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电针对青霉素所致大脑皮层痫样放电的抑制作用 总被引:5,自引:0,他引:5
青霉素置于大鼠大脑皮层感觉运动区所诱发的皮层痫样放电,可被一些“穴位”电针所抑制,表现为放电频率、振幅及时程之减少。青霉素使逆向刺激锥体束所产生的感觉运动皮层表面负波减小,而电针则促进其恢复。因此电针制痫与它促进回返抑制的恢复有关。将微量纳洛酮注入腹腔、脑室及中脑导水管周围灰质、伏隔核均能翻转电针的作用。将纳洛酮直接注入放置青霉素处的皮层感觉运动区,针效亦被阻断。这表明电针制痛中有内啡肽参与。电刺激中脑导水管周围灰质及伏隔核有显著制痫作用。 相似文献
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本实验观察刺激中缝背核对大鼠视交叉上核光敏神经元单位放电的影响,并进行药理学分析。结果表明,刺激DR能明显抑制SCN神经元光诱发放电,这种抑制作用能被单胺氧化酶抑制剂优降宁增强,能被5-HT合成抑制剂对氯苯丙氨酸减弱,还能被5-HT受体拮抗剂赛庚啶阻断。结果提示,5-HT参与了刺激DR对SCN光敏神经元放电的抑制。 相似文献
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注射6-羟多巴胺于中缝背核后对针刺镇痛和单胺能神经元荧光组织化学反应的影响 总被引:3,自引:2,他引:1
新近的研究资料表明,在针刺镇痛过程中,中缝背核的5-羟色胺(5-HT)荧光增强,蓝斑核的去甲肾上腺素(NA)荧光减弱;分别损毁中缝背核和蓝斑核或从蓝斑核发出的上行背束时,前者减弱针刺镇痛效应,后者加强这个效应;若刺激中缝背核和蓝斑核,它们对针刺镇痛效应分别表现为易化和压抑的作用。这些结果从正反两方面肯定了中缝背核和蓝斑核在针刺镇痛中的作用,并揭示它们的作用是拮抗性的。但迄今为止,没有资料证明这两个核团及其所含的5-HT 和 NA 在针刺镇痛中的相互关系。因 相似文献
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中缝背核5-羟色胺能神经元在睡眠调节中的作用研究 总被引:1,自引:0,他引:1
目的:研究中缝背核(DRN)5-羟色胺(5-HT)能神经元在睡眠中的调节作用。方法:运用脑立体定位、核团微量注射和多导睡眠描记(PSG),观察DRN 5-HT能神经元对大鼠睡眠的影响。结果:DRN微量注射谷氨酸钠(L-Glu),大鼠睡眠减少,特别是深慢波睡眠(SWS2)明显减少,觉醒(W)增加;DRN微量注射海人酸(KA)和对氯苯丙氨酸(PCPA),大鼠SWS2和异相睡眠(PS)增加,W减少。结论:DRN 5-HT能神经元参与睡眠的调节,兴奋DRN 5-HT能神经元睡眠时间减少,抑制DRN 5-HT能神经元则具有促进睡眠的作用。 相似文献
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大量资料表明,中缝背核(DR)在痛觉调节中具有重要作用。本实验用电生理学方法研究DR在痛觉调制中的下行性抑制作用,主要观察刺激DR对清醒制动大鼠脊髓背角神经元伤害性放电的影响。其主要结果是:①刺激DR或电针可以抑制脊髓背角神经元的伤害性反应,吗啡可加强这种抑制效应;②损毁中缝大核(NRM)、纳洛酮、麦角酰二乙胺(LSD)、赛庚啶及对氯苯丙氨酸(PCPA)均能部分阻断DR对脊髓背角神经元伤害性反应的抑制,实验结果表明:刺激DR抑制脊髓背角神经元的伤害性反应,部分是通过NRM间接控制背角神经元的伤害性传入;还有一部分是不通过NRM,可能是DR直接对脊髓背角伤害性信息的调制。在这种下行性抑制通路中有5-HT和阿片样物质的参与。 相似文献
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家兔杏仁核内的5-羟色胺和内源性吗啡样物质在电针镇痛和吗啡镇痛中起重要作用 总被引:2,自引:0,他引:2
本工作的目的是要确定杏仁核内的吗啡样物质(内啡素)和5-羟色胺(5-HT)是否参与电针镇痛和吗啡镇痛。经慢性埋植套管向家兔杏仁核内微量注射阿片受体阻断剂纳洛酮,或5-HT受体阻断剂肉桂硫胺,可使电针的镇痛效果显著减弱,尤以注入中央杏仁核作用最为显著,双侧注射效果大于单侧,注入核外则无效。杏仁核内注入5-HT 的前体5-HTP,或脑啡肽降解酶抑制剂 D-苯丙氨酸可使电针镇痛显著加强。上述措施凡是加强或对抗电针镇痛的,也能加强或对抗吗啡镇痛。以上结果表明,电针刺激或注射吗啡可能在杏仁核内引起5-HT 和内啡素(很可能是脑啡肽)的释放,而发挥镇痛效应。 相似文献
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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
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C M Contreras M L Marván A Mu?oz-Méndez A Ramírez-Morales 《Boletín de estudios médicos y biológicos》1992,40(1-4):3-7
In cerebral cortex and lateral septal nuclei different serotonergic receptor subtypes coexist, thus a different action on neuronal firing may be expected depending on the receptor activated. Dorsal raphe nucleus stimulation produced an increased rate of firing in cortical layer V, and in lateral septal nuclei. However, firing rate in cortical layer VI remained unchanged after stimulating the dorsal raphe nucleus. Clomipramine is a tricyclic which exerts its main actions on serotonergic receptors, and long-term treatment with this antidepressant produced a selective increased firing rate in lateral septal neurons, but not in cortical neurons. From an electrophysiological point of view, it is concluded that the excitatory actions on firing rate elicited by dorsal raphe nucleus stimulation or clomipramine treatment are mediated by 5-HT2 receptor subtype activation which is likely to be acting as a 5-HT1A modulator in such places where both receptor subtypes coexist. 相似文献
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Effect of p-chlorophenylalanine on development of cross-tolerance between pentobarbital and ethanol.
D Frankel J M Khanna A E LeBlanc H Kalant 《Canadian journal of physiology and pharmacology》1977,55(4):954-957
Rats developed cross-tolerance to the motor-impairing effects of ethanol after daily oral administration of pentobarbital. Chronic administration of p-chlorophenylalanine (p-CPA), in a dosage regimen previously demonstrated to maintain extensive brain serotonin (5-HT) depletion, slowed down cross-tolerance development. p-CPA did not appear to exert this effect by altering the disposition of ethanol, since blood ethanol levels measured 20 min after ethanol administration were not affected by p-CPA treatment. This study extends our previous findings with respect to the inhibitory effects of p-CPA on tolerance development to ethanol and pentobarbital, and suggests that 5-HT may play a role in cross-tolerance development between ethanol and pentobarbital. 相似文献
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p-chlorophenylethylamine (p-CPEA), a metabolite of p-chlorophenylalanine (p-CPA) induces the “serotonin syndrome” which consists of lateral head weaving, Straub tail, hindlimb abduction, tremor, hyperactivity, reciprocal fore-paw treading, salivation and piloerection. These p-CPEA-induced behavioral signs were partially prevented by pretreatment with serotonin (5-HT) uptake blockers (fluoxetine, chlorimipramine, Org 6582) and 5-HT receptor blockers (methiothepin, methysergide, cinnanserin) but not by two depletors of brain 5-HT (p-CPA, reserpine). p-CPEA (50 mg/kg) produces an initial decrease in 5-HT associated with a concurrent increase in 5-hydroxyindoleacetic acid with a maximum change at 30 minutes after injection; these early biochemical changes are prevented by pretreatment with fluoxetine (10 mg/kg). p-CPEA also competes with (3H)-5-HT for 5-HT receptors. The reported paradoxical effects of p-CPA on several behavioral paradigms could be due to its decarboxylation to p-CPEA which may both stimulate 5-HT receptors and enhance 5-HT release. 相似文献
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Adayev T El-Sherif Y Barua M Penington NJ Banerjee P 《Journal of neurochemistry》1999,72(4):1489-1496
Previous studies have indicated that stimulation of neuronal inhibitory receptors, such as the serotonin1A receptor (5-HT1A-R), could cause attenuation of the activity of both N-type Ca2+ channels and N-methyl-D-aspartic acid receptors, thus resulting in protection of neurons against excitotoxicity. The purpose of this study was to investigate if the 5-HT1A-R is also coupled to an alternative pathway that culminates in suppression of apoptosis even in cells that are deficient in Ca2+ channels. Using a hippocampal neuron-derived cell line (HN2-5) that is Ca2+ channel-deficient, we demonstrate here that an alternative pathway is responsible for 5-HT1A-R-mediated protection of these cells from anoxia-triggered apoptosis, assessed by deoxynucleotidyl-transferase-mediated dUTP nick end-labeling (TUNEL). The 5-HT1A-R agonist-evoked protection was eliminated in the presence of pertussis toxin and also required phosphorylation-mediated activation of mitogen-activated protein kinase (MAPK), as evidenced by the elimination of the agonist-elicited rescue of neuronal cells by the MAPK kinase inhibitor PD98059 but not by the phosphatidylinositol 3-kinase (PI-3K) inhibitor wortmannin. Furthermore, agonist stimulation of the 5-HT1A-R caused a 60% inhibition of anoxia-stimulated caspase 3-like activity in the HN2-5 cells, and this inhibition was abrogated by PD98059 but not by wortmannin. Although agonist stimulation of the 5-HT1A-R caused an activation of PI-3Kgamma in HN2-5 cells, our results showed that this PI-3Kgamma activity was not linked to the 5-HT1A-R-promoted regulation of caspase activity and suppression of apoptosis. Thus, in the neuronal HN2-5 cells, agonist binding to the 5-HT1A-R results in MAPK-mediated inhibition of a caspase 3-like enzyme and a 60-70% suppression of anoxia-induced apoptosis through a Ca2+ channel-independent pathway. 相似文献
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T. Sh. Labakhua Т. K. Dzhanashiya G. I. Gedevanishvili Е. V. Abzianidze Т. Т. Тkemaladze 《Neurophysiology》2009,41(2):137-147
In experiments on cats, we studied the effects of electrical stimulation of the cerebral central grey (CG), locus coeruleus (LC), and substantia nigra (SN) on postsynaptic processes evoked by nociceptive volleys in somatosensory cortex neurons. Nineteen cells activated exclusively
by stimulation of nociceptors (intense stimulation of the dental pulp) and 26 cells activated by both nociceptive and non-nociceptive
(near-threshold) stimulations of the n. infraorbitalis and thalamic nucl. ventroposteromedialis (VPM) were intracellularly recorded (nociceptive and convergent cortical neurons, respectively). In neurons of both groups,
stimulation of both nociceptive afferents and the VPM evoked complex responses having on EPSP-spike-IPSP patterns (duration
of IPSPs about 200-300 msec). Electrical stimulation of the СG, which per se could activate the examined cortical neurons, induced prolonged suppression of synaptic responses evoked by stimulation of
nociceptors; maximum inhibition was observed at 600- to 800-msec-long conditioning–test intervals. A certain parallelism was
observed between the conditioning effects of СG stimulation and effects of systemic introduction of morphine. Isolated stimulations
of the LC and SN by short high-frequency pulse series evoked primary complex EPSPs in a part of the examined cortical neurons,
while high-amplitude IPSPs (up to 120 msec long) were observed in other units. Independently of the type of the primary response,
conditioning stimulations of the LC and SN induced long-lasting (several seconds) suppression of synaptic responses evoked
in cortical neurons by stimulation of nociceptive inputs. Mechanisms of modulating influences coming from opioidergic, noradrenergic,
and dopaminergic cerebral systems to neurons of the somatosensory cortex activated upon excitation of high-threshold (nociceptive)
afferent inputs are discussed. 相似文献
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S González-Barón J Jiménez-Vargas J Marcó F Hernández 《Revista Espanola de Fisiología》1976,32(1):29-32
Influence of 5-HT on the rat follicle rupture mechanism was studied by the administration of p-clorophenyl-alanine (p-CPA) (300 mg/kg) at different stages of the ovarian cycle. The ovarian cycle of treated rats was subject of investigation, as well as the histology of tubes and ovaries. Administration of p-CPA at 10 hours of metestrus phase induces an inhibition of ovulation. Predominant diestrus phases in the ovarian cycle and luteinitation of ovaries suggested an increase in progesterone secretion probably owed to a correspondingly greater prolactine secretion. Adequate 5-HT levels in central structures proved to necessary for normal ovulation. 相似文献
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Recovery cycles of primary evoked potentials to light flashes in the visual cortical area of waking rats were studied under conditions of pharmacological and electrical influences on serotonin (5-HT)- and noradren (NA)ergic brain systems. All factors used induced oscillations of the recovery cycles. Periods of oscillations were similar (300-400 ms) during pharmacological suppression of the NA-system and during high-frequency (500 Hz) electrical stimulation or lesion of locus coeruleus. Analogous influences on 5-HT-system were accompanied by oscillations of recovery cycles with a period of 200 ms. Mechanism of inhibitory action of high-frequency electrical stimulation on activity of monoaminergic systems is discussed. 相似文献
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Simultaneous single-unit and intracortical activity were recorded from neocortical neurons in urethane-anaesthetized rats to investigate the role of serotonin (5-HT) in modifying cortical excitability. Units, at a depth of 775-1100 microns from the pial surface, discharged in a burst-pause pattern that was correlated with slow wave activity. Application of noxious somatic stimulation resulted in cortical desynchronization and altered the pattern of unit activity such that firing was continuous, i.e., the pauses were eliminated. Intravenous administration of the mixed 5-HT1C/5-HT2 antagonists (cinanserin, cyproheptadine, ketanserin, and ritanserin) prevented both desynchronization and the change in unit activity induced by noxious stimulation within 2.5-15 min of the injection. The basic pattern of burst-pause activity remained intact, but the number of spikes per burst was typically reduced, whereas interburst intervals were increased. Iontophoretic application of these antagonists onto cortical neurons resulted in actions similar to those observed following systemic administration. Intravenous and iontophoretic application of m-trifluomethylphenylpiperazine (5-HT1C agonist, 5-HT2 antagonist) resulted in actions indistinguishable from those observed with the above antagonists, from which we conclude 5-HT2 and not 5-HT1C receptors mediate the alteration in unit activity observed with noxious stimulation. The results are discussed with respect to an interaction between N-methyl-D-aspartate and 5-HT2 receptors leading to the enhanced unit activity observed with noxious stimulation. 相似文献