دورية أكاديمية
Chronic lithium treatment up-regulates cell surface Na(V)1.7 sodium channels via inhibition of glycogen synthase kinase-3 in adrenal chromaffin cells: enhancement of Na(+) influx, Ca(2+) influx and catecholamine secretion after lithium withdrawal.
| العنوان: | Chronic lithium treatment up-regulates cell surface Na(V)1.7 sodium channels via inhibition of glycogen synthase kinase-3 in adrenal chromaffin cells: enhancement of Na(+) influx, Ca(2+) influx and catecholamine secretion after lithium withdrawal. |
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| المؤلفون: | Yanagita T; Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889-1692, Japan. yanagita@med.miyazaki-u.ac.jp, Maruta T, Nemoto T, Uezono Y, Matsuo K, Satoh S, Yoshikawa N, Kanai T, Kobayashi H, Wada A |
| المصدر: | Neuropharmacology [Neuropharmacology] 2009 Sep; Vol. 57 (3), pp. 311-21. Date of Electronic Publication: 2009 May 30. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Pergamon Press Country of Publication: England NLM ID: 0236217 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7064 (Electronic) Linking ISSN: 00283908 NLM ISO Abbreviation: Neuropharmacology Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Oxford : Pergamon Press Original Publication: Oxford, New York, Pergamon. |
| مواضيع طبية MeSH: | Antimanic Agents/*pharmacology , Chromaffin Cells/*drug effects , Glycogen Synthase Kinase 3/*antagonists & inhibitors , Lithium Chloride/*pharmacology , Sodium Channels/*metabolism, Animals ; Calcium/metabolism ; Calcium Channels/metabolism ; Catecholamines/metabolism ; Cattle ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Cells, Cultured ; Chromaffin Cells/metabolism ; Glycogen Synthase Kinase 3/metabolism ; Membrane Potentials/drug effects ; Membrane Potentials/physiology ; Protein Stability/drug effects ; RNA, Messenger/metabolism ; Sodium/metabolism ; Sodium Channels/genetics ; Transcription, Genetic/drug effects |
| مستخلص: | In cultured bovine adrenal chromaffin cells expressing Na(V)1.7 isoform of voltage-dependent Na(+) channels, we have previously reported that lithium chloride (LiCl) inhibits function of Na(+) channels independent of glycogen synthase kinase-3 (GSK-3) (Yanagita et al., 2007). Here, we further examined the effects of chronic lithium treatment on Na(+) channels. LiCl treatment (1-30 mM, > or = 12 h) increased cell surface [(3)H]saxitoxin ([(3)H]STX) binding by approximately 32% without altering the affinity of [(3)H]STX binding. This increase was prevented by cycloheximide and actinomycin D. SB216763 and SB415286 (GSK-3 inhibitors) also increased cell surface [(3)H]STX binding by approximately 31%. Simultaneous treatment with LiCl and SB216763 or SB415286 did not produce an increased effect on [(3)H]STX binding compared with either treatment alone. LiCl increased Na(+) channel alpha-subunit mRNA level by 32% at 24 h. LiCl accelerated alpha-subunit gene transcription by 35% without altering alpha-subunit mRNA stability. In LiCl-treated cells, LiCl inhibited veratridine-induced (22)Na(+) influx as in untreated cells. However, washout of LiCl after chronic treatment enhanced veratridine-induced (22)Na(+) influx, (45)Ca(2+) influx and catecholamine secretion by approximately 30%. Washout of LiCl after 24 h treatment shifted concentration-response curve of veratridine upon (22)Na(+) influx upward, without altering its EC(50) value. Ptychodiscus brevis toxin-3 allosterically enhanced veratridine-induced (22)Na(+) influx by two-fold in untreated and LiCl-treated cells. Whole-cell patch-clamp analysis indicated that I-V curve and steady-state inactivation/activation curves were comparable between untreated and LiCl-treated cells. Thus, GSK-3 inhibition by LiCl up-regulated cell surface Na(V)1.7 via acceleration of alpha-subunit gene transcription, enhancing veratridine-induced Na(+) influx, Ca(2+) influx and catecholamine secretion. |
| المشرفين على المادة: | 0 (Antimanic Agents) 0 (Calcium Channels) 0 (Catecholamines) 0 (RNA, Messenger) 0 (Sodium Channels) 9NEZ333N27 (Sodium) EC 2.7.11.26 (Glycogen Synthase Kinase 3) G4962QA067 (Lithium Chloride) SY7Q814VUP (Calcium) |
| تواريخ الأحداث: | Date Created: 20090603 Date Completed: 20091127 Latest Revision: 20181201 |
| رمز التحديث: | 20231215 |
| DOI: | 10.1016/j.neuropharm.2009.05.006 |
| PMID: | 19486905 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1873-7064 |
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| DOI: | 10.1016/j.neuropharm.2009.05.006 |