Voltage-dependent Facilitation Research Articles

Double-pulse facilitation of smooth muscle alpha 1-subunit Ca2+ channels expressed in CHO cells.

Frequent strong depolarizations facilitate Ca2+ channels in various cell types by shifting their gating behavior towards mode 2, which is characterized by long openings and high probability of being open. In cardiac cells, the same type of gating behavior is potentiated by beta-adrenoceptors presumably acting via phosphorylation of a protein identical to or associated with the channel. Voltage-dependent phosphorylation has also been reported to underlie Ca2+ channel facilitation in chromaffin adrenal medulla and in skeletal muscle cells. We studied a possible voltage-dependent facilitation of the principal channel forming alpha 1-subunit of the dihydropyridine-sensitive smooth muscle Ca2+ channel. Single channel and whole-cell Ca2+ currents were recorded in Chinese hamster ovary cells stably expressing the class Cb Ca2+ channel alpha 1-subunit. Strong depolarizing voltage-clamp steps preceding the test pulse resulted in a 2- to 3-fold increase of the single Ca2+ channel activity and induction of mode 2-like gating behavior. Accordingly we observed a significant potentiation of the whole-cell current by approximately 50%. In contrast to the previous suggestions we found no experimental evidence for involvement of channel phosphorylation by protein kinases (cAMP-dependent protein kinase, protein kinase C and other protein kinases utilizing ATP gamma S) in the control and facilitated current. The data demonstrate that the L-type Ca2+ channel alpha 1-subunit solely expressed in Chinese hamster ovary cells is subject to a voltage-dependent facilitation but not to phosphorylation.(ABSTRACT TRUNCATED AT 250 WORDS)

Associative neural and behavioral change in Hermissenda: consequences of nervous system orientation for light and pairing specificity.

Associative neural and behavioral change in Hermissenda: consequences of nervous system orientation for light and pairing specificity.J Farley, and D L AlkonJ Farley, and D L AlkonPublished Online:01 Sep 1982https://doi.org/10.1152/jn.1982.48.3.785MoreSectionsPDF (4 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByProtein Tyrosine Kinase Involvement in Learning-Produced Changes in Hermissenda Type B PhotoreceptorsIksung Jin, Haojiang Huang, Benjamin Smith, and Joseph Farley1 December 2009 | Journal of Neurophysiology, Vol. 102, No. 65-HT and GABA Modulate Intrinsic Excitability of Type I Interneurons in HermissendaNan Ge Jin, Lian-Ming Tian, and Terry Crow1 November 2009 | Journal of Neurophysiology, Vol. 102, No. 5Random Noise Paradoxically Improves Light-Intensity Encoding in Hermissenda Photoreceptor NetworkChristopher R. Butson, and Gregory A. Clark1 January 2008 | Journal of Neurophysiology, Vol. 99, No. 1Pavlovian Conditioning in Hermissenda: A Circuit AnalysisThe Biological Bulletin, Vol. 210, No. 3Ionic Currents Underlying Difference in Light Response Between Type A and Type B PhotoreceptorsK. T. Blackwell1 May 2006 | Journal of Neurophysiology, Vol. 95, No. 5Involvement of the Ryanodine Receptor in Morphologic Modification of Hermissenda Type B Photoreceptors After In Vitro ConditioningRyo Kawai, Tetsuro Horikoshi, and Manabu Sakakibara1 February 2004 | Journal of Neurophysiology, Vol. 91, No. 2Protein Kinase A Mediates Voltage-Dependent Facilitation of Ca2+ Current in Presynaptic Hair Cells inHermissenda crassicornisCatherine T. Tamse, Yanfang Xu, Haitao Song, Liping Nie, and Ebenezer N. Yamoah1 March 2003 | Journal of Neurophysiology, Vol. 89, No. 3Calcium Waves and Closure of Potassium Channels in Response to GABA Stimulation in Hermissenda Type B PhotoreceptorsK. T. Blackwell1 February 2002 | Journal of Neurophysiology, Vol. 87, No. 2PP1 Inhibitors Depolarize HermissendaPhotoreceptors and Reduce K+ CurrentsHaojiang Huang, and Joseph Farley1 September 2001 | Journal of Neurophysiology, Vol. 86, No. 3Synaptic depression at type B to A photoreceptor connections in HermissendaNeuroReport, Vol. 9, No. 3Ionic Basis of Learning-Correlated Excitability Changes in Hermissenda Type A PhotoreceptorsJoseph Farley, and Yunru Han1 April 1997 | Journal of Neurophysiology, Vol. 77, No. 4Associative learning in a network model of Hermissenda crassicornisBiological Cybernetics, Vol. 69, No. 1Associative learning in a network model of Hermissenda crassicornisBiological Cybernetics, Vol. 68, No. 2Serotonin modulation ofHermissenda type B photoreceptor light responses and ionic currents: Implications for mechanisms underlying associative learningBrain Research Bulletin, Vol. 22, No. 2Serotonin involvement during in vitro conditioning ofhermissendaBrain Research Bulletin, Vol. 22, No. 2Motor correlates of phototaxis and associative learning in Hermissenda crassicornisBrain Research Bulletin, Vol. 19, No. 2Extinction of associative learning in Hermissenda: Behavior and neural correlatesBehavioural Brain Research, Vol. 14, No. 3Depolarization-induced effects of Ca2+-calmodulin-dependent protein kinase injection, in vivo, in single neurons of cat motor cortexBrain Research, Vol. 321, No. 1In vitro expression of in vivo learning by an isolated molluscan CNSBrain Research, Vol. 304, No. 2Correlated receptor and motorneuron changes during retention of associative learning of Hermissenda crassicornisComparative Biochemistry and Physiology Part A: Physiology, Vol. 73, No. 2 More from this issue > Volume 48Issue 3September 1982Pages 785-807 https://doi.org/10.1152/jn.1982.48.3.785PubMed6290619History Published online 1 September 1982 Published in print 1 September 1982 Metrics

Voltage-dependent facilitation of Ca2+ entry in voltage-clamped, aequorin-injected molluscan neurons.

Voltage-clamp experiments were performed on giant neurons of the nudibranch Anisodoris nobilis injected with the Ca-sensitive photoprotein, aequorin. Depolarization beyond -10 to +5 m V produced an aequorin signal, the amplitude of which depended on the extracellular Ca2+ concentration, the amplitude of the depolarization, and its duration. In paired pulse experiments, the amplitude of the aequorin signal produced in response to the second of two identical depolarizing pulses was larger than that produced during the first, resulting from an increased entry of Ca2+ during the second pulse. The increment in Ca conductance inferred from the augmented signal during the second pulse was independent of Ca2+ influx during the first pulse but, instead, was related to the amplitude and duration of the first pulse.