VASOPRESSIN BINDING IN THE CEREBRAL-CORTEX OF THE MONGOLIAN GERBIL ISREDUCED BY TRANSIENT CEREBRAL-ISCHEMIA

In Mongolian gerbils, the content of vasopressin in the cerebral corte x, 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 vasopr essin V-1 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 imme diately or 10, 30, or 100 hours after transient bilateral occlusion of the common carotid arteries. In control animals, specific [I-125]-VPA binding sites were present in various structures of the brain (olfact ory bulb, anterior olfactory nucleus, lateral septum, bed nucleus of t he stria terminalis, median preoptic area, ventral pallidum, substanti a innominata, amygdala, thalamus, hypothalamic mammillary nuclei, supe rior colliculus, subiculum, central gray, nucleus of the solitary trac t, hypoglossal nucleus). The strongest labeling was detected in the ce rebral cortex, layers 5-6. After 30-100 hours of survival time followi ng ischemia there was a marked decrease in [I-125]-VPA binding site de nsity 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) a nd striatum, In addition, ischemia induced concomitant and proliferati ve changes in cortical and hippocampal astrocytes assessed by glial fi brillary acid protein immunoreactivity. These observations indicate a role for vasopressin in the cerebral cortex either on neurons or on gl ial cells and the modulation of vasopressin receptor expression by tra nsient cerebral ischemia. (C) 1995 Wiley-Liss, Inc.