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中文摘要
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A. CCK拮抗剂丙谷胺, 大鼠的丘脑核,部分阻断hypermotorism在一个 暗的Digiscan活动监视器 这一发现是第一个 内源性CCK有助于中脑边缘功能的证据。 B。 胆囊收缩素腹侧被盖区药理学特性 发现CCK调节DA,即CCK单独没有作用,但 增强DA诱导的低运动,当微量注射到 VTA。 这种作用被未硫酸化的CCK-8模仿。还有CCK-4 并且不被丙谷胺阻断,这表明 中枢型CCK受体亚型。 中枢型CCK激动剂 模仿了这种效果。 C. 甘丙肽是一种29个氨基酸的肽, 乙酰胆碱在大鼠隔-海马通路。 脑室内或海马内微量注射纳克 一定剂量的甘丙肽阻断了乙酰胆碱逆转 大鼠在t-迷宫延迟交替任务中的记忆缺陷 Meynert-内侧隔区基底核病变。 一个 正在寻找这种抑制肽的拮抗剂作为一种可能的 治疗某些认知功能障碍的方法 与老年痴呆症有关。 D. 神经肽的微透析正在开发, 不同的塑料,允许更大的通道, 带电肽 放射免疫分析检测到了可测量的 胆囊收缩素水平在脑桥核,和可测量 麻醉大鼠腹侧海马中甘丙肽的水平。
英文摘要
A. Microinjection of the CCK antagonist, proglumide, in the nucleus accumbens of rats, partially blocked hyperlocomotion in a darkened Digiscan activity monitor. This finding is the first evidence that endogenous CCK contributes to mesolimbic functions. B. Characterization of the ventral tegmental pharmacology of CCK found that CCK modulated DA, i.e. CCK had no effect alone, but potentiated DA-induced hypolocomotion, when microinjected into the VTA. This effect was mimicked by unsulfated CCK-8. and by CCK-4. and was not blocked by proglumide, suggesting mediation by a central-type CCK receptor subtype. A central-type CCK agonist mimicked this effect. C. Galanin is a 29-amino acid peptide which coexists with acetylcholine in the septo-hippocampal pathway of the rat. Intraventricular or intrahippocampal microinjection of nanogram doses of galanin blocked the ability of acetylcholine to reverse memory deficits on a t-maze delayed alternation task in rats lesioned in the nucleus basalis of Meynert-medial septal area. An antagonist of this inhibitory peptide is being sought as a possible approach for the treatment of some cognitive dysfunctions associated with Alzheimers disease. D. Microdialysis for neuropeptides is being developed using different plastics which allow greater passage of the large, highly charged peptides. Radioimmunoassays have detected measurable levels of cholecystokinin in the nucleus accumbens, and measurable levels of galanin in the ventral hippocampus, of anesthetized rats.
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