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Reelin-Dab1 signaling is indispensable for proper positioning of neurons in mammalian brain. Reelin is a glycoprotein secreted from Cajal-Reztuis cells in marginal zone of cerebral cortex, and its receptors are Apolipoprotein E receptor 2 (ApoER2) or very low density lipoprotein receptor (VLDLR) expressed on migrating neurons. When Reelin binds to ApoER2 or VLDLR, an adaptor protein Dab1 bound to the receptors undergoes Tyr phosphorylation that is essential for Reelin signaling. We reported previously that Cdk5-p35 phosphorylates Dab1 at Ser400 and Ser491 and the phosphorylation regulates its binding to CIN85, which is an SH3-containing multiadaptor protein involved in endocytic downregulation of receptor-tyrosine kinases. However, the interaction of CIN85 with Dab1 has not been addressed in neurons. We examined here a possibility that CIN85 has a role in Reelin signaling. We found nonphosphorylated Dab1-mediated colocalization of CIN85 with ApoER2. The colocalization of CIN85 with ApoER2 was increased in neurons stimulated with Reelin repeats 3-6, an active Reelin fragment. The stimulation recruited CIN85 to domains in plasma membrane where it colocalized with ApoER2 and Dab1 and then to EEA1-labeled early endosomes in the cytoplasm. In addition, Tyr phosphorylation of Dab1 strengthened the binding to CIN85. These results suggest that CIN85 participates in Reelin signaling through the binding to Dab1.

Objective We aimed to investigate the usefulness of glucose administration for maintaining perioperative glycemic control in patients with dietary restrictions during 4 h prior to impacted mandibular third molar extraction under intravenous sedation. Methods Fifty-four individuals scheduled to undergo extraction of impacted mandibular third molars under intravenous sedation, with preoperative blood glucose levels (GL) of 70-110 mg/dL, were evaluated and divided into 3 groups (n = 18 each): control group receiving glucose-free sodium lactate Ringer's solution, perioperative GL group receiving 100 mL of 5% glucose solution immediately after local anesthesia, and postoperative GL group receiving 100 mL of 5% glucose solution immediately after surgery completion. Blood glucose levels, systolic blood pressure, diastolic blood pressure, and heart rate were measured. Results Glucose levels of those in the control and perioperative GL groups decreased within the standard range 90 min after surgery, compared with the preoperative blood glucose level. However, in the postoperative GL group, glucose levels were similar to the preoperative levels. Systolic and diastolic blood pressure and heart rate were not affected by glucose administration, and sedation could be maintained without an invasive procedure. Conclusions Following a restriction on eating and drinking 4 h prior to surgery, the blood glucose level gradually decreased in the perioperative period but remained within the reference range until 90 min following surgery. The administration of 100 mL 5% glucose solution immediately after surgery was sufficient for the prevention of postoperative hypoglycemia. This approach may be useful for perioperative glycemic control during third molar extraction.

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