电刺激大鼠束旁核对底丘脑核和丘脑腹内侧核神经元的影响

本工作旨在探讨电刺激束旁核（parafascicular nucleus,PF）对帕金森病模型（Parkinson’s disease,PD）大鼠神经行为的改善作用及其机制。成年雄性Sprague—Dawley大鼠黑质致密部注射6一羟基多巴胺建立PD大鼠模型。采用行为学方法观察电刺激PF对阿朴吗啡诱发的大鼠旋转行为的作用,并应用在体细胞外记录法观察电刺激PF对大鼠底丘脑核（subthalamic nucleus,STN）及丘脑腹内侧核（ventromedial nucleus,VM）神经元放电的影响。结果发现,高频电刺激（130Hz,0．4mA,5s）PF一周,明显改善PD大鼠旋转行为。细胞外放电记录显示,高频电刺激PF使PD大鼠STN神经元自发放电减少,且该作用具有频率依赖性。另外,高频电刺激PF可使VM神经元兴奋,该作用也是频率依赖性的。我们在实验中同时观察到微电泳谷氨酸（glutamicacid,Glu）受体拮抗剂MK-801使STN神经元放电频率减少或完全抑制,微电泳t氨基丁酸（T-amino butyricacid,GABA）受体拮抗剂印防己毒素（picrotoxin,Pic）则使神经元放电频率增加。以上结果表明,GABA能和GIu能传入纤维可会聚于同-STN神经元,并对后者有紧张性作用。高频刺激PF,使该核团到STN神经元的Glu能兴奋性输出减少,导致STN的失活。这一作用通过基底神经节的间接通路,最终释放了丘脑运动核团VM的活性。高频刺激PF经PF,STN和VM的神经通路而改善PD大鼠神经行为。     

损毁丘脑腹内侧核对大鼠行为的影响

黑质(SN)-纹状体多巴胺(DA)能神经元系统在调节躯体运动方面起着重要作用;但这一作用的传出神经通路尚无定论。在大鼠,丘脑腹内侧核(VM)是基底神经节的传出投射之一,主要接受SN网状部(SNR的投射纤维。本实验观察电损毁VM后,腹腔注射去水吗啡对大鼠姿势与行为的影响,以探讨SN-纹状体DA能神经元系统与VM在调节躯体运动中的功能联系。1 材料与方法 实验采用Sprague-Dawley系雄性大鼠,体重为200～300g,分为对照组(n=10)和实验组(n=11)。在1％成巴比妥钠麻醉下,将动物固定于立     

微电泳乙酰胆碱和阿托品对大鼠丘脑束旁核痛敏神经元电活动的影响

在30只大鼠上,用多管微电极细胞外记录和离子微电泳方法,观察了乙酰胆碱(ACh)和阿托品对丘脑束旁核(Pf)神经元电活动的影响。结果表明,微电泳ACh可加强痛敏神经元的电活动,并使部分自发放电神经元对伤害性刺激产生反应。阿托品可以阻断ACh的上述作用。微电泳阿托品能减少痛敏神经元的电活动。这些结果提示,在Pf神经元的活动中,ACh可以直接作用于M受体发挥其兴奋作用。     

微电泳GABA和5－HT对大鼠丘脑束旁核单位痛放电的影响

本实验用多管微电极细胞外记录和离子微电泳方法,在水含氯醛麻醉的ＳＤ大鼠上观察了γ－氨基丁酸（ＧＡＢＡ）和５－羟色胺（５－ＨＴ）以及它们的受体阻断剂（印防已毒素和赛庚啶）对丘脑束旁核（Ｐｆ）单位痛放电的影响。结果表明：（１）电泳ＧＡＢＡ可抑制Ｐｆ神经元的痛放电,这作用可被电泳印防已毒素所阻断,而单独电泳印防己毒素可加强Ｐｆ的痛放电。（２）电泳５－ＨＴ对Ｐｆ单位痛放电在有些单位表现加强作用,另一些单位表现抑制作用,仅前者可被电泳赛庚啶所阻断。上述结果提示：在Ｐｆ神经元的痛放电活动中,ＧＡＢＡ可能起抑制性作用,而５－ＨＴ可能通过不同的受体亚型既发挥其兴奋作用,也可有抑制作用。     

乙酰胆碱对大鼠丘脑束旁核和中脑网状结构痛反应神经元电活动的影响

在54只大鼠上,用两支微电极同时记录神经元放电的方法,研究了脑室注射乙酰胆碱(ACh)对丘脑束旁核(Pf)和中脑网状结构(RF)痛反应神经元电活动的影响。结果表明,当脑内ACh含量增加时,Pf和RF中两个痛兴奋神经元(PEN)的电活动同时减弱,两个痛抑制神经元(PIN)的电活动同时加强,Pf中一个PEN电活动减弱的同时RF中一个PIN电活动加强,或者相反。阿托品可以阻断ACh的上述作用。这提示,ACh对不同中枢痛反应神经元的电活动的影响是通过M胆碱能受体而实现的。     

损毁成体鸽下丘脑腹内侧核对神经元增生的影响

本实验应用（＾３Ｈ）放射自显影和免疫组织化学方法首次报道了高等脊椎动物成体鸟脑损伤引起神经元增生的观察结果。电损毁非鸣禽成体环鸽下丘脑腹内侧核后能引起端脑外侧室带区中（＾３Ｈ）标记细胞的大量增生和在端脑尾部ＬＶＺ中的特异性分布。     

微电泳GABA和5—HT对大鼠丘脑束核单位痛放电的影响

本实验用多管微电极细胞外记录和离子微电泳方法，在水合氯醛麻醉的ＳＤ大鼠上观察了γ－氨基丁酸和５－羟色胺以及它们的受体阻断剂（印防已毒素和赛庚啶）对丘脑束旁核单位痛放电的影响。结果表明：（１）电泳ＧＡＢＡ可抑制Ｐｆ神经元的痛放电，这作用可被电泳印防已毒素所阻断，而单独电泳印防已毒素可加强Ｐｆ的痛放电。（２）电泳５－ＨＴ对Ｐｆ单位痛放电在有些单位表现加强作用，另一些单位表现抑制作用，仅前者可被电泳赛庚     

面神经核腹内侧区微量注射三种递质的呼吸效应

实验用兔,在乌拉坦静脉麻醉、切断双侧颈迷走神经、自主呼吸条件下进行,以膈神经放电作呼吸指标。观察了面神经核腹内侧区(VMNF)微量注射三种递质对呼吸节律的影响。结果如下:(1)VMNF 区微量注射肾上腺素呼吸频率增加,膈神经吸气性放电的递增速度加快,积分幅度升高,VMNF 区微量注射妥拉苏林,呼吸频率下降且妥拉苏林可阻断肾上腺素的呼吸效应。(2)VMNF 区微量注射γ-氨基丁酸、甘氨酸导致呼吸频率下降,吸气时程、呼气时程延长。提示肾上腺素、γ-氨基丁酸、甘氨酸可能作为递质作用于 VMNF 区的神经元而发挥呼吸调节作用。     

GABA IN THE OLFACTORY BULB AND OLFACTORY NUCLEUS OF THE RAT: THE DISTRIBUTION OF GAMMA-AMINOBUTYRIC ACID, GLUTAMIC ACID DECARBOXYLASE, GABA TRANSAMINASE AND SUCCINATE SEMIALDEHYDE DEHYDROGENASE

Abstract— The distribution of GABA and enzymes involved in its metabolism was investigated in the different regions of the olfactory bulb and olfactory nucleus. The highest levels of GABA in the olfactory bulb were found in the layers rich in nerve terminals (31 μmol/g dry wt.). A similar distribution was found in the olfactory nucleus although the overall level of GABA was only a quarter of that measured in the bulb. Glutamic acid decarboxylase (GAD) levels in the various layers of the olfactory nucleus were similar in distribution to those of GABA. However, the correlation between GAD and GABA did not hold for the olfactory bulb, particularly in the granule cell layer and the medulla. The activities of GAD and the levels of GABA are significantly higher in the bulb than in the nucleus but succinic acid scmialdehyde dehydrogenase and GABA aminotransaminase activities are almost identical in both regions.     

刺激猫下丘脑LHA和VMN对小脑皮层神经元电活动的影响

在戊巴比妥钠麻醉的猫,电刺激下丘脑外侧区(LHA)和腹内侧核(VMN)可引起小脑皮层第Ⅵ和Ⅶ小叶浦肯野细胞和非浦肯野细胞抑制性、兴奋性和抑制-兴奋性的电活动,但以抑制性活动为主;这些反应的潜伏期多数为10-20ms,但也可长达90ms;一般刺激LHA比刺激VMN更有效。刺激下丘脑所激发的小脑神经元抑制性电活动可为静脉注射组胺H_1受体阻断剂扑尔敏所阻断。本文对上述观察的可能作用作了讨论。     

丘脑网状核及其GABAB受体在癫痫小发作形成中的作用

目的和方法：实验选用ＳＤ大鼠戊四氮（ＰＴＺ）模型,结合电刺激或电解毁损丘脑网状核、丘脑接替核（丘脑腹后外侧核）、丘脑前核（丘脑前内侧核）,并用蝇蕈醇、氯苯氨丁酸、３疏基丙酸等药物在丘脑网状核内微量注射或腹腔注射后观察棘慢波的变化。结果：电刺激丘脑网状核可增强癫痫小发作,毁损丘脑网状核可抑制癫痫小发作,ＧＡＢＡＢ受体的激活不利于小发作的消除     

猫丘脑腹后外侧核的超微结构

采用电镜技术观察了猫丘脑腹后外侧核的超微结构。该核内的神经元可分为大小两种类型，大型直径在１５—４０μｍ，小型小于１５μｍ，其胞质内容无明显差别。树突较多见，直径从１—１０μｍ不等。轴突可分为三种类型：含圆形小泡的小终末、终末及扁平小泡的终末。突触类型主要为轴树突触，此外还可见到轴体、轴轴、轴轴树、树树突触以及以树突为中心的突触复合体。在树突之间、树突与胞体之间还存在有非突触的丝状连接。     

INTRACELLULAR AMINO ACID CONTENT OF NEURONAL, GLIAL, AND NON-NEURAL CELL CULTURES: THE RELATIONSHIP TO GLUTAMIC ACID COMPARTMENTATION

Abstract— A protocol for the accurate determination of intracellular levels of amino acids in tissue cultured cells has been developed and used in the measurement of intracellular amino acids levels in neuronal, glial, and non-neural cell lines, with the objective of establishing morphological correlates for large and small glutamic acid compartments and of examining hypotheses for the morphological basis of glutamic acid compartmentation. This survey of intracellular amino acid levels has revealed striking differences among the cell lines tested, but these differences did not correlate with cell type, i.e. neuronal vs glial, in contrast to earlier results (R ose , 1968) based on bulk separated neuronal and pial fractions from rat brain. Amino acid levels were found to be dependent upon tissue culture conditions, yet reproducible differences could be observed when growth and experimental conditions were carefully controlled. Glutamic acid levels for various cell lines ranged from 50.8 ± 14.3 to 158 ± 8.5 nmol/mg protein. Intracellular glutamine levels demonstrated even greater difference, with values ranging from 0.8 ± 0.2 to 107 ± 42.4 nmol/mg protein. Statistically significant differences in intracellular amino acid levels between cell lines were also observed for aspartic acid, praline, glycine, alanine, valine, cystathionine, isoleucine, and leucine. A number of cell lines demonstrating highly elevated elevated levels of γ-aminobutyrate and β-alanine were identified. The significance of neuronal and glial levels of glutamic acid, glutamine and γ-aminobutyrate to models for glutamic acid compartmentation is discussed.     

INTERACTION OF TAURINE, GABA AND GLUTAMIC ACID WITH SYNAPTIC MEMBRANES

Abstract— Sodium-independent but calcium-dependent binding of taurine, GABA and glutamate to synaptic membranes from calf brain cortex is demonstrated. Binding constants of 1.5 μ m for taurine, 46 μ m for GABA and 45 μ m for glutamate were obtained, being largely mixed with transport constants derived from the influx to empty membrane-pouches (particularly in the case of GABA and glutamate), and in the case of GABA also with the non-specific binding. Certain structural analogues of amino acids inhibited the binding, aspartate being the most potent inhibitor for glutamate, and β -alanine for GABA and taurine, but KCN and 2,4-dinitrophenol had no effect. The membrane-attached [³⁵S]taurine was divided by differential elution into easily extractable and firmly bound components.