title: ATP-sensitive K+ channels are functional in expiratory neurones of normoxic cats.
abstract: 1. We analysed spontaneously active expiratory neurones (n = 48) of anaesthetized cats for the presence of ATP-sensitive K+ (KATP) channels. 2. Intracellular injection of ATP reversibly depolarized neurones during all phases of the respiratory cycle. During expiration, membrane potential depolarized by an average of 1.5 +/- 0.1 mV leading to a 25% increase of discharge frequency. During inspiration, ATP induced a 1.8 +/- 0.2 mV depolarization, which was accompanied by a maximum of 20% increase of input resistance (Rn). 3. Extracellular application of diazoxide, an agonist of KATP channels, resulted in reversible membrane hyperpolarization in 68% of neurones (n = 19). This hyperpolarization (2.5 mV during expiration and 3.1 mV during inspiration) was accompanied by a 22% decrease in Rn. 4. Extracellular application of tolbutamide and glibenclamide, two antagonists of KATP channels, evoked reversible depolarizations in 76% of neurones (n = 21). The depolarization was relatively constant throughout the respiratory cycle (1.4 mV during expiration and 2.3 mV during inspiration). Rn increased by 22%. 5. The same sulphonylureas also changed the steepness of membrane depolarization when neurones escaped spontaneous synaptic inhibition during postinspiration. Extracellularly applied tolbutamide and glibenclamide increased the steepness of depolarization by 21%, while diazoxide reduced it by 20%. 6. Antagonism of drugs was verified by simultaneous extra- and intracellular application of diazoxide and glibenclamide, respectively. 7. During voltage clamp at holding potential at -60 to -67 mV, intracellular or extracellular application of tolbutamide and glibenclamide blocked a persistent outward current. 8. We conclude that KATP channels are functional in expiratory neurones of adult cats and contribute to the control of excitability even during normoxia.
authors.affiliation: II. Physiologisches Institut, Universität Göttingen, Germany.
authors.forename: O
authors.initials: O
authors.lastname: Pierrefiche
authors.forename: A M
authors.initials: AM
authors.lastname: Bischoff
authors.forename: D W
authors.initials: DW
authors.lastname: Richter
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D001812:Blood-Brain Barrier; D001933:Brain Stem / Q000502:physiology*; D002415:Cats; D005260:Female; D005905:Glyburide / Q000494:pharmacology; D000860:Hypoxia; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D010791:Phrenic Nerve / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D012016:Reference Values; D012119:Respiration / Q000502:physiology*; D014044:Tolbutamide / Q000494:pharmacology
chemical_list: D015221:Potassium Channels; D000255:Adenosine Triphosphate; D014044:Tolbutamide; D005905:Glyburide; D001640:Bicuculline