Agonists at μ‐opioid, M2 ‐muscarinic and GABAB ‐receptors increase the same potassium conductance in rat lateral parabrachial neurones

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Abstract
1 Intracellular recordings of membrane potential and current were made from neurones in the lateral parabrachial nucleus in slices of rat brain in vitro. 2 The membrane was hyperpolarized by the opioid peptides Tyr-d-Ala-Gly-MePhe-Gly-ol (DAGOL, 0.01–1μm) and [Met5]enkephalin (3–30μm), though not by Tyr-d-Pen-Gly-Phe-d-Pen and U50488. In two experiments, naloxone competitively antagonized the effects of DAGOL and [Met]enkephalin with equilibrium dissociation constants of 0.8 and 3.2 nM, respectively. 3 Baclofen (0.3–30 μm) also hyperpolarized the neurones; this action was unaffected by naloxone. 4 DAGOL, [Met5]enkephalin and baclofen caused outward currents at the resting potential. These currents reversed polarity at a membrane potential which changed with the logarithm of the extracellular potassium concentration. 5 Muscarine has been shown previously to increase the potassium conductance by an action at M2-receptors: the potassium currents induced by maximal concentrations of muscarine, baclofen and [Met5]enkephalin were non-additive, indicating that these agonists opened the same population of potassium channels. 6 Noradrenaline, UK14304, carboxamidotryptamine, dopamine, adenosine and somatostatin had little or no effect on membrane potential. 7 It is concluded that rat lateral parabrachial neurones express μ-opioid, γ-aminobutyric acidB (GABAB), and M2-muscarinic receptors: activation of any of these receptors increases the potassium conductance of the membrane and inhibits the neurones through hyperpolarization.