Involvement of Supraoptic Astrocytes in Basilar Artery Occlusion-Evoked Differential Activation of Vasopressin Neurons and Vasopressin Secretion in Rats

Vasopressin (VP) is a key factor in the development of brain injury in ischemic stroke. However, the regulation of VP secretion in basilar artery occlusion (BAO) remains unclear. To clarify the regulation of VP secretion in BAO and the underlying mechanisms, we performed this study in a rat model of BAO with (BC) or without common carotid artery occlusion (CCAO). The results showed that BAO and BC time-dependently increased neurological scores and that BC also increased water contents in the medulla at 2 h and in the pontine at 8 h. Moreover, plasma VP level increased significantly at BAO-8 h, CCAO and BC-2 h but not at BC-8 h; however, VP expressions increased in the supraoptic nucleus (SON) at BC-8 h. The neurological scores were highly correlated with pontine water contents and plasma VP levels. The number of phosphorylated extracellular signal-regulated protein kinase1/2-positive VP neurons increased significantly in the SON at BC-8 h. Similarly, the number of c-Fos-positive VP neurons increased significantly in the SON at BAO-8 h and BC-8 h. In addition, the length of glial fibrillary acidic protein (GFAP) filaments increased significantly in BC compared to BAO only. Aquaporin 4 (AQP4) puncta around VP neurons increased significantly at BC-8 h relative to BC-2 h, which had negative correlation with plasma VP levels. These findings indicate that BAO facilitates VP secretion and increases VP neuronal activity in the SON. The peripheral VP release is possibly under a negative feedback regulation of central VP neuronal activity through increasing GFAP and AQP4 expression in astrocytic processes.

Automated summary

The study found that basilar artery occlusion facilitates vasopressin secretion and increases vasopressin neuronal activity in the supraoptic nucleus (SON). Peripheral vasopressin release is possibly under negative feedback regulation of central vasopressin neuronal activity through increasing glial fibrillary acidic protein (GFAP) and aquaporin 4 (AQP4) expression in astrocytic processes.