caa a22 4500 445353732 CHVBK 20180317142853.0 cr unu---uuuuu 170323e20110801xx s 000 0 eng 10.1007/s00221-011-2759-z doi (NATIONALLICENCE)springer-10.1007/s00221-011-2759-z Apamin increases post-spike excitability of supraoptic nucleus neurons in anaesthetized morphine-naïve rats and morphine-dependent rats: consequences for morphine withdrawal excitation [Elektronische Daten] [Philip Bull, John Russell, Victoria Scott, Colin Brown] Supraoptic nucleus (SON) oxytocin neurons develop morphine dependence when chronically exposed to this opiate and undergo excitation when morphine is subsequently withdrawn. Morphine withdrawal excitation is evident as an increased action potential (spike) firing rate and is associated with an increased post-spike excitability that is consistent with the expression of an enhanced post-spike afterdepolarization (ADP) during withdrawal. Here, we administered apamin (which inhibits the medium afterhyperpolarization [mAHP] in vitro and unmasks an ADP) into the SON of urethane-anaesthetized rats to determine its effects on oxytocin neurons in vivo. As predicted, intra-SON apamin administration increased the propensity to fire a spike soon (<100ms) after each spike (post-spike excitability) more in oxytocin neurons recorded from morphine-treated rats than in morphine-naïve rats. However, intra-SON apamin did not alter the overall firing rate of oxytocin neurons recorded from morphine-treated rats or morphine-naïve rats, indicating that an increase in post-spike excitability alone is not sufficient to trigger withdrawal excitation of oxytocin neurons. Nevertheless, bilateral intra-SON apamin infusion increased oxytocin secretion (which depends on firing pattern as well as firing rate) by 90±46% in morphine-dependent rats (P<0.01 compared to aCSF). Hence, an increase in post-spike excitability does not appear to drive morphine withdrawal-induced increases in oxytocin neuron firing rate, but does contribute to withdrawal-induced hyper-secretion of oxytocin. Springer-Verlag, 2011 Apamin nationallicence Intrinsic excitability nationallicence Naloxone nationallicence Opioid nationallicence Oxytocin nationallicence Vasopressin nationallicence Bull Philip Centre for Integrative Physiology, University of Edinburgh, EH8 9XD, Edinburgh, UK aut Russell John Centre for Integrative Physiology, University of Edinburgh, EH8 9XD, Edinburgh, UK aut Scott Victoria Centre for Neuroendocrinology and Department of Physiology, Otago School of Medical Sciences, University of Otago, P.O. Box 913, 9054, Dunedin, New Zealand aut Brown Colin Centre for Neuroendocrinology and Department of Physiology, Otago School of Medical Sciences, University of Otago, P.O. Box 913, 9054, Dunedin, New Zealand aut Experimental Brain Research Springer-Verlag 212/4(2011-08-01), 517-528 0014-4819 212:4<517 2011 212 221 https://doi.org/10.1007/s00221-011-2759-z text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00221-011-2759-z text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Bull Philip Centre for Integrative Physiology, University of Edinburgh, EH8 9XD, Edinburgh, UK aut NATIONALLICENCE 700 1- Russell John Centre for Integrative Physiology, University of Edinburgh, EH8 9XD, Edinburgh, UK aut NATIONALLICENCE 700 1- Scott Victoria Centre for Neuroendocrinology and Department of Physiology, Otago School of Medical Sciences, University of Otago, P.O. Box 913, 9054, Dunedin, New Zealand aut NATIONALLICENCE 700 1- Brown Colin Centre for Neuroendocrinology and Department of Physiology, Otago School of Medical Sciences, University of Otago, P.O. Box 913, 9054, Dunedin, New Zealand aut NATIONALLICENCE 773 0- Experimental Brain Research Springer-Verlag 212/4(2011-08-01), 517-528 0014-4819 212:4<517 2011 212 221 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer