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κ‐Opioid Receptor Activation Inhibits Post‐Spike Depolarizing After‐Potentials in Rat Supraoptic Nucleus Neurones In Vitro
Author(s) -
Colin H. Brown,
Masoud GhamariLangroudi,
Gareth Leng,
Charles W. Bourque
Publication year - 1999
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1999.00419.x
Subject(s) - supraoptic nucleus , depolarization , medicine , endocrinology , nucleus , in vitro , opioid , receptor , chemistry , neuroscience , hypothalamus , biology , biochemistry
Endogenous agonists acting at κ ‐opioid receptors modulate the discharge activity of hypothalamic supraoptic nucleus vasopressin cells in vivo . Phasic activity in vasopressin cells is known to depend critically on intrinsic mechanisms involving post‐spike depolarizing after‐potentials and we hypothesized that inhibition of phasic bursting by an endogenous κ ‐agonist may result from reducing the magnitude of depolarizing after‐potentials. To investigate this possibility, intracellular sharp electrode recordings were obtained from supraoptic nucleus cells impaled in superfused explants of rat hypothalamus. Bath application of the selective κ ‐agonist, U50,488H (0.1–1 μM), decreased the spontaneous firing rate of magnocellular neurosecretory cells (by 94.0±4.5% at 1 μM, mean±SEM; P=0.02, n=4). U50,488H did not alter membrane potential (0.9±0.8 mV hyperpolarization at 1 μM, P=0.17, n=8) or input resistance (11.0±4.5% increase at 1 μM, P=0.09, n=5). U50,488H (0.1 and 1 μM, both n=5) reduced depolarizing after‐potential amplitude (by 29.9±9.3 and 78.0±10.6%, respectively, P<0.001) in eight cells in which the baseline membrane potential was kept constant by dc‐current injection and in which a depolarizing after‐potential was evoked every 25–40 s by a brief (40–80 ms) train of 3–6 action potentials (the number of spikes in the trains was kept constant for each cell). Thus, κ ‐opioid receptor activation reduces depolarizing after‐potential amplitude in supraoptic nucleus cells and this may underlie the reduction in burst duration of vasopressin cells caused by an endogenous κ ‐agonist in vivo .