Memantine has no effect on K(ATP) channels in pancreatic β cells

OBJECTIVE: Memantine, a drug for Alzheimer’s disease, is considered to suppress excessive stimulation of N-methyl-d-aspartic acid receptors and to prevent neuronal death. However, a recent report indicated that the neuronal K(ATP) channel also can become a target of memantine. The K(ATP) channel is a key regulator of insulin secretion in pancreatic β cells. Therefore, if memantine could inhibit the K(ATP) channel in pancreatic β cells, it would be an effective drug for both Alzheimer’s disease and diabetes. However, there is no report on the effect of memantine on the K(ATP) channel in pancreatic β cells. Therefore, we investigated whether memantine affect the blood glucose level, insulin secretion and K(ATP) channel activity in pancreatic β cells. RESULTS: An intraperitoneal glucose tolerance test was performed with or without memantine (1 mg/kg) injection in intact mice. Insulin secretion from isolated islets was measured under low (2 mM) and high (20 mM) glucose concentrations with or without memantine (1 μM). The effect of memantine (1 μM) on K(ATP) channel currents in isolated pancreatic β cells was recorded using the whole-cell patch-clamp technique. Memantine had no effect on the blood glucose level, insulin secretion from isolated islets or K(ATP) channel current in pancreatic β cells.