Subarachnoid Hemorrhage Induces Na+/myo-Inositol Cotransporter in the Rat Brain.

Abstract

Neurons and glial cells respond to extracellular hyperosmolarity by accumulating small organic solutes, called``osmolytes.'' Na ＋ /myo-inositol is one of the major organic osmolytes in the brain and Na ＋ /myo-inositol cotransporter (SMIT) regulates extracellular Na ＋ /myo-inositol content. Subarachnoid hemorrhage (SAH) is an osmotic stress-inducing event of the brain. The expression of SMIT messenger ribonucleic acid (mRNA) and protein was investigated with in situ hybridization and immunohistochemistry in rat brains with SAH induced by endovascular perforation. SMIT riboprobe was raised from a 490-bp rat SMIT complementary deoxyribonucleic acid. Anti-SMIT antibody was raised in rabbits. SMIT mRNA was expressed strongly in the cortex, hippocampus, and hypothalamus of the perforated side at 6 to 24 hours after SAH. Mild upregulation was noted in the contralateral cortex, hippocampus, and hypothalamus. The ventral aspect of the pons showed mild upregulation. Microautoradiography and immunostaining showed SMIT expression mainly in the neurons, but also in some non-neural cells in the hippocampus. The present results indicate that diffuse osmotic stress occurs in the host brain after SAH.

The blood–brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments

“…Areas like the hypothalamus, the amygdala, and the temporal cortex are directly affected by blood-borne materials. In these areas, expression of Na + /myo-inositol cotransporter (SMIT) reflecting osmotic stress is upregulated between 6 to 24 h after SAH [ 414 ].…”