刺激蓝斑及电针对大鼠脊髓背角神经元伤害性反应的影响

以往的工作表明,蓝斑（LC）-去甲肾上腺素能神经元系统在痛觉调制和针刺镇痛中起着重要作用,本文用电生理学方法研究刺激LC和电针对大鼠脊髓背角神经元伤害性反应的影响,其主要结果如下：1、刺激LC或电针有明显抑制脊髓背角神经元伤害性反应的作用。2、损毁中缝大核和腹腔注射纳洛酮并不明显影响刺激LC的抑制效应。3、α2受体激动剂氯压啶能加强刺激LC或电针的抑制效应,而α受体阻断剂酚妥拉明在一定程度上能削弱这种抑制效应,这些实验结果提示,刺激LC和电针可激活LC神经元,通过其下行纤维,在脊髓水平释放NE,通过α2受体,阻断伤害性信息的传递。     

刺激大鼠外侧缰核对脊髓背角神经元伤害性反应的影响

电刺激大鼠一侧外侧缰核可对脊髓疹角广动力型神经元的伤害性放电产生明显抑制;这种抑制效应可部分地被静脉注射赛庚啶及酚妥拉明所阻断,电解损毁ＬＨｂ对ＷＤＲ神经元的放电无影响,本文结果表明,ＬＨｂ参与了脊髓上结构对脊髓背角ＷＤＲ神经元伤害性反应的下行抑制,这种下行抑制为位相性抑制。     

多巴胺对大鼠背角WDR神经元的抑制不被酚妥拉明...

The inhibitory effects of dopamine (DA) applied spinally on the wide dynamic range (WDR) neurons of dorsal horn in rats were studied with extracellular recording technique. 54 WDR units were tested from 43 rats. With a dosage of DA from 0.26 x 10(-6) to 1.58 x 10(-6) mol/kg, the inhibitory effect of the neurotransmitter on the responses of dorsal horn neurons to noxious transcutaneous electrical stimulation exhibited a gradual increase. After DA (0.52 x 10(-6) mol/kg) administration, the inhibitory effect of DA began to appear in 5 min and reach to maximum in 15 min, whereupon the maximum level could be maintained for about 25 min. This effect of DA could be reversed completely by dopaminergic receptor antagonist, droperidol (0.66 x 10(-6) mol/kg) but not by 2.65 x 10(-6) mol/kg phentolamine or 1.37 x 10(-6) mol/kg naloxone. The results of the present investigation suggest that DA may be involved in the modulation of nociception at the spinal level as an independent neurotransmitter.     

电刺激猫中脑导水管周围灰质和中缝大核对脊髓背角神经元伤害性感受反应的抑制

1.在氯醛糖麻醉的猫上,观察了电刺激中脑导水管周围灰质(PAG)和中缝大核(NRM)对脊髓腰段背角神经元传入活动的影响。2.按照对刺激的反应型式,在背角记录到非伤害性低阈值传入、广动力范围、伤害性热敏以及高阈值传入诱发的自发放电抑制等四类神经元。3.刺激 PAG和 NRM对记录到的多数背角神经元皮肤传入反应有明显抑制效应,而对自发放电抑制性神经元产生去抑制。4.比较刺激两脑区的抑制效应:NRM 作用较PAG 强;PAG 活动对背角伤害性反应抑制的选择性较 NRM强;阿片肽拮抗剂-纳洛酮拮抗NRM刺激的抑制。5.这些结果提示PAG和NRM对脊髓的下行抑制,可能有一部分是通过不同神经机制实现的。     

刺激中缝背核对大鼠脊髓背角神经元伤害性反应的影响及其传出途径的分析

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。     

半胱胺对猫脊髓背角神经元伤害性热反应的抑制

在戊巴比妥钠麻醉和脊髓腰-1段全横切的16只猫上,观察生长抑素(somatostatin,SOM)的耗竭剂半胱胺对伤害性热刺激脚跖皮肤和电刺激胫后神经所引起的脊髓背角Ⅳ-Ⅵ层神经元单位反应的影响。静脉注射半胱胺50mg/kg对电刺激神经引起的伤害性反应无影响,100mg/kg可使被测试的13个神经元单位中的8个单位反应明显抑制。而静脉注射半胱胺50mg/kg可明显抑制伤害性热刺激所引起的脊髓背角神经元单位反应。用微电极将半胱胺微压注入背角胶质层也使背角神经元的伤害性热反应明显抑制,但只使13个单位中的7个单位对电刺激神经引起的伤害性反应轻度抑制。半胱胺对背角神经元伤害性反应的抑制可能由于耗竭了背角中的生长抑素。本文讨论了半胱胺对背角神经元伤害性热反应的抑制明显强于电刺激神经所诱发的伤害性反应的抑制的可能机制。     

多巴胺对大鼠背角WDR神经元的抑制不被酚妥拉明和纳洛酮所拮抗

本实验用微电极细胞外记录方法研究了脊髓局部应用多巴胺对大鼠背角WDR神经元的抑制作用。实验在43只SD大鼠上共记录到54个WDR神经元。多巴胺的剂量从0.26×10~(-6)mol/kg-1.58×10~(-6)mol/kg逐步增加,其对伤害性经皮电刺激诱发的背角神经元后串放电的抑制作用也随之加强;0.52×10~(-6)mol/kg多巴胺的作用在给药后5min即出现,15min达高峰并在此后的25min基本维持在同一水平,这个作用可被静注多巴胺能受体拮抗剂氟哌啶(0.66×10~(-6)mol/kg)完全翻转,而不受静注酚妥拉明(2.65×10~(-6)mol/kg)和纳洛酮(1.37×10~(-6)mol/kg)影响。上述结果表明,多巴胺可能是参与脊髓水平伤害性信息传递调控的另一单胺类神经递质。     

刺激大脑皮层体感Ⅰ区和大脑脚对大鼠脊髓背角神经元伤害感受性反应的影响

在大鼠用玻璃微电极细胞外记录的方法,观察了刺激皮层体感Ⅰ区(SI区)和大脑脚(CP)对皮肤强电刺激诱发的脊髓背角广动力范围(WDR)神经元长潜伏期反应(C-反应)的影响。结果表明刺激SI区对背角WDR神经元C-反应的影响以抑制为主,刺激CP的作用与刺激SI区的作用相似,但刺激CP更为有效。抑制作用的持续时间在不同神经元差别很大,短者在刺激停止后仅持续400ms,长者可达10min以上。静注纳洛酮对抑制作用无明显影响,静注二甲麦角新碱在部分神经元可使抑制作用明显减弱或完全消失,提示5-HT部分参与皮层下行抑制作用的实现,而内鸦片肽则否。     

氯胺酮对单足致炎大鼠脊髓背角神经元活动的影响

在大鼠脊髓背角用细胞外记录技术共记录到３２个单位。角叉菜胶一侧足底注射致炎后,电刺激该侧足底内外侧神经激动其中Ａ、Ｃ纤维时,脊髓背角神经元诱发放电数均显著增加;静脉注射ＮＭＤＡ受体拮抗剂氯胺酮后,Ａ、Ｃ纤维刺激诱发的放电反应均显著下降甚至消失。致炎后脊髓背角深层单位出现Ｗｉｎｄｕｐ现象,静脉注射氯胺酮后该现象减轻消失。结果提示：角叉菜胶致炎导致脊髓背角神经元兴奋性升高和Ｗｉｎｄｕｐ;ＮＭＤＡ受体参     

The effect of different activating influences on the self stimulation reaction]

A study was made of the influence on self-stimulation of non-painful sensory stimuli of different modalities, and of intra-brain stimulations of emotionally positive and neutral points with the wiew to elucidate the specificity of certain functional relations appearing during interaction between emotionally negative and positive conditions. The data obtained attest that the influence of various excitation sites on self-stimulation reactions depends not so much on the strength of the stimuli, as on the specific neurophysiological organization of emotionally negative zones in the brain. A reciprocal enhancement of excitation of self-stimulation zones points to a certain non-specificity of positively reinforced structures.     

Nutritional influences on sexual maturation in the rat

The effect of altered nutrition on sexual maturation may depend in part on the nature and timing of the dietary change. The data are conflicting as to whether rats undernourished before weaning but normally fed after weaning have delayed puberty, but such undernourished rats clearly weigh less at vaginal opening than do normally fed animals. Altered nutrition after weaning can change the timing of puberty, and in such cases the body weight at puberty of the animals given the modified diet is frequently abnormal. The factors regulating the age and weight at puberty of rats fed altered diets seem to include the degree of underfeeding, as reflected in the growth rate, and the composition of the diet. Undernourished immature male rats have low serum testosterone secondary to gonadotropin deficiency. Basal luteinizing hormone (LH) in these animals is either low or "inappropriately normal" relative to their hypoandrogenic state (low serum testosterone and sexual accessory gland weights), and serum LH increases after luteinizing hormone-releasing hormone (LHRH) or castration are normal or minimally reduced. Serum follicle-stimulating hormone (FSH) in undernourished rats is subnormal basally and after administration of LHRH, but not after castration, which suggests that the low basal serum FSH is due to inhibition of FSH output by a testicular factor. Spermatogenesis may be unaltered by dietary changes severe enough to cause hypoandrogenism, although very severe under-nutrition will impair sperm production.     

Phasic influences of vagal stimulation on atrioventricular conduction

The beat-by-beat changes in atrioventricular (AV) conduction evoked by constant frequency and phase-coupled vagal stimulation were examined both qualitatively and quantitatively in 13 anesthetized dogs. The effects of pacing cycle length and sympathetic activity on the vagally induced phasic changes in AV conduction were also characterized. When the vagal stimulus interval was nearly equal to the pacing cycle length and the vagal stimulus moved progressively through the cardiac cycle, AV interval oscillated in a rhythmic fashion. The rhythmicity of the vagally induced AV interval oscillations was altered substantially by changes in either the vagal stimulus interval or the pacing cycle length. The vagally induced AV interval oscillations were abolished during phase-coupled vagal stimulation; however, the magnitude of the resultant steady-state AV interval depended on the time relative to the phase of the cardiac cycle that the vagal stimulus was delivered. In the presence or absence of sympathetic stimulation, a vagal stimulus falling approximately 200 ms prior to atrial depolarization evoked the greatest prolongation in AV interval, regardless of the pacing cycle length. Additionally, the effects of combined sympathetic and phase-dependent vagal stimulation on the AV interval were additive. These data confirm that the influence of a vagal stimulus on AV interval can be predicted from the phase in the cardiac cycle that the vagal stimulus is delivered. Moreover, this phase dependency of vagal effects evokes marked qualitative variations in AV interval response patterns when either the vagal stimulus interval or the pacing cycle length is altered.     

Rubrospinal synaptic influences on the lumbar motoneurons of the rat

Intracellular recording was employed in experiments on rats with the nervous system intact and after acute pyramidotomy to study the postsynaptic effects produced in the lumbar motoneurons on stimulation of the nucleus ruber. Stimulation of this nucleus with single stimuli and with a short series of stimuli caused excitatory and inhibitory postsynaptic potentials (EPSP and IPSP) to develop in the motoneurons. Most of the EPSP recorded were disynaptic, but response development involved a monosynaptic segmental delay in five of the 124 cells that exhibited EPSP. A capacity for high-frequency potentiation was a characteristic feature of the disynaptic excitatory and inhibitory effects. Transmembrane polarization of the motoneurons had a marked influence on the amplitude of the disynaptic EPSP and IPSP. The properties of the disynaptic rubrospinal influences were similar to those described for the cat.I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Translated from Neirofiziologiya, Vol. 3, No. 3, pp. 266–273, May–June, 1971.     

The influence of hypothyroidism on the adrenergic stimulation of glycogenolysis in perfused rat liver

The ability of noradrenaline (1 microM), phenylephrine (10 microM), and isoproterenol (1 microM) to stimulate glycogenolysis in euthyroid and hypothyroid perfused rat livers was investigated. It was found that hypothyroidism severely impaired alpha-receptor-mediated (noradrenaline, phenylephrine) glucose release. The initial Ca2+ efflux and K+ influx induced by these agonists in the euthyroid control group were almost totally absent in the hypothyroid group, while glycogen phosphorylase a activity in the hypothyroid rat livers was markedly lower than in the controls after infusing noradrenaline for 1 min. Diminished CA2+ efflux (and possibly diminished K+ influx) is likely to play a role in the large impairment in the action of noradrenaline or phenylephrine on glycogenolysis in the perfused hypothyroid rat liver. After prolonged stimulation (15 min) with noradrenaline, however, the phosphorylase a activity in the hypothyroid and euthyroid groups did not differ significantly. This was accompanied by Ca2+ influx in the hypothyroid livers, probably facilitated by a beta-adrenergic effect of noradrenaline in this group. Hypothyroidism potentiated the effect of isoproterenol on glycogenolysis. The glucose 6-phosphate content in the hypothyroid rat livers was markedly higher than in the euthyroid group after stimulation by noradrenaline or isoproterenol.     

The influence of tactile stimulation of nipples on the milk ejection reflex in the rat

Summary Changes of positive pressure exerted by pups on nipples during sucking were investigated using anesthetized, lactating dams. It was found that, every 50–60 s, individual pups performed bouts of pressure oscillations (3/s) of high amplitude which lasted about 10–12 s and coincided with periods of increased motor activity. During the intervals, when pups were quiet, series of low-amplitude oscillations (3/s) were also observed. Using a strain measuring method to record the activity of sucking pups, synchronization of activity of two or more pups was found to occur periodically every 25–30 s and, most frequently, 10–30 s before the reflex increase of milk pressure. In further experiments, artificial tactile stimulation was applied to the dam's nipples using the joint action of suction and positive pressure. Following a short-term (10–20 s) increase in frequency and amplitude of artificial nipple stimulation, 60%–80% of all reflexive peaks of milk pressure were elicited with a latency of 19 ± 5 s. This suggests that there are specific conditions under which the stimulation of nipples by pups may trigger the formation of the milk ejection reflex in the rat.Abbreviation MER milk ejection reflex