title: Sustained outward rectification of oxytocinergic neurones in the rat supraoptic nucleus: ionic dependence and pharmacology.
abstract: 1. Intracellular recordings were obtained in vitro from oxytocin and vasopressin neurones from dioestrous and lactating female rats. Oxytocin neurones were characterized under current clamp by the expression of a depolarization-activated, sustained outward rectification (SOR) and a rebound depolarization (RD). 2. An increment in extracellular K+ shifted the expression of the SOR and RD towards a more depolarized membrane potential, indicating that the mechanisms underlying these events are dependent on extracellular potassium. 3. The SOR and RD were blocked by external tetraethylammonium (10 mM) and Ba2+ (0.1-0.5 mM). Cs+ (2 mM) blocked the hyperpolarization-activated inward rectification without affecting the expression of the SOR and RD. 4. The SOR was not affected by 4-aminopyridine (6 mM). However, the rebound amplitude was significantly enhanced, indicating that the activation of a transient outward current interacts with the expression of the rebound. 5. Iberiotoxin (100 nM) and apamin (50 nM), toxins known to block some calcium-dependent potassium conductances, did not affect the expression of the SOR and RD. 6. The SOR and RD were significantly reduced by Cd2+ (0.5 mM) but not by Ni2+ (0.25 mM). 7. Muscarine (10 microM) did not affect the SOR or the RD. 8. These results indicate that the SOR and RD depend upon a depolarization-activated, sustained outward potassium current, which might be calcium dependent. A current with these characteristics has never been described before in the magnocellular system. Voltage-clamp experiments are needed to completely characterize this potassium conductance selectively expressed by oxytocin neurones.
authors.affiliation: Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis 38163, USA. javier@nb.utmem.edu
authors.forename: J E
authors.initials: JE
authors.lastname: Stern
authors.forename: W E
authors.initials: WE
authors.lastname: Armstrong
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001464:Barium / Q000494:pharmacology; D002118:Calcium / Q000502:physiology; D004594:Electrophysiology; D005260:Female; D007774:Lactation / Q000502:physiology; D009116:Muscarine / Q000494:pharmacology; D018721:Muscarinic Agonists / Q000494:pharmacology; D009474:Neurons / Q000737:chemistry / Q000187:drug effects* / Q000502:physiology*; D010121:Oxytocin / Q000502:physiology*; D010455:Peptides / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000819:agonists / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012604:Scorpion Venoms / Q000494:pharmacology; D013495:Supraoptic Nucleus / Q000166:cytology* / Q000502:physiology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D018721:Muscarinic Agonists; D010455:Peptides; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D012604:Scorpion Venoms; D013757:Tetraethylammonium Compounds; D001464:Barium; D013779:Tetrodotoxin; D010121:Oxytocin; D019789:Tetraethylammonium; C064719:iberiotoxin; D009116:Muscarine; D015761:4-Aminopyridine; D011188:Potassium; D002118:Calcium