下丘脑背内侧核注射纳洛酮对束旁核痛兴奋单位放电的影响

用玻璃微电极记录大鼠丘脑束旁核痛兴奋单位(PfPE)放电。观察到下丘脑背内侧核(DMH)微量注射纳洛酮(Nx)后:(1)PfPE的自发和痛诱发放电频率增加,时程延长;(2)部份PfPE的自发放电类型由散在单脉冲变成散在间簇状或完全的簇状发放,而窟诱发放电类型由持续性发放转变为间断性暴发式放电。本实验提示:DMH局部的内源性阿片肽对PfPE放电活动有抑制性调控作用。     

The subcortical generated somatosensory evoked potentials in non-cephalic,cephalic, and anterior neck referenced recordings in a patient with a cervico-medullary lesion: a clue to the identification of the P14/N14 and N13 generators

Summary Median nerve somatosensory evoked potentials (SEPs) were studied in a patient before and after the development of a cervico-medullary lesion. The first examination demonstrated normal subcortical generated potentials N13 and N14. The second examination, following a subarachnoid haemorrhage at the cervico-medullary junction, displayed a delayed and reduced amplitude P14/N14 peak on both sides. P14/N14 showed the same latency in all montages, using noncephalic, cephalic and anterior neck references. The N13 component was not significantly changed in latency compared with the first examination. The latencies of the N13 peak were variable in the different montages. They increased from the lower (C7) to the upper (C2) neck, whereas the latency of the N13 onset was identical in all montages. This alteration might be caused by a delayed near-field activity at C2 overlapping the N13 component. These results fit the hypothesis of two major generators responsible for subcortical SEPs; a near-field N13 component at the level of the lower neck and a far-field P14 component arising from the level of the cervico-medullary junction. An additional minor near-field activity generated by the cuneate nucleus is suspected.     

苍白球在电针镇痛及兴奋尾壳核镇痛中的作用

用行为学和电生理学的方法 ,探讨苍白球在电针镇痛及兴奋尾壳核镇痛中的作用。结果表明 :电针可以延长辐射热引起的缩腿潜伏期 ,电针或兴奋尾壳核可抑制丘脑束旁核神经元的伤害性反应 ;苍白球微量注射红藻氨酸 7d后 ,电针对辐射热引起的大鼠缩腿潜伏期无明显影响 ,电针或兴奋尾壳核对丘脑束旁核神经元的伤害性反应亦无明显影响 ,与毁损前相比有显著性差异 (P <0 .0 5 ) ,与苍白球微量注射生理盐水 7d后 ,电针可延长大鼠缩腿潜伏期 ,及电针或兴奋尾壳核对束旁核神经元伤害性反应的抑制作用相比有显著性差异 (P <0 .0 5 )。结果提示 :苍白球在电针及兴奋尾壳核镇痛中发挥重要作用     

Short-term lithium treatment enhances responsiveness of postsynaptic 5-HT1A receptors without altering 5-HT autoreceptor sensitivity: an electrophysiological study in the rat brain

Short-term lithium administration to rats has previously been shown to enhance 5-HT neurotransmission through a modification of 5-HT neuron properties. In the first part of the present study, the effect of lithium on the function of terminal 5-HT autoreceptors was assessed by comparing in controls and lithium-treated rats the differential effect of two frequencies of stimulation (0.8 and 5 Hz) and that of methiothepin, a terminal 5-HT autoreceptor antagonist, on the effectiveness of the electrical activation of the ascending 5-HT pathway in suppressing dorsal hippocampus pyramidal neuron firing activity. Both procedures produced similar effects in controls and lithium-treated rats. In the second part of the study, the function of somatodendritic 5-HT autoreceptors was studied. The effect of intravenous LSD, an agonist of the somatodendritic 5-HT autoreceptor, on the firing activity of 5-HT neurons was not modified by the lithium treatment, whereas that of intravenous 8-OH-DPAT, a 5-HT1A receptor agonist, was increased two-fold. However, lithium did not alter the responsiveness of 5-HT neurons to direct microiontophoretic applications of 8-OH-DPAT as well as of LSD and 5-HT. It is concluded that short-term lithium treatment does not alter the function of terminal and somatodendritic 5-HT autoreceptors and that it enhances the sensitivity of a subset of postsynaptic 5-HT1A receptors involved in controlling 5-HT neuron firing activity, presumably through a feedback loop.     

Immunocytochemical localization of aromatase in the brain

An immunocytochemical peroxidase-antiperoxidase procedure using a purified polyclonal antibody raised against human placental aromatase was used to localize aromatase-containing cells in the Japanese quail brain. Immunoreactive cells were found only in the preoptic area and hypothalamus, with a high density of positive cells being present in the sexually dimorphic medial preoptic nucleus, in the ventromedial nucleus of the hypothalamus and in the infundibulum. The positive material was localized in the perikarya and in adjacent cytoplasmic processes. Aromatase-containing cells were a specific marker for the sexually dimorphic preoptic nucleus. Treatment with testosterone produced a 6-fold increase in the aromatase activity of the preoptic area and a 4-fold increase in the number of immunoreactive cells in the medial preoptic nucleus. Thus, the increase in aromatase activity observed after testosterone administration is caused by a change in enzyme concentration.     

Role of the hippocampus in development of the seizure syndrome induced by kindling stimulation of the caudate nucleus

Institute of Biomedical Technology, Ministry of Health of the USSR, Moscow (Presented by Academician of the Academy of Medical Sciences of the USSR G. N. Kryzhanovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 108, No. 8, pp. 145–147, August, 1989.     

An HRP study of the central projections from primary sensory neurons innervating the rat masseter muscle

Retrograde and transganglionic transport of horseradish peroxidase has been used to study the cell bodies of origin and the central projections of neurons innervating the rat masseter muscle. Labeled cell bodies were observed both in the trigeminal ganglion and in the mesencephalic trigeminal nucleus. Major central projections from mesencephalic trigeminal neurons were traced to the supratrigeminal nucleus and to the brainstem reticular formation. Smaller projections from these neurons could be followed to the borders of the solitary tract and hypoglossal nuclei as well as to lamina V of nucleus caudalis and corresponding areas in the dorsal horn at C₁−C₂ spinal cord segments. Labeling from trigeminal ganglion neurons was observed close to the trigeminal tract in all subdivisions of the trigeminal sensory nuclear complex and in the dorsal horn lamina I at C₁ and C₂ levels.     

硬膜外移植自体髓核大鼠背根神经节的非压迫性损伤

背景：最新的研究表明，髓核所致的炎性反应是导致坐骨神经痛的重要原因之一，在此过程中背根神经节可能起重要作用，但是其病理生理变化目前尚不完全清楚。 目的：探讨在无机械压迫情况下，腰椎间盘髓核突出引起坐骨神经痛的发病机制。 方法：10月龄雄性SD大鼠24只，随机分成实验组和对照组，每组12只。切开大鼠尾椎椎间盘，髓核呈胶冻样，取5个髓核并加入50 µL生理盐水，充分搅拌稀释成混悬液备用。实验组大鼠行硬膜外穿刺，注射混悬液到腰椎硬膜外腔制作动物模型。对照组硬膜外腔注射生理盐水。测定大鼠后肢机械刺激缩爪阈值并对疼痛相关行为和背根神经节组织形态学进行观察。 结果与结论：在无机械压迫情况下，硬膜外移植自体髓核能使大鼠后肢产生明显的痛觉过敏，背根神经节会出现节细胞肿胀、核膜不清晰、核仁变淡或消失、胞浆出现空泡、尼氏小体颜色变浅分布不均匀、内膜间质增宽、充血和水肿等形态学改变。结果表明，移植自体髓核所致的炎性反应是引起大鼠背根神经节损伤和坐骨神经痛的重要原因之一。     

A review on the effect of the photoperiod and melatonin on interactions between ghrelin and serotonin

Ghrelin and serotonin, which exhibit rhythmic secretion profiles under feeding/fasting conditions, are sensitive to increases and decreases in the day length and form a close web of interrelationships in the regulation of energy homeostasis. Ghrelin and serotonin are biochemically and functionally linked to the suprachiasmatic nucleus, which is a circadian pacemaker, and melatonin, which is an internal transducer of photic environmental changes. Ghrelin and serotonin might be candidates for integrating photic and nonphotic signals, such as light and food availability in the central nervous system. The mechanisms that convert a light signal into a variety of physiological and behavioral rhythms remain unknown. However, we know that the conversion of light signals is necessary to maximize an animal’s chances of survival and reproduction.     

An fMRI case report of photophobia: Activation of the trigeminal nociceptive pathway

Photophobia, or painful oversensitivity to light, occurs in a number of clinical conditions, which range from superficial eye irritation to meningitis. In this case study, a healthy subject with transient photophobia (induced by the overuse of contact lenses) was examined using functional magnetic resonance imaging (fMRI). While being scanned in a darkened environment, the subject was presented with intermittent 6-s blocks of bright light. The subject was scanned twice, once during his photophobic state and once after recovery. The subject reported that the visual stimuli produced pain (pain intensity = 3/10 and unpleasantness = 7/10) only during the photophobic state. During photophobia, specific activation patterns in the trigeminal system were seen at the level of the trigeminal ganglion, trigeminal nucleus caudalis, and ventroposteromedial thalamus. The anterior cingulate cortex, a brain structure associated with unpleasantness, was also active during photophobia. After recovery from photophobia, no significant activations were detected in these areas. This study may contribute to a better understanding of the pathways involved in photophobia in the human condition.