6—羟多巴胺损毁的大鼠纹状体内多巴胺排空与左旋千金藤啶碱引起的？…

用高效液相－电化学检测器和旋转计数的方法检测６－羟多巴胺（６－ｈｙｄｒｏｘｙｄｏｐａｍｉｎｅ，６－ＯＨＤＡ）损毁大鼠纹状体多巴胺（ｄｏｐａｍｉｎｅ，ＤＡ）排空与旋转的关系，Ｄ１／Ｄ２混合性激动剂阿扑吗啡（ａｐｏｍｏｒｐｈｉｎｅ，ＡＰＯ，０．２ｍｇ／ｋｇ，ｉｐ）可使３３只大鼠中的２０只出现旋转，其中１５只旋转强度〉５次／分钟，平均为１２．１±５．８次／分钟。Ｄ１选择性激动剂ＳＫＦ３８３９３，Ｄ２选择     

谷氨酸树突处局部给药所引起的前额皮层锥体细胞爆发式放电：NM …

AIM: To investigate whether in the prefrontal cortical (PFC) pyramidal cells, focal glutamate application to the apical dendrite induces bursting and whether the effect of glutamate involves activation of both NMDA and non-NMDA receptors. METHODS: Pyramidal cells in layers V and VI of the PFC were visualized in rat brain slices using infrared videomicroscopy and recorded with whole-cell electrodes. Glutamate and its agonists were focally applied to the apical dendrite and the soma using microiontophoresis. RESULTS: Dendritic glutamate application (0-20 nA, 10 mmol/L) induced repetitive bursts in most cells tested (12/17). In the same cells, somatic glutamate (5-20 nA, 10 mmol/L) induced only regular spiking. The bursting effect is likely to be direct since applications 5 microns away from the dendrite resulted in either a much reduced effect or no effect. Both CGP 37849 1 mumol/L and NBQX 1 mumol/L reduced the effect, suggesting an involvement of both NMDA and non-NMDA receptors. However, when non-NMDA receptors were selectively activated using AMPA (2-50 nA, 10 mmol/L), only regular spiking was observed. In contrast, selective NMDA receptor activation (NMDA 1.3-25 nA, 100 mmol/L) reliably induced bursting. CONCLUSION: In most PFC pyramidal cells tested, dendritic glutamate application induces repetitive bursting, whereas somatic glutamate application induces only regular spiking. Both NMDA and non-NMDA receptors are activated during dendritic glutamate application. However, bursting is primarily mediated by NMDA receptors.     

左旋千金藤立定和12-氯斯阔任旋光异构体对黑质多巴胺神经元放电活动的比较(英文)

目的:比较左旋千金藤立定((-)-stepholidine,(-)-SPD)和12-氯斯阔任(12-chloroscoulerine,CSL)对黑质(substantia nigra,SN)多巴胺(DA)神经元放电的影响。方法:麻痹大鼠上的胞外单单位记录。结果:在大鼠,(-)-SPD,(-)-,(±)-和( )-CSL减弱iv 10μg·kg~(-1)阿朴吗啡引起的放电抑制。ED_(50)值分别为15.1(11.9—19.4),7.8(7.0—8.7),12.6(2.0—17.9)μg·kg~(-1)和2.9(2.6—3.3)mg·kg~(-1)。(-)-CSL比(-)-SPD强1倍,比( )-CSL强371倍。在利血平化大鼠,(-)-SPD,(-)-,(±)-,和( )-CSL减弱4mg·kg~(-1)SKF-38393引起的放电抑制。ED_(50)值为0.53(0.51—0.55),0.51(0.43—0.60),1.2(0.7—2.0)和5.9(4.9—7.1)mg·kg~(-1)。(-)-CSL的强度与(-)-SPD相似,比( )-CSL强11倍。结论:(-)-SPD和CSL是D_1/D_2混合性阻滞剂。(-)-CSL最强,( )-CSL最弱。     

氯代斯阔任对D2自身受体反馈调控作用的阻滞

研究氯代斯阔任对Ｄ２自身受体是激动作用或阻滞作用。     

Effects of tetrahydroprotoberberines on dopamine D_2 receptors in ventral tegmental area of rat

阐明四氢原小檗碱同类物（ＴＨＰＢ）对大鼠中脑腹侧被盖区（ＶＴＡ）多巴胺（ＤＡ）受体的作用特性，并比较它们的作用强度．方法：采用大鼠在体胞外单位放电记录．结果：观察了１１个ＴＨＰＢ均可完全地翻转ＤＡ受体激动剂阿扑吗啡（２０μｇ·ｋｇ－１）所产生的放电抑制作用，为Ｄ２受体拮抗剂的作用特性．ＴＨＰＢ对Ｄ２受体的作用与Ｃ２位上的ＯＨ基团有密切的关系．它们的作用强度（ＥＤ５０，μｇ·ｋｇ－１）：ＴＨＰＢ１４３（５６）＞ＳＰＤ（８５）＞Ｉｓｏ（１７０）＞ＴＨＰ（３３）＞ＴＨＢ（４８）＞ＴＨＰＢ１８（６６）＞ＴＨＰＢ１（１７９）＞ＴＨＰＢ１９（４０８）＞ＴＨＰＢ１２６（５１０）＞ＴＨＰＢ１０４（１０１９）＞ＴＨＰＢ１０（４８１５）．结论：１１个ＴＨＰＢ均为ＶＴＡＤ２受体拮抗剂，以Ｃ２位上有ＯＨ基团的ＴＨＰＢ１４３作用最强．     

谷氨酸树突处局部给药所引起的前额皮层锥体细胞爆发式放电:NMDA和非NMDA受体的作用(英文)

AIM: To investigate whether in the prefrontal cortical(PFC) pyramidal eells, focal glutamate application tothe apical dendrite induces bursting and whether theeffect of glutamate involves activation of both NMDAand non-NMDA receptors. METHODS: Pyramidalcells in layers Ⅴ and Ⅵ of the PFC were visualized inrat brain slices using infrared videomicroscopy andrecorded with whole-cell electrodes. Glutamate and itsagonists were focally applied to the apical dendrite andthe soma using microiontophoresis. RESULTS:Dendritic glutamate application (0--20 nA, 10 mmol/L) induced repetitive bursts in most cells tested (12/     

6-羟多巴胺损毁的大鼠纹状体内多巴胺排空与左旋千金藤啶碱引起的旋转关系(英文)

用高效液相－电化学检测器和旋转计数方法检测6－羟多巴胺（6－hydroxydopamine，6－OHDA）损毁大鼠纹状体多巴胺（dopamine，DA)排空与旋转的关系。D1/D2混合性激动剂阿扑吗啡（apomorphine，APO，0．2mg/kg，iP）可使33只大鼠中的20只出现旋转．其中15只旋转强度＞5次／分钟，平均为12．l±5．8次／分钟。D1选择性激动剂SKF38393、D2选择性激动剂LY171555有类似APO的作用。然而，左旋千金藤啶碱（（-）－stepholidine,SPD)仅使14只大鼠出现旋转，其中6只旋转＞5次/分钟，平均为6．41±1．3次/分钟。33只损毁大鼠健测纹状体DA合量平均为9．9±1．1μg/g湿组织，损侧为2．8±2．9μg/g湿组织。旋转＞5次／分钟的大鼠，其健侧和损侧纹状体内DA含量分别为10．1±0．8和0．3±0．1μg/g湿组织。说明纹状体内DA排空程度与旋转行为有密切关系。当损侧纹状体排空小于51％时．APO不能引起任何旋转，而SPD的阈值为88．2％。APO、SKF38393、LY171555和SPD引起＞5次／分钟的旋转，分别需要损侧纹状体内DA排空达96±4％，94±4％，95±4％和98±2％以上。     

左旋千金藤立定和DA受体激动剂对6—OHDA损毁大鼠旋转行为和基底？…

AIM: To elucidate the action sites of l-stepholidine (SPD) in the basal ganglia. METHODS: Counting the rotations after intra-nucleus microinjection and recording the neuron firing by microiontophoresis of SPD and DA agonists in the basal ganglia of 6-hydroxydopamine (6-OHDA)-lesioned rats. RESULTS: The DA immunoreactive substance was markedly reduced in the 6-OHDA-lesioned rats. The intra-neostriatum microinjection of apomorphine (Apo, D1/D2), SK&F 38393 (D1), and SPD elicited remarkable rotation, and the characteristics of SK&F 38393-produced rotation were of long latency and long duration. The intra-substantia nigra pars reticulata (SNR) injection of Apo, SK&F 38393, and SPD induced the rotation response, while the selective D2 agonist quinpirole hydrochloride (Ly171555) did not because of scarce D2 receptors in the SNR. The intraglobus pallidus (GP) injection of DA agonists and SPD failed to evoke rotation, but the GP nucleus still had the contribution to rotation elicited by i.p. injection of DA agonists and SPD in the 6-OHDA-lesioned rats with successive kainic acid (KA) lesion. Besides, the successive lesion of entopeduncular nucleus (EP) on rotation was less important than that of GP nucleus. The microiontophoresis of Apo and SPD into the SNR could evoke the neuron firing, but failed to activate the GP neurons, which were activated by sodium glutamate (Glu) and inhibited by gamma-aminobutyric acid (GABA). CONCLUSION: The action sites of SPD-induced rotation and neuron firing via the D1 receptors are in the neostriatum and SNR instead of GP. The direct neurocircuit through SNR is the most important for rotation of 6-OHDA-lesioned rats.     

左旋千金藤立定和DA受体激动剂对6-OHDA损毁大鼠旋转行为和基底核神经元放电的作用部位(英文)

目的:确定l-SPD在基底神经核的作用部位。方法:6-OHDA损毁大鼠单侧黑质致密区(SNC),核团内微注或微电泳给予l-SPD或DA激动剂,作旋转实验和神经元放电记录。结果:1)大鼠纹状体损毁侧DA免疫反应物减少。2)新纹状体或黑质网质区(SNR)内微注DA激动剂Apo(D_1/D_2),SK＆F38393(D_1)或SPD引起大鼠强烈旋转,而微注Ly171555(D_2)于SNR或DA激动剂和l-SPD于苍白球(GP)均不引起旋转。卡英酸进一步损毁GP或脚间核(EP),DA激动剂或l-SPD诱发大鼠旋转显著下降。3)微电泳Apo或SPD引起SNR神经元放电,但对GP神经元无效。结论:l-SPD诱发大鼠旋转和神经元放电由D_1受体介导,基底核新纹状体和SNR是其作用部位,而不是GP。通过SNR的直接环路在旋转行为中起重要作用。