Cerebellar benzodiazepine receptors: cellular localization and consequences of neurological mutations in mice.
Cerebellar benzodiazepine receptors: cellular localization and consequences of neurological mutations in mice.
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小脑苯二氮卓受体：小鼠神经突变的细胞定位和后果。
DOI：
10.1016/0006-8993(88)90920-1
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发表时间：
1988
期刊：
影响因子：
2.9
通讯作者：
Frostholm,A
中科院分区：
文献类型：
--
作者：
Rotter,A;Frostholm,A
在浦肯野细胞变性（pcd/pcd）、weaver（wv/wv）、staggerer（sg/sg）和reeler（rl/rl）突变小鼠中，通过放射自显影研究了小脑[3H]氟硝西泮结合位点的分布。在正常的 78 天龄 C57BL/6J 小鼠小脑中，在分子层上观察到最高浓度的 [3H]氟硝西泮结合位点。浦肯野细胞层上存在中等颗粒密度，小脑深核上存在中等至高密度。在颗粒细胞层上观察到低标记。在白质中观察到的结合位点浓度可以忽略不计。在 45-49 天龄的浦肯野细胞变性突变体中，到第 45 天基本上所有浦肯野细胞都消失了，小脑皮质上的颗粒密度略有下降。同时，与同窝对照相比，在pcd/pcd突变体的小脑深部核上观察到颗粒密度显着增加。在 81-86 日龄 wv/wv 突变体的小脑皮质中观察到[3H]氟硝西泮标记显着增加；这在蚓部最为明显，那里的颗粒细胞损失最多。在半球上，颗粒细胞退化较少，结合位点密度较低。 wv/wv 小脑深部核上的颗粒密度与同窝出生的小鼠相当。在 25-27 日龄儿童 g/sg 突变体的小脑皮质中检测到显着较低的 [3H]氟硝西泮标记，其中颗粒数量较多。浦肯野细胞和高尔基细胞大大减少；然而，深部核上的标记显着增加。在 27-29 天大的rl/rl 突变小脑中，所有类别的细胞都错位，小脑皮质所有区域（包括浦肯野细胞团）的标记密度。增加了。我们的放射自显影数据表明，部分小脑皮质苯二氮卓受体与浦肯野细胞相关。我们认为其余的受体位于高尔基细胞上，而颗粒细胞则缺乏受体。在小脑深部核中，所观察到的 PCD/PCDANDSG/SG 突变体中苯二氮卓受体的增加可能是浦肯野细胞轴突末端失去神经支配后去神经超敏性的表现。在therl/rl突变体的浦肯野细胞团中发现高受体密度，其中浦肯野细胞缺乏传入篮细胞输入，这表明苯二氮卓受体在缺乏完整的GABA能传入神经的情况下表达和维持。
The distribution of cerebellar [3H]flunitrazepam binding sites was studied autoradiographically in Purkinje cell degeneration (pcd/pcd), weaver (wv/wv), staggerer (sg/sg) and reeler (rl/rl) mutant mice. In the normal 78-day-old C57BL/6J mouse cerebellum, the highest concentration of [3H]flunitrazepam binding sites was observed over the molecular layer. Intermediate grain density was present over the Purkinje cell layer and intermediate to high density over the deep cerebellar nuclei. Low labeling was observed over the granule cell layer. Negligible concentrations of binding sites were seen in the white matter. In 45–49-day-old Purkinje cell degeneration mutants, where essentially all Purkinje cells have disappeared by day 45, there was a small decrease in grain density over the cerebellar cortex. Concomitantly, a substantial increase in grain density was observed over the deep cerebellar nuclei of thepcd/pcdmutants when compared to littermate controls. A significant increase in [3H]flunitrazepam labeling was observed over the cerebellar cortex of 81–86-day-oldwv/wvmutants; this was most pronounced in the vermis where the granule cell loss was greatest. Over the hemispheres, where fewer granule cells degenerate, a lower density of binding sites was seen. Grain density over thewv/wvdeep cerebellar nuclei was comparable to that of littermates. Substantially lower [3H]flunitrazepam labeling was detected over the cerebellar cortex of 25–27-day-oldsg/sgmutants in which the number of granule. Purkinje and Golgi cells is greatly reduced; the labeling over the deep nuclei, however, was significantly increased. In 27–29-day-oldrl/rlmutant cerebella, where all classes of cells are malpositioned, labeling density over all areas of the cerebellar cortex, including the Purkinje cell masses. was increased. Our autoradiographic data suggest that a proportion of cerebellar cortical benzodiazepine receptors are associated with Purkinje cells; we propose that the remainder of the receptors are localized on Golgi cells, while granule cells are devoid of receptors. In the deep cerebellar nuclei, the observed increase in benzodiazepine receptors in thepcd/pcdandsg/sgmutants may be a manifestation of denervation supersensitivity subsequent to the loss of innervation by Purkinje cell axon terminals. The finding of a high receptor density in the Purkinje cell masses of therl/rlmutant, where Purkinje cells are devoid of afferent basket cell input, suggests that benzodiazepine receptors are expressed and maintained in the absence of a full complement of GABAergic afferents.