重复经颅磁刺激安全性的初步研究

目的 探讨重复经颅磁刺激的安全性。方法 对接受不同刺激频率和刺激量组经颅磁刺激大鼠的行为、组织病理形态、血清髓鞘碱性蛋白（MBP）及神经元特异性烯醇化酶（NSE）含量进行观察。结果 低频刺激组（5Hz）和高频刺激组（20Hz）在刺激过程中均未出现异常活动,无肢体强直、阵挛等,脑组织形态学包括大体观察、普通光镜改变不明显,其血清MBP和NSE含量与正常对照组比较,无显著性差异（P＞0．05）。结论 在一定强度和频率内经颅磁刺激是比较安全的。     

川芎嗪对大鼠局部脑缺血星形胶质细胞的影响

目的 :观察川芎嗪对缺血后神经元改变和星形胶质细胞GFAP表达的影响。方法 :制作大鼠单侧局灶性脑缺血模型 ,HE染色观察神经元的形态学改变 ,免疫组化染色观察星形胶质细胞GFAP表达的变化。结果 :川芎嗪可提高星形胶质细胞GFAP表达。结论 :川芎嗪对缺血神经元有保护作用     

Proton-gated ion channels in cultured mouse cortical neurons

Proton-gated ion channels in cultured mouse cortical neurons were characterized using the patch clamp technique. In voltage clamp, rapid shifts of the extracellular saline from pH 7.4 to <7.0 invariably triggered inward currents carried by sodium. The currents were inhibited by Amiloride (IC₅₀: 6.2 μM). In current clamp, acidic saline depolarized the neurons and triggered trains of action potentials. Concentration–response experiments revealed an extreme intercell variance as the EC₅₀-value for protons varied from pH 6.8 to 5.6, indicating heterogeneity in channel type expression from cell to cell. The possible involvement of acid sensing ion channels in ischemic neurodegeneration is discussed.     

Onset and regression of neuroaxonal lesions in sheep with mannosidosis induced experimentally with swainsonine

Summary A group of young sheep were fed a diet containing the-mannosidase inhibitor swainsonine, which resulted in the induction of a neuronal lysosomal mannoside storage disease. Sheep were killed at various intervals during and following the treatment period and the nature and distribution of neuronal and axonal lesions in the brain were assessed by routine light and electron microscopy and by the rapid Golgi impregnation technique. Neuronal mannoside storage, axonal dystrophy and meganeurite formation were induced by 80 days of treatment and the lesions had regressed by 40 days after the end of treatment. The results are discussed in relation to their relevance to the current widespread interest in the pathobiology of neuronal lysosomal storage.Supported by the Australian Research Grants Scheme and the Australian Brain Foundation (Huxtable and Dorling) and NIH Grant No. NS-07512 (Walkley)     

神经元特异性烯醇化酶与脑损伤

神经元特异性烯醇化酶 ( NSE)为烯醇化酶的γ二聚体同工酶 ,特征性地位于神经元和神经内分泌细胞胞质中 ,血清和脑脊液中亦含有少量 NSE。若神经元发生坏死 ,NSE会漏至胞外 ,使体液浓度升高。在脑损伤性疾病中 ,如脑梗死、脑出血、蛛网膜下腔出血、癫、脑外伤、脑缺氧、脑炎、Creutzfeldt-Jakob病 ,血清和 /或脑脊液 NSE显著升高 ,与脑损伤范围或疾病严重程度密切相关 ,是早期预测预后的重要指标     

Lateral asymmetries in the trigeminal ganglion of the male rat

We have applied stereological methods to estimate the number and perikaryal size of primary sensory neurons in celloidin-embedded trigeminal ganglia of male albino rats, specifically looking for inter-individual and side variability. The mean total number of neurons per ganglion was 35,300, with a moderate variability among ganglia. On average, 66% of the neurons were classified as A-type and 34% as B-type. Although for individual cases there could be notable side differences in the number of neurons of each type, on a population basis these differences were not significant. Mean neuronal volume was four times larger for A- than for B-cells, and both populations exhibited a moderate variability among individuals. High intra-animal side differences were found for A-cells, which were on average a significant 23.5% larger in the right ganglia. B-cells did not show significant side differences. The distribution of individual volumes around the mean value was consistently skewed to the right, particularly in the case of A-cells, which partially overlapped with the largest B-cells. In the right ganglion the distribution of A-cells, but not of B-cells, showed a rightward bias, revealing the increase in bigger neurons. The existence of larger A-type neurons in the right trigeminal ganglion may provide a structural substrate for some somesthetically based complex behaviors which are best performed by rats using their right vibrissae.     

Expression of connexin36 in the adult and developing rat brain

The distribution of connexin36 (Cx36) in the adult rat brain and retina has been analysed at the protein (immunofluorescence) and mRNA (in situ hybridization) level. Cx36 immunoreactivity, consisting primarily of round or elongated puncta, is highly enriched in specific brain regions (inferior olive and the olfactory bulb), in the retina, in the anterior pituitary and in the pineal gland, in agreement with the high levels of Cx36 mRNA in the same regions. A lower density of immunoreactive puncta can be observed in several brain regions, where only scattered subpopulations of cells express Cx36 mRNA. By combining in situ hybridization for Cx36 mRNA with immunohistochemistry for a general neuronal marker (NeuN), we found that neuronal cells are responsible for the expression of Cx36 mRNA in inferior olive, cerebellum, striatum, hippocampus and cerebral cortex. Cx36 mRNA was also demonstrated in parvalbumin-containing GABAergic interneurons of cerebral cortex, striatum, hippocampus and cerebellar cortex. Analysis of developing brain further revealed that Cx36 reaches a peak of expression in the first two weeks of postnatal life, and decreases sharply during the third week. Moreover, in these early stages of postnatal development Cx36 is detectable in neuronal populations that are devoid of Cx36 mRNA at the adult stage. The developmental changes of Cx36 expression suggest a participation of this connexin in the extensive interneuronal coupling which takes place in several regions of the early postnatal brain.     

Immunohistochemical examination of the INK4 and Cip inhibitors in the rat neonatal cerebellum: cellular localization and the impact of protein calorie malnutrition

Expression of the cyclin-dependent kinase inhibitors (CKIs) has been linked to the inhibition of cellular proliferation and the induction of differentiation. Based on structure function analysis, two distinct families of CDKIs, the INK4 and the Cip/Kip family have been identified. The INK4 family member p16(Ink4), and the Cip/Kip protein p27(Kip1) have been implicated in normal development of the CNS and cerebellum. Recent studies have suggested a functional inter-dependence between the CKI and the abundance of cyclin D1 in orchestrating growth factor-induced cellular proliferation. The neonatal rat cerebellum undergoes proliferative growth and differentiation, localized to distinct topographical regions and cell types. The cell type and the temporal profile of CKI expression during postnatal cerebellar development had not been described. The current studies determined the specific cerebellar cell types in which the CKIs were expressed during post natal development by co-staining for cell-type specific markers. p16(Ink4a) and p27(Kip1) immunostaining was identified in both neurons and glial cells, increasing progressively between postnatal days 6 to 13 into adulthood. By contrast, neuronal and glial cell p21(Cip1) staining was prominent at days 6-11 and decreased thereafter. Cyclin D1 was expressed in the proliferating external granular cells, with occassional staining in the molecular, and internal granular layers. Dual immunostaining demonstrated cyclin D1 within cells expressing CKI (p16(Ink4a), p21(Cip1),p27(Kip1)). Cerebellar cellular growth arrest, induced by protein-calorie malnutrition, inhibited cyclin D1 protein levels without affecting CKI immunostaining suggesting CKI do not mediate the developmental arrest. These results demonstrate that the CKIs are induced by differentiation cues in specific cell types with distinct kinetics in the developing cerebellum in vivo.     

An adenoviral vector expressing the glucose transporter protects cultured striatal neurons from 3-nitropropionic acid

Considerable interest has focused on the possibility of using gene transfer techniques to introduce protective genes into neurons around the time of necrotic insults. We have previously used herpes simplex virus amplicon vectors to overexpress the rat brain glucose transporter, Glut-1 (GT), and have shown it to protect against a variety of necrotic insults both in vitro and in vivo, as well as to buffer neurons from the steps thought to mediate necrotic injury. It is critical to show the specificity of the effects of any such transgene overexpression, in order to show that protection arises from the transgene delivered, rather than from the vector delivery system itself. As such, we tested the protective potential of GT overexpression driven, in this case, by an adenoviral vector, against a novel insult, namely exposure of primary striatal cultures to the metabolic poison, 3-nitropropionic acid (3NP). We observed that GT overexpression buffered neurons from neurotoxicity induced by 3NP.     

新生儿窒息后血清神经元特异性烯醇化酶与Apgar评分关系分析

目的 :探讨新生儿窒息后血清神经元特异性烯醇化酶 (NSE)浓度与Apgar评分关系。方法 :选择窒息新生儿52例 ,同期健康无窒息对照22例 ,采用免疫放射分析法 (RIA)测定其生后24小时血清NES水平。结果 :(1)1分钟和5分钟Apgar评分时 ,4～7分组与≤3分组之间血清NSE浓度差异均无显著性。 (2)5分钟复苏组、10分钟复苏组、>10分钟复苏组与对照组间血清NSE浓度差异具有统计学意义 (F=6.21,P<0.05)。>10分钟复苏组的血清NSE浓度较10分钟复苏组、5分钟复苏组及对照组明显升高 (P均<0.01)。结论 :新生儿窒息时 ,血清中NSE浓度与Apgar评分关系并非一致 ,而与复苏时间变化一致 ,复苏时间越长 ,NSE升高越明显