Allen E E, Trombley P Q, Gordon B
Institute of Neuroscience, University of Oregon, Eugene 97403.
Exp Brain Res. 1988;72(3):605-10. doi: 10.1007/BF00250605.
Under some circumstances intraventricular administration of 6-OHDA decreases visual cortical plasticity of kittens; the mechanism for this change is not known, but depletion of norepinephrine (NE) is not the entire explanation. We have examined the effects of 6-OHDA treatment on beta adrenergic receptor binding in kitten visual cortex. Subjects were given vehicle solution alone, a low dose of 6-OHDA which depleted cortical NE without affecting visuocortical plasticity, or a higher dose of 6-OHDA which depleted cortical NE and decreased visuocortical plasticity. Drugs were administered in single daily injections via intraventricular cannulas. Saturation assays were performed on homogenates of visual cortical tissue using 125I-pindolol (30-400 pM) along w/ isoproterenol (237 microM) as a cold competitor. We measured radioactivity bound to tissue and retained on filters and analyzed the data using the EBDA computer program (McPherson 1983, 1985); we determined the affinity constant (Kd) and receptor density (Bmax) in multiple assays for each animal. Despite 75-90% NE depletion in both experimental groups, only the group receiving the lower dose of 6-OHDA showed any evidence of supersensitivity. The Kds did not differ among the groups. The data suggest that the effects of 6-OHDA on visuocortical plasticity are not secondary to beta adrenergic supersensitivity.
在某些情况下，脑室内注射6-羟基多巴胺会降低小猫视皮层的可塑性；这种变化的机制尚不清楚，但去甲肾上腺素（NE）的耗竭并非全部原因。我们研究了6-羟基多巴胺处理对小猫视皮层β肾上腺素能受体结合的影响。实验对象分别接受单独的赋形剂溶液、低剂量的6-羟基多巴胺（其耗尽皮层NE但不影响视皮层可塑性）或高剂量的6-羟基多巴胺（其耗尽皮层NE并降低视皮层可塑性）。药物通过脑室内插管每日单次注射给药。使用125I-吲哚洛尔（30 - 400 pM）并以异丙肾上腺素（237 microM）作为冷竞争剂对视皮层组织匀浆进行饱和分析。我们测量了与组织结合并保留在滤膜上的放射性，并使用EBDA计算机程序（麦克弗森，1983年，1985年）分析数据；我们在对每只动物的多次分析中确定了亲和常数（Kd）和受体密度（Bmax）。尽管两个实验组的NE均耗竭了75 - 90%，但只有接受低剂量6-羟基多巴胺的组显示出任何超敏反应的迹象。各组之间的Kd没有差异。数据表明，6-羟基多巴胺对视皮层可塑性的影响并非继发于β肾上腺素能超敏反应。
