楔状核内微量注射谷氨酸对中缝大核痛放电的影响

用玻璃微电极细胞外记录法，探讨楔状核内注入胞体兴奋剂谷氨酸对中缝大核内痛兴奋性神经元痛放电的影响。结果表明，楔状核内注入谷氨酸可明显抑制中缝大核内痛兴奋性神经元痛放电。示楔状核内神经与抗伤害感受作用有关。     

Postnatal development of [D-Ala2]deltorphin-I-like immunoreactive structures in the rat brain

[D-Ala²]deltorphin-I, a highly selective ligand for δ opioid receptors, is a heptapeptide originally purified from frog skin. Previous immunohistochemical studies indicate that [D-Ala²]deltorphin-I-like molecule(s) may be present in adult rat brain, including specific neuronal cells and fibers partially overlapping with the mesocortical and nigrostriatal dopaminergic systems. Here, we examined the developmental aspect of such immunoreactive brain structures in early postnatal rats. In newborn to 21-day-old rats, positive staining in the brain occurred mainly in subpopulations of neurons and occasionally in tanycytes. On postnatal day 0, neuronal cell bodies containing [D-Ala²]deltorphin-I-like immunoreactivity were found in various brain regions, including the olfactory tubercle, ventral pallidum, hippocampus, ventral tegmental area, pars compacta of the substantia nigra, supramammillary nucleus, and dorsal raphe nucleus. Immunoreactive nerve fibers were observed in the main and accessory olfactory bulbs, olfactory tubercle, prelimbic area, anterior cingulate cortex, neostriatum, accumbens, lateral septal nucleus, lateral habenular nucleus, and superior colliculus. As pups grew, positive staining of cell bodies decreased gradually in both density and intesity, and those in the olfactory tubercle and ventral pallidum were no longer visible on postnatal day 14. On postnatal day 21, positive cells were found only in the ventral midbrain, including the pars compacta of the substantia nigra, ventral tegmental area, A8 region, and supramammillary nucleus. Positive fibers also decreased in density with age except in the accessory olfactory bulb, olfactory tubercle, prelimbic area, and anterior cingulate cortex. © 1994 Wiley-Liss, Inc.     

Evidence for, and nature of, the tonic inhibitory influence of habenulointerpeduncular pathways upon cerebral dopaminergic transmission in the rat

The potential role of the habenula in the transsynaptic regulation of the activity of ascending dopaminergic systems has been investigated in the rat by studying the effect of an acute interruption of impulse traffic in the diencephalic conduction system (stria medullaris-habenula-fasciculus retroflexus) and of pharmacological manipulation of various neurotransmitter systems in the interpeduncular nucleus on dopamine metabolism in several dopaminergic projection fields. The bilateral infusion of tetrodotoxin into the fasciculus retroflexus (which conveys the habenulointerpeduncular tract) of conscious rats markedly increased homovanillic acid levels and dopamine synthesis and utilization in the medial prefrontal cortex, nucleus accumbens, olfactory tubercle and striatum. Similar changes in dopamine metabolism were observed in these areas after bilateral infusion of tetrodotoxin into the stria medullaris (which conveys most of the afferents to the habenula). Infusion of atropine (0.4-1 micrograms) into the interpeduncular nucleus increased homovanillic acid concentrations and dopamine utilization in the medial prefrontal cortex and nucleus accumbens but not in the olfactory tubercle and striatum. Moreover, intra-interpeduncular injection of oxotremorine (17 micrograms) antagonized the increase in dopamine utilization in the nucleus accumbens (but not in the olfactory tubercle) induced by an intrafasciculus retroflexus infusion of tetrodotoxin. Local infusion of naloxone (20 micrograms) into the interpeduncular nucleus increased homovanillic acid concentrations in the nucleus accumbens and olfactory tubercle but not in the medial prefrontal cortex and striatum. In contrast, intra-interpeduncular nucleus infusion of the substance P antagonist D-Arg1, D-Pro2, D-Trp7,9, Leu11-substance P or of substance P antiserum failed to alter homovanillic acid levels in the 4 dopamine-rich areas investigated. Finally, intraraphé medianus (but not intraraphé dorsalis) infusion of muscimol (25 ng) moderately increased dopamine synthesis in the nucleus accumbens and striatum. The present findings suggest that the habenulointerpeduncular pathways exert a tonic inhibitory influence on mesocortical, mesolimbic and mesostriatal dopaminergic neurons. Cholinergic and/or opioid peptidergic neurons coursing through the fasciculus retroflexus as well as ascending serotonergic neurons originating in the raphé medianus could take part in this inhibitory control of ascending dopaminergic neurons.     

Sensory neurons supplying touch domes near the body midlines project bilaterally in the thoracic spinal cord of rats

Sensory neurons that project bilaterally to laminae III-V of the dorsal horns in the thoracic spinal cord of rats were described in a previous anatomical study. The electrophysiological experiments reported here show that these neurons innervate skin near the dorsal and ventral midlines. Three series of experiments were undertaken: (1) the regions of skin supplied by subdivisions of thoracic nerves were mapped by recording from the subdivisions while mechanically stimulating the skin; (2) subdivisions containing the axons of contralaterally projecting sensory neurons were identified by antidromic activation from the contralateral dorsal horn; (3) the receptive fields of individual sensory neurons and dorsal horn neurons were characterized by single-unit recording methods. Contralaterally projecting sensory neurons had axons in subdivisions of the thoracic nerves that supply skin adjacent to the body midlines. Their receptive fields were located near the dorsal or ventral midline but did not extend onto the contralateral side of the body. Most of the neurons were slowly adapting “type I” units supplying touch domes. Dorsal horn neurons receiving input from contralateral sensory neurons had receptive fields that overlapped the dorsal or ventral midline. This bilateral representation of skin near the midlines may be important for the fusion of the sensory maps of the right and left sides of the body.     

Shenfu injection attenuates neurotoxicity of bupivacaine in cultured mouse spinal cord neurons

Background Our previous in vivo study in the rat demonstrates that Shenfu injection, a clinically used extract preparation from Chinese herbs, attenuates neural and cardiac toxicity induced by intravenous infusion of bupivacaine, a local anesthetic. This study was designed to investigate whether bupivacaine could induce a toxic effect in primary cultured mouse spinal cord neuron and if so, whether the Shenfu injection had a similar neuroprotective effect in the cell model. Methods The spinal cords from 11- to 14-day-old fetal mice were minced and incubated. Cytarabine was added into the medium to inhibit the proliferation of non-neuronal cells. The immunocytochemical staining of β-tubulin was used to determine the identity of cultured cells. The cultured neurons were randomly assigned into three sets treated with various doses of bupivacaine, Shenfu and bupivacaine+Shenfu, for 48 hours respectively. Cell viability in each group was analyzed by methyl thiazoleterazolium (MTT) assay. Results The viability of the cultured neurons treated with bupivacaine at concentrations of 0.01%, 0.02%, 0.04% and 0.08% was decreased in a dose-dependent manner. Although the Shenfu injection at concentrations ranging from 1/50 to 1/12.5 (V/V) had no significant influence on the viability of cultured neurons (P<0.05 vs control), the injection significantly increased the cellular viability of cultured neurons pretreated with 0.03% bupivacaine (P<0.05). Conclusion Although Shenfu injection itself has no effect on spinal neurons, it was able to reduce the bupivacaine- induced neurotoxicity in vitro.     

Structural asymmetry of the basal nucleus of Meynert in men and women

The structure of Meynert’s nucleus was studied using quantitative neurohistological measures in 11 cases from the collection of the Institute of the Brain, Russian Academy of Medical Sciences. The set consisted of seven men and four women aged 19–60 years (apart from one aged 70 years) and were patients who had died suddenly with no history of neurological or mental diseases. The following parameters were measured: neuron field profile, neuron density, total and satellite glial density, and the proportion of glia consisting of satellite glia and the proportion of neurons surrounded by satellites. All individual measures were analyzed statistically and differences between the hemispheres were determined. On a background of a large spread in individual values, there was significant asymmetry in neuron field profile area in different directions in men and women and tendencies to a greater neuron density on the left and a greater glial cell density on the right. Measures of satellite glia showed particularly large variation, with the result that the only identifiable result was a greater proportion of satellite-surrounded neurons in the right hemisphere. Overall, there was a tendency to somewhat greater asymmetry in the structure of this nucleus in men. __________ Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 106, No. 4, pp. 50–54, April, 2006.     

Effects of protein synthesis inhibitors on the sensitization of a defensive response in common snails and potentiation of the cholinosensitivity of command neurons

The effects of protein synthesis inhibitors on short-term sensitization of a defensive reaction in common snails and the potentiation of the cholinosensitivity of command neurons were studied. The protein synthesis inhibitor anisomycin did not prevent behavioral sensitization. Anisomycin and the irreversible protein synthesis inhibitor saporin changed the dynamics of potentiation of command neuron cholinosensitivity. We suggest that the sensitization of the defensive response of the common snail studied here does not require the synthesis of new proteins. __________ Translated from Zhurnal Vysshei Nervnoi Deyatel’nosti imeni I. P. Pavlova, Vol. 56, No. 3, pp. 355–362, May–June, 2006.     

Neurons and satellite glial cells in adult rat lumbar dorsal root ganglia express connexin 36

Previous studies have shown that following peripheral nerve injury there was a downregulation of the gap junction protein connexin 36 (Cx36) in the spinal cord; however, it is not known whether Cx36 protein is expressed in the dorsal root ganglia (DRGs), nor if its levels are altered following peripheral nerve injuries. Here we address these aspects in the adult rat lumbar DRG. Cx36 mRNA was detected using qRT-PCR, and Cx36 protein was identified in DRG sections using immunohistochemistry (IHC) and immunofluorescence (IF). Double staining revealed that Cx36 co-localizes with both anti-β-III tubulin, a neuronal marker, and anti-glutamine synthetase, a satellite glial cell (SGC) marker. In neurons, Cx36 staining was mostly uniform in somata and fibers of all sizes and its intensity increased at the cell membranes. This labeling pattern was in contrast with Cx36 IF dots mainly found at junctional membranes in islet beta cells used as a control tissue. Co-staining with anti-Cx43 and anti-Cx36 showed that whereas mostly uniform staining of Cx36 was found throughout neurons and SGCs, Cx43 IF puncta were localized to SGCs. Cx36 mRNA was expressed in normal lumbar DRG, and it was significantly down-regulated in L4 DRG of rats that underwent sciatic nerve injury resulting in persistent hypersensitivity. Collectively, these findings demonstrated that neurons and SGCs express Cx36 protein in normal DRG, and suggested that perturbation of Cx36 levels may contribute to chronic neuropathic pain resulting from a peripheral nerve injury.     

4-PBA通过抑制内质网应激减轻原代海马神经元的损伤

目的:探讨内质网应激后原代海马神经元树突棘密度及突触蛋白表达的变化,以及通过内质网应激分子伴侣4-苯基丁酸(4-phenylbutyric acid,4-PBA)抑制内质网应激对这种神经元损伤的抑制作用。方法:原代培养新生大鼠海马神经元,将表达增强型绿色荧光蛋白的质粒转染到原代培养5～7 d(DIV 5～7)的大鼠海马神经元内持续培养,DIV 20时分为对照组、衣霉素(tunicamycin,Tm)处理组和Tm+4-PBA预处理组(Tm处理前1 h给予4-PBA),采用Western blot法检测内质网应激标志蛋白Bi P和突触蛋白的表达水平,激光共聚焦显微镜下观察神经元,分析树突棘密度,采用MTT法分析细胞活力。结果:Tm处理后使Bi P蛋白水平明显升高,而4-PBA预处理使Bi P蛋白水平显著下降(P 0. 05)。Tm引起的原代海马神经元树突棘密度下降及突触蛋白的表达下降能够被4-PBA抑制。Tm引起的细胞活力下降可被4-PBA抑制。结论:Tm能够通过诱导内质网应激而引起原代海马神经元树突棘密度下降及突触蛋白表达下降,而提前给予4-PBA预处理可明显降低内质网应激反应,抑制树突棘密度下降及突触蛋白表达下降,从而减轻原代海马神经元的损伤。