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The Noradrenergic Inhibition of an Apamin-Sensitive, Small-Conductance Ca2+-Activated K+ Channel in Hypothalamic γ-Aminobutyric Acid Neurons: Pharmacology, Estrogen Sensitivity, and Relevance to the Control of the Reproductive Axis

Abstract The present study sought to determine whether small-conductance, Ca 2+ -activated K + currents underlie the afterhyperpolarization (AHP) in neurons of the preoptic area (POA), a brain region important in controlling reproduction. We used an ovariectomized, female guinea pig model to test two hypotheses: 1) the current associated with the AHP (I AHP ) regulates the firing rate of POA neurons and 2) amine neurotransmitters modulate it in a gonadal steroid-sensitive manner. Intracellular recordings followed by combined histofluorescence/in situ hybridization for glutamic acid decarboxylase, 65-kDa isomer, revealed that POA neurons, including γ-aminobutyric acid (GABA)ergic neurons, exhibited an AHP and spike frequency adaptation. The corresponding I AHP was sensitive to antagonism by CdCl 2 (200 μM), apamin (0.3–1 μM), and dequalinium (3 μM). The β-adrenergic receptor agonist isoproterenol inhibited the I AHP in a dose-dependent, timolol-sensitive fashion. In addition, the α 1 -adrenergic receptor agonist methoxamine dose dependently inhibited the I AHP in a prazosin-sensitive manner and increased neuronal firing rate. Twenty-four-hour pretreatment with estradiol benzoate (EB; 25 μg, s.c.) markedly potentiated the inhibitory effect of methoxamine on the I AHP , whereas that for isoproterenol was unaffected. Similarly, bath application of 17β-estradiol (100 nM; 15–20 min) mimicked the effect of EB on the methoxamine-induced inhibition of the I AHP . Thus, POA GABAergic neurons express an apamin-sensitive channel that mediates, at least in part, the I AHP , and tempers the excitability of these cells. Furthermore, these studies demonstrate that estrogen enhances the α 1 -adrenergic receptor-mediated inhibition of this current. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Pharmacology and Experimental Therapeutics Am. Soc for Pharma & Experimental Therapeutics

The Noradrenergic Inhibition of an Apamin-Sensitive, Small-Conductance Ca2+-Activated K+ Channel in Hypothalamic γ-Aminobutyric Acid Neurons: Pharmacology, Estrogen Sensitivity, and Relevance to the Control of the Reproductive Axis

Abstract

Abstract The present study sought to determine whether small-conductance, Ca 2+ -activated K + currents underlie the afterhyperpolarization (AHP) in neurons of the preoptic area (POA), a brain region important in controlling reproduction. We used an ovariectomized, female guinea pig model to test two hypotheses: 1) the current associated with the AHP (I AHP ) regulates the firing rate of POA neurons and 2) amine neurotransmitters modulate it in a gonadal steroid-sensitive manner. Intracellular recordings followed by combined histofluorescence/in situ hybridization for glutamic acid decarboxylase, 65-kDa isomer, revealed that POA neurons, including γ-aminobutyric acid (GABA)ergic neurons, exhibited an AHP and spike frequency adaptation. The corresponding I AHP was sensitive to antagonism by CdCl 2 (200 μM), apamin (0.3–1 μM), and dequalinium (3 μM). The β-adrenergic receptor agonist isoproterenol inhibited the I AHP in a dose-dependent, timolol-sensitive fashion. In addition, the α 1 -adrenergic receptor agonist methoxamine dose dependently inhibited the I AHP in a prazosin-sensitive manner and increased neuronal firing rate. Twenty-four-hour pretreatment with estradiol benzoate (EB; 25 μg, s.c.) markedly potentiated the inhibitory effect of methoxamine on the I AHP , whereas that for isoproterenol was unaffected. Similarly, bath application of 17β-estradiol (100 nM; 15–20 min) mimicked the effect of EB on the methoxamine-induced inhibition of the I AHP . Thus, POA GABAergic neurons express an apamin-sensitive channel that mediates, at least in part, the I AHP , and tempers the excitability of these cells. Furthermore, these studies demonstrate that estrogen enhances the α 1 -adrenergic receptor-mediated inhibition of this current.
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