Vallet P, Bouras C, Barberis C, Dreifuss J J, Dubois-Dauphin M
Department of Psychiatry, University Medical Center, Geneva, Switzerland.
J Comp Neurol. 1995 Nov 13;362(2):223-32. doi: 10.1002/cne.903620206.
In Mongolian gerbils, the content of vasopressin in the cerebral cortex, the striatum, and the hypothalamus is increased after induction of acute cerebral ischemia. We used an iodinated vasopressin analogue and light microscopic autoradiography to study the distribution of vasopressin V1 receptors in the brain of adult male gerbils and to evaluate the effects of a transient bilateral cerebral ischemia (6 minutes) on the density of this receptor population. The animals were killed immediately or 10, 30, or 100 hours after transient bilateral occlusion of the common carotid arteries. In control animals, specific [125I]-VPA binding sites were present in various structures of the brain (olfactory bulb, anterior olfactory nucleus, lateral septum, bed nucleus of the stria terminalis, median preoptic area, ventral pallidum, substantia innominata, amygdala, thalamus, hypothalamic mammillary nuclei, superior colliculus, subiculum, central gray, nucleus of the solitary tract, hypoglossal nucleus). The strongest labeling was detected in the cerebral cortex, layers 5-6. After 30-100 hours of survival time following ischemia there was a marked decrease in [125I]-VPA binding site density in these cerebral cortex layers. To a lesser degree, a decrease was also detected in the lateral septal nucleus. In contrast, labeling in other noncortical structures remained unchanged. All animals with 100 hours recovery showed a loss of cells in hippocampus (CA1 layer) and striatum. In addition, ischemia induced concomitant and proliferative changes in cortical and hippocampal astrocytes assessed by glial fibrillary acid protein immunoreactivity. These observations indicate a role for vasopressin in the cerebral cortex either on neurons or on glial cells and the modulation of vasopressin receptor expression by transient cerebral ischemia.
在蒙古沙鼠中，急性脑缺血诱导后，大脑皮质、纹状体和下丘脑的血管加压素含量增加。我们使用碘化血管加压素类似物和光学显微镜放射自显影术来研究成年雄性沙鼠大脑中血管加压素V1受体的分布，并评估短暂双侧脑缺血（6分钟）对该受体群体密度的影响。动物在双侧颈总动脉短暂闭塞后立即或10、30或100小时处死。在对照动物中，特异性[125I]-VPA结合位点存在于大脑的各种结构中（嗅球、前嗅核、外侧隔、终纹床核、视前正中区、腹侧苍白球、无名质、杏仁核、丘脑、下丘脑乳头体核、上丘、海马下脚、中央灰质、孤束核、舌下神经核）。在大脑皮质第5 - 6层检测到最强的标记。缺血后存活30 - 100小时，这些大脑皮质层中[125I]-VPA结合位点密度显著降低。外侧隔核也有程度较轻的降低。相比之下，其他非皮质结构中的标记保持不变。所有恢复100小时的动物海马（CA1层）和纹状体均出现细胞丢失。此外，通过胶质纤维酸性蛋白免疫反应性评估，缺血诱导皮质和海马星形胶质细胞出现伴随性和增殖性变化。这些观察结果表明血管加压素在大脑皮质中对神经元或胶质细胞起作用，以及短暂性脑缺血对血管加压素受体表达的调节作用。
