Pflügers Archiv

, Volume 415, Issue 4, pp 479–483

Glucose-induced excitation of hypothalamic neurones is mediated by ATP-sensitive K+ channels

Authors

  • Michael L. J. Ashford
    • Department of PharmacologyUniversity of Cambridge
  • Philip R. Boden
    • Parke-Davis Research UnitAddenbrooke's Hospital Site
  • J. Mark Treherne
    • Department of PharmacologyUniversity of Cambridge
Excitable Tissues and Central Nervous Physiology

DOI: 10.1007/BF00373626

Cite this article as:
Ashford, M.L.J., Boden, P.R. & Treherne, J.M. Pflügers Arch (1990) 415: 479. doi:10.1007/BF00373626

Abstract

Intracellular recordings were made from neurones located in the ventromedial hypothalamic nucleus (VMHN) of slices from rat hypothalamus. These neurones were hyperpolarized on removal of extracellular glucose, resulting in an inhibition of firing, actions which were reversed on the re-introduction of glucose. No reversal of the inhibition of firing was observed when 10 mM mannoheptulose an inhibitor of glucose metabolism, was present in addition to glucose. Increasing the mannoheptulose concentration to 20 mM resulted in further hyperpolarization. Cell-attached recordings from isolated neurones revealed that an increase in extracellular glucose inhibited a K+ channel and increased action current activity. ATP induced closure of this K+ channel when applied to inside-out membrane patches. Closure was also induced by Mg-free ATP or the nonhydrolysable ATP-analogue, adenylylimidodiphosphate indicating no requirement for ATP metabolism. We suggest that the closure of ATP-sensitive potassium channels underlies increased hypothalamic firing following an increase in extracellular glucose.

Key words

GlucoseHypothalamic neuronesATP-K+ channels

Copyright information

© Springer-Verlag 1990