疗效优于颈椎椎旁神经阻滞。  相似文献   

5.
Yi BD  Ma B  Xing BR 《生理学报》1999,(2):147-152
在离体灌流的牛蛙交感神经节标本上,电刺激节前纤维,细胞内记录B细胞的电活动,观察给予皮质醇对B细胞突触传递作用。主要结果有:(1)电刺激节前纤维,细胞内记录170个B细胞的动作电位,给予皮质醇后0.5 ̄3min内,52个B细胞的突触传递发生脱漏甚至完全阻断,有明显的量效关系。甾体激素胞内受体阻断剂RU38486可部分阻断这种作用。(2)蛋白合成抑制剂放线菌酮不能阻断皮质醇的快速阻断作用。(3)阿托  相似文献   

6.
The effects of L-glutamate and acetylcholine on the ventral muscle fibres of the larval mealworm Tenebrio molitor were studied by means of microelectrodes. Bath application of L-glutamate at concentrations higher than 1 × 10 4M suppressed excitatory postsynaptic potentials (EPSPs) and evoked both a depolarisation and a reduction in the input resistance of the muscle fibre. In contrast, acetylcholine chloride (up to 1 mM) had no effect at all. Circumscribed spots could be detected on the fibre surface where iontophoretic applications of L-glutamate caused transient depolarizations (glutamate potentials). Focal extracellular recordings revealed that the glutamate sensitive spots were identical with synaptic sites. The reversal potentials of the EPSP and the L-glutamate potential were identical. These results are compatible with the hypothesis that L-glutamate is an excitatory transmitter at the neuromuscular junction.  相似文献   

7.
The kinetics of sodium dependency of GABA uptake by satellite glial cells was studied in bullfrog sympathetic ganglia. GABA uptake followed simple Michaelis-Menten kinetics at all sodium concentrations tested. Increasing external sodium concentration increased bothK m andV max for GABA uptake, with an increase in theV max/K m ratio. The initial rate of uptake as a function of the sodium concentration exhibited sigmoid shape at 100 M GABA. Hill number was estimated to be 2.0. Removal of external potassium ion or 10 M ouabain reduced GABA uptake time-dependently. The effect of ouabain was potentiated by 100 M veratrine. These results suggest that at least two sodium ions are involved with the transport of one GABA molecule and that sodium concentration gradient across the plasma membrane is the main driving force for the transport of GABA. The essential sodium gradient may be maintained by Na+, K+-ATPase acting as an ion pump.  相似文献   

8.
A nonlinear dependence of the amplitude of excitatory postsynaptic potentials on the membrane potentials was derived. The existence of a region of oscillation stability with an increase in the mean value of nonspecific afferent inflow was demonstrated. A high-frequency oscillation component (40–60 Hz) appears with a pronounced increase in the afferent inflow; this can cause instability in oscillations and abnormal brain activity.  相似文献   

9.
Two types of slow excitatory postsynaptic potentials (EPSPs) with different properties were found in neurons of the rabbit superior cervical sympathetic ganglion. In our group of neurons slow EPSPs increased during artificial hyperpolarization and decreased during depolarization of the membrane. The input resistance of the cells fell or remained unchanged during the development of slow EPSPs. In the second group of cells slow EPSPs increased during depolarization and decreased during hyperpolarization. The reversal potential of these responses, determined by extrapolation, was –78.9±3.6 mV. Depolarization responses to activation of muscarinic cholinergic receptors by acetylcholine or carbachol developed in 53% of neurons with an increase in input resistance and had a reversal potential of –83.2±6.7 mV. It is suggested that in cells of the first group the ionic mechanism of the slow EPSPs is similar to that of the fast EPSPs, whereas in cells of the second group its main component is a decrease in the potassium conductance of the membrane.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 13, No. 4, pp. 371–379, July–August, 1981.  相似文献   

10.
11.
12.
The kinetics and specificity of GABA and taurine uptake were studied in the bullfrog sympathetic ganglia. GABA uptake system consisted of simple saturable component and taurine uptake system consisted of two saturable components exclusive of non-saturable influx. Taurine unaffected GABA uptake while GABA inhibited taurine uptake competitively with theK i/Km ratio of 38. GABA (5.14 M) uptake was inhibited by -aminovaleric acid and slightly by 2,4-diaminobutyric acid (5 mM, each) among ten structural analogs. Taurine uptake under high-affinity conditions was most strongly suppressed by hypotaurine and -alanine competitively with theK i/Km ratio of 1.0 and 1.9, respectively. Autoradiography showed that glial cells were heavily labeled by both [3H]GABA and [3H]taurine. These results suggest that GABA is transported by a highly specific carrier system distinct from the taurine carrier and that taurine, hypotaurine, and -alanine may share the same high-affinity carrier system in the glial cells of the bullfrog sympathetic ganglia.  相似文献   

13.
Summary Paravertebral (superior cervical and stellate), prevertebral (coeliac-superior mesenteric, inferior mesenteric) and pelvic (hypogastric) sympathetic ganglia of the rat were investigated by enzyme histochemistry to ascertain the distribution of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase) activity. In the paravertebral ganglia the majority of the sympathetic neuronal perikarya contained lightly and homogeneously distributed formazan reaction product but there was a range of staining intensities amongst the neuron population. In contrast, in the prevertebral ganglia, intense NADPH-diaphorase staining was present in certain neurons. Firstly, a population of neurons of the coeliac-superior mesenteric ganglion complex were surrounded by densely NADPH-diaphorase-positive baskets of fibres and other stained fibres were seen in interstitial nerve bundles and in nerve trunks connected to the ganglion complex. Secondly, in both the inferior mesenteric ganglion and hypogastric ganglion there were many very intensely NADPH-diaphorase positive neurons. Stained dendritic and axonal processes emerged from these cell bodies. In both ganglia this population of neurons was smaller in size than the lightly stained ganglionic neurons and commonly had only one long (presumably axonal) process. The similarity of these highly NADPH-diaphorase-positive neurons with previously described postganglionic parasympathetic neurons in the hypogastric ganglion is discussed.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号