دورية أكاديمية
Heteromeric canonical transient receptor potential 1 and 4 channels play a critical role in epileptiform burst firing and seizure-induced neurodegeneration.
| العنوان: | Heteromeric canonical transient receptor potential 1 and 4 channels play a critical role in epileptiform burst firing and seizure-induced neurodegeneration. |
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| المؤلفون: | Phelan KD; Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA., Mock MM, Kretz O, Shwe UT, Kozhemyakin M, Greenfield LJ, Dietrich A, Birnbaumer L, Freichel M, Flockerzi V, Zheng F |
| المصدر: | Molecular pharmacology [Mol Pharmacol] 2012 Mar; Vol. 81 (3), pp. 384-92. Date of Electronic Publication: 2011 Dec 05. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Society for Pharmacology and Experimental Therapeutics Country of Publication: United States NLM ID: 0035623 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1521-0111 (Electronic) Linking ISSN: 0026895X NLM ISO Abbreviation: Mol Pharmacol Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Bethesda, MD : American Society for Pharmacology and Experimental Therapeutics |
| مواضيع طبية MeSH: | Seizures/*physiopathology , TRPC Cation Channels/*physiology, Animals ; Immunohistochemistry ; Mice ; Mice, Knockout ; Microscopy, Electron ; Real-Time Polymerase Chain Reaction |
| مستخلص: | Canonical transient receptor potential channels (TRPCs) are receptor-operated cation channels that are activated in response to phospholipase C signaling. Although TRPC1 is ubiquitously expressed in the brain, TRPC4 expression is the most restrictive, with the highest expression level limited to the lateral septum. The subunit composition of neuronal TRPC channels remains uncertain because of conflicting data from recombinant expression systems. Here we report that the large depolarizing plateau potential that underlies the epileptiform burst firing induced by metabotropic glutamate receptor agonists in lateral septal neurons was completely abolished in TRPC1/4 double-knockout mice, and was abolished in 74% of lateral septal neurons in TRPC1 knockout mice. Furthermore, neuronal cell death in the lateral septum and the cornu ammonis 1 region of hippocampus after pilocarpine-induced severe seizures was significantly ameliorated in TRPC1/4 double-knockout mice. Our data suggest that both TRPC1 and TRPC4 are essential for an intrinsic membrane conductance mediating the plateau potential in lateral septal neurons, possibly as heteromeric channels. Moreover, excitotoxic neuronal cell death, an underlying process for many neurological diseases, is not mediated merely by ionotropic glutamate receptors but also by heteromeric TRPC channels activated by metabotropic glutamate receptors. TRPC channels could be an unsuspected but critical molecular target for clinical intervention for excitotoxicity. |
| References: | J Neurosci. 1993 Oct;13(10):4445-55. (PMID: 8410197) Neurosci Lett. 1991 Apr 29;125(2):147-50. (PMID: 1881593) Brain Res. 1997 Nov 21;776(1-2):75-87. (PMID: 9439798) Cell Calcium. 2003 May-Jun;33(5-6):419-32. (PMID: 12765687) Neuroreport. 1998 Feb 16;9(3):507-15. (PMID: 9512398) Exp Neurol. 2003 Jul;182(1):21-34. (PMID: 12821374) Neuropharmacology. 1995 Aug;34(8):905-17. (PMID: 8532172) Neuron. 2008 Aug 14;59(3):392-8. (PMID: 18701065) EMBO J. 1996 Nov 15;15(22):6166-71. (PMID: 8947038) Pflugers Arch. 2007 Dec;455(3):465-77. (PMID: 17647013) Pflugers Arch. 2005 Oct;451(1):11-8. (PMID: 16078044) Brain Res. 2005 Feb 21;1035(1):24-31. (PMID: 15713273) Neuron. 1988 Oct;1(8):623-34. (PMID: 2908446) N Engl J Med. 1994 Mar 3;330(9):613-22. (PMID: 7905600) Nature. 2003 Nov 20;426(6964):285-91. (PMID: 14614461) Nature. 2007 Jan 11;445(7124):168-76. (PMID: 17151600) Pflugers Arch. 2005 Oct;451(1):29-34. (PMID: 16133266) Nat Cell Biol. 2001 Feb;3(2):121-7. (PMID: 11175743) Curr Opin Pharmacol. 2003 Feb;3(1):101-9. (PMID: 12550750) Neuroscience. 1995 Sep;68(2):423-34. (PMID: 7477953) J Neurochem. 2007 Apr;101(2):411-21. (PMID: 17402970) Cell. 1996 May 31;85(5):661-71. (PMID: 8646775) Mol Cell Biol. 2005 Aug;25(16):6980-9. (PMID: 16055711) J Physiol. 2003 Feb 1;546(Pt 3):655-64. (PMID: 12562994) Nat Neurosci. 2007 May;10(5):537-8. (PMID: 17453053) J Neurosci. 1996 Oct 1;16(19):6079-88. (PMID: 8815890) Annu Rev Biochem. 2007;76:387-417. (PMID: 17579562) Epilepsia. 1996 Oct;37(10):1015-9. (PMID: 8822702) Cell Calcium. 2005 Sep-Oct;38(3-4):233-52. (PMID: 16098585) |
| معلومات مُعتمدة: | NS047546 United States NS NINDS NIH HHS; NS050381 United States NS NINDS NIH HHS; R03 NS050381 United States NS NINDS NIH HHS; P30 NS047546 United States NS NINDS NIH HHS; R01 NS058503 United States NS NINDS NIH HHS; Z01 ES101684 United States ImNIH Intramural NIH HHS |
| المشرفين على المادة: | 0 (TRPC Cation Channels) 0 (TRPC4 ion channel) 0 (transient receptor potential cation channel, subfamily C, member 1) |
| تواريخ الأحداث: | Date Created: 20111207 Date Completed: 20120411 Latest Revision: 20211021 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC3286301 |
| DOI: | 10.1124/mol.111.075341 |
| PMID: | 22144671 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1521-0111 |
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| DOI: | 10.1124/mol.111.075341 |