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J Physiol. 1985 Jul;364:265-80.

On the potassium conductance increased by opioids in rat locus coeruleus neurones.


Intracellular recordings were made from locus coeruleus neurones in slices cut from rat pons and superfused in vitro. Membrane currents were recorded with a single-electrode switch-clamp amplifier. Opioids, enkephalin analogues or morphine, caused a concentration-dependent potassium current, which had a maximum value of about 300 pA at -60 mV. The opioid-sensitive potassium conductance was independent of membrane potential between -60 and -130 mV, but became less as the membrane potential was changed from -60 to -30 mV. The opioid outward current was reduced by quinine (100 microM-1 mM) and barium (30 microM-2 mM), but not by 4-aminopyridine (100 microM-1 mM) or tetraethylammonium (10 mM). A potassium current with similar properties flowed for several seconds after a burst of action potentials; this appeared to result from calcium entering the neurone during the action potentials. The alpha 2-adrenoceptor agonists noradrenaline and clonidine caused a concentration-dependent potassium conductance increase which had the same maximum value as that caused by opioids in the same neurones. Experiments in which an opioid and an alpha 2-adrenoceptor agonist were superfused together indicated that the same potassium conductance is increased by both agonists.

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