Inward rectification of resting and opiate-activated potassium currents in rat locus coeruleus neurons

• Published in: The Journal of neuroscience 1988-11, Vol.8 (11), p.4299-4306
• Main Authors: Williams, JT, North, RA, Tokimasa, T
• Format: Article
• Language: English
• Subjects: Adrenergic alpha-Agonists - pharmacology; Animals; Biological and medical sciences; Cell Membrane - physiology; Central nervous system; Electric Conductivity; Electrophysiology; Fundamental and applied biological sciences. Psychology; Locus Coeruleus - cytology; Locus Coeruleus - physiology; Narcotics - pharmacology; Neurons - physiology; Neurons - ultrastructure; Potassium - physiology; Rats; Rest; Vertebrates: nervous system and sense organs
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/jneurosci.08-11-04299.1988

Intracellular recordings were made from rat locus coeruleus neurons in vitro, and membrane currents were measured at potentials from -50 to -130 mV. In the absence of any applied agonists, the slope conductance of the cells increased 3-fold when the cell was hyperpolarized from -60 to -120 mV. This conductance increase was complete within 5 msec of the onset of a hyperpolarizing command and was subsequently independent of time for several seconds. The conductance increase was blocked by cesium chloride (1-2 mM), rubidium chloride (1-2 mM), or barium chloride (1-100 microM). The membrane potential range over which the conductance increased was centered at the potassium equilibrium potential (EK; extracellular potassium concentration, 2.5-10.5 mM): the current/voltage (I/V) relation of the cell could be well described by supposing that there were 2 potassium conductances, one voltage independent (G1) and the other (inward rectifier, Gir) activated according to the expression Gir = Gir,max/(1 + exp[(V - EK)/k]), where k ranged from 15 mV in 2.5 mM potassium to 6 mV in 10.5 mM potassium. The additional membrane potassium conductance that developed when agonists at mu-opioid and alpha 2-adrenoceptors were applied also became larger with membrane hyperpolarization, and this voltage dependence was also reduced or blocked by rubidium, cesium, and barium; in the presence of these agonists the current also reached its final value within 5 msec. However, the conductance increased by the agonists (Gag) was not well expressed by simply increasing the values of G1 and Gir,max. It was best described by a potassium conductance that increased according to Gag,max/(1 + exp[(V - Vm)/k]), where Vm (the potential at which the conductance was half-maximum) was close to the resting potential of the cell.