title: Predominant functional expression of Kv1.3 by activated microglia of the hippocampus after Status epilepticus.
abstract: BACKGROUND
  Growing evidence indicates that the functional state of microglial cells differs according to the pathological conditions that trigger their activation. In particular, activated microglial cells can express sets of Kv subunits which sustain delayed rectifying potassium currents (Kdr) and modulate differently microglia proliferation and ability to release mediators. We recently reported that hippocampal microglia is in a particular activation state after a status epilepticus (SE) and the present study aimed at identifying which of the Kv channels are functionally expressed by microglia in this model.
  
  
  RESULTS
  SE was induced by systemic injection of kainate in CX3CR1(eGFP/+) mice and whole cell recordings of fluorescent microglia were performed in acute hippocampal slices prepared 48 h after SE. Microglia expressed Kdr currents which were characterized by a potential of half-maximal activation near -25 mV, prominent steady-state and cumulative inactivations. Kdr currents were almost abolished by the broad spectrum antagonist 4-Aminopyridine (1 mM). In contrast, tetraethylammonium (TEA) at a concentration of 1 mM, known to block Kv3.1, Kv1.1 and 1.2 subunits, only weakly reduced Kdr currents. However, at a concentration of 5 mM which should also affect Kv1.3 and 1.6, TEA inhibited about 30% of the Kdr conductance. Alpha-dendrotoxin, which selectively inhibits Kv1.1, 1.2 and 1.6, reduced only weakly Kdr currents, indicating that channels formed by homomeric assemblies of these subunits are not important contributors of Kdr currents. Finally, agitoxin-2 and margatoxin strongly inhibited the current.
  
  
  CONCLUSIONS
  These results indicate that Kv1.3 containing channels predominantly determined Kdr currents in activated microglia after SE.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Unité 603, Paris, France.
authors.forename: Alexis
authors.initials: A
authors.lastname: Menteyne
authors.forename: Françoise
authors.initials: F
authors.lastname: Levavasseur
authors.forename: Etienne
authors.initials: E
authors.lastname: Audinat
authors.forename: Elena
authors.initials: E
authors.lastname: Avignone
mesh_terms: D000818:Animals; D006624:Hippocampus / Q000503:physiopathology*; D051664:Kv1.3 Potassium Channel / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000502:physiology*; D013226:Status Epilepticus / Q000503:physiopathology*
chemical_list: D051664:Kv1.3 Potassium Channel
references.citation: Mol Cell Neurosci. 2006 Dec;33(4):401-11
references.pmid: 17055293
references.citation: J Neurosci. 2005 Aug 3;25(31):7139-49
references.pmid: 16079396
references.citation: Biochemistry. 1994 Jun 7;33(22):6834-9
references.pmid: 8204618
references.citation: J Neurosci. 1999 Dec 15;19(24):10680-93
references.pmid: 10594052
references.citation: Nat Neurosci. 2007 Nov;10(11):1387-94
references.pmid: 17965659
references.citation: J Biol Chem. 2006 Dec 8;281(49):37675-85
references.pmid: 17038323
references.citation: Neuroscience. 1999;89(4):1379-90
references.pmid: 10362322
references.citation: Brain Res Brain Res Rev. 2005 Apr;48(2):133-43
references.pmid: 15850652
references.citation: Eur J Neurosci. 2000 Jun;12(6):2049-58
references.pmid: 10886344
references.citation: Biochem Biophys Res Commun. 2007 Jan 26;352(4):913-8
references.pmid: 17157812
references.citation: J Neurosci. 2001 Feb 15;21(4):1160-8
references.pmid: 11160386
references.citation: Brain Res. 2007 Dec;1186:21-8
references.pmid: 18005942
references.citation: J Neurosci Res. 1990 Jul;26(3):278-87
references.pmid: 1697905
references.citation: Glia. 2007 Feb;55(3):233-8
references.pmid: 17106878
references.citation: Eur Biophys J. 1992;21(3):185-91
references.pmid: 1425474
references.citation: Am J Physiol. 1998 Jun;274(6):C1485-95
references.pmid: 9696690
references.citation: Science. 2005 May 27;308(5726):1314-8
references.pmid: 15831717
references.citation: J Neurosci. 2007 Jan 3;27(1):234-44
references.pmid: 17202491
references.citation: J Neurochem. 2008 Sep;106(5):2093-105
references.pmid: 18627436
references.citation: J Pharmacol Exp Ther. 2006 Jun;317(3):1054-63
references.pmid: 16522807
references.citation: EMBO J. 1989 Nov;8(11):3235-44
references.pmid: 2555158
references.citation: Neuroscience. 2009 Feb 18;158(4):1500-8
references.pmid: 19118603
references.citation: J Neurosci Res. 1995 Nov 1;42(4):439-51
references.pmid: 8568930
references.citation: J Neurosci. 2006 Nov 8;26(45):11652-64
references.pmid: 17093087
references.citation: Trends Pharmacol Sci. 1993 Dec;14(12):434
references.pmid: 8122319
references.citation: Neuron. 2004 Feb 19;41(4):535-47
references.pmid: 14980203
references.citation: Neuroscience. 2005;133(4):1007-19
references.pmid: 15964489
references.citation: Brain Res. 2004 Oct 22;1024(1-2):59-76
references.pmid: 15451367
references.citation: Eur J Neurosci. 2003 Nov;18(10):2893-8
references.pmid: 14656339
references.citation: J Biol Chem. 1997 Jan 24;272(4):2389-95
references.pmid: 8999950
references.citation: Neurosci Lett. 1992 Dec 7;147(2):171-4
references.pmid: 1491802
references.citation: J Neurosci. 2008 Sep 10;28(37):9133-44
references.pmid: 18784294
references.citation: Nat Neurosci. 2005 Jun;8(6):752-8
references.pmid: 15895084
references.citation: Biochim Biophys Acta. 1993 Nov 21;1153(1):111-21
references.pmid: 7694656
references.citation: Mol Cell Biol. 2000 Jun;20(11):4106-14
references.pmid: 10805752
references.citation: FEBS Lett. 1991 Jan 14;278(1):55-60
references.pmid: 1993474
references.citation: EMBO J. 1990 Jun;9(6):1749-56
references.pmid: 2347305
references.citation: Mol Pharmacol. 1994 Jun;45(6):1227-34
references.pmid: 7517498
references.citation: J Biol Chem. 1993 Sep 5;268(25):18866-74
references.pmid: 8360176
references.citation: Eur Biophys J. 1994;23(5):379-84
references.pmid: 7835322
references.citation: Gen Pharmacol. 1998 Jan;30(1):13-24
references.pmid: 9457476