Memantine has no effect on KATP channels in pancreatic β cells

BMC Res Notes. 2018 Aug 25;11(1):614. doi: 10.1186/s13104-018-3715-9.

Abstract

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 KATP channel also can become a target of memantine. The KATP channel is a key regulator of insulin secretion in pancreatic β cells. Therefore, if memantine could inhibit the KATP 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 KATP channel in pancreatic β cells. Therefore, we investigated whether memantine affect the blood glucose level, insulin secretion and KATP 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 KATP 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 KATP channel current in pancreatic β cells.

Keywords: Alzheimer’s disease; Diabetes; Insulin secretion; KATP channel; Memantine; Pancreatic β cells.

MeSH terms

  • Animals
  • Dopamine Agents / pharmacology*
  • Glucose
  • Insulin
  • Insulin-Secreting Cells / drug effects*
  • Islets of Langerhans
  • Japan
  • KATP Channels / drug effects*
  • KATP Channels / physiology
  • Male
  • Memantine / pharmacology*
  • Mice
  • Mice, Inbred C57BL

Substances

  • Dopamine Agents
  • Insulin
  • KATP Channels
  • Glucose
  • Memantine