「カリウムチャネル」の版間の差分

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{| class="wikitable"
{| class="wikitable"
|+Potassium channel classes, function, and pharmacology.<ref name=Rang60>{{cite book | author=Rang, HP | title = Pharmacology | publisher = Churchill Livingstone | location = Edinburgh | year = 2003 | isbn = 0-443-07145-4 | oclc = | doi = | page = 60 }}</ref>
|+カリウムチャネルのクラス、機能、薬理学<ref name="pmid16382103"/><ref name="pmid16382104"/><ref name="16382105"/><ref name="pmid16382106"/>
 
|-
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|'''Class'''
|'''Class'''
! Subclasses
! IUPHAR Name
!Function
!Human Gene Name
!Blockers
!Other Name
!Activators
!補助サブユニット
!分子機能
!生理的意義
!阻害薬(IC<sub>50</sub>)
!活性化薬(EC<sub>50</sub>)
|-
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| [[Calcium-activated potassium channel|Calcium-activated]] <br /> 6[[transmembrane helix|T]] & 1[[pore-forming loop|P]]
|rowspan=5 | [[Calcium-activated potassium channel|Calcium-activated]] <br /> 6[[transmembrane helix|T]] & 1[[pore-forming loop|P]]
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* [[BK channel]]
K<sub>Ca</sub>1.1
* [[SK channel]]
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* inhibition following stimuli increasing intracellular calcium
KCNMA1
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* [[charybdotoxin]], [[iberiotoxin]]
Slo, Slo1, BK
* [[apamin]]
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脱分極によって活性化、細胞内Ca<sup>2+</sup>濃度上昇による活性化
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書く
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charybdotoxin(2.9 nM), iberiotoxin(1.7 nM), TEA(0.14 mM)
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K<sub>Ca</sub>2.1-2.3
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KCNN1-3
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SK<sub>Ca</sub>1-3
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calmodulin
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細胞内Ca<sup>2+</sup>濃度上昇による活性化
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書く
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UCL1684(1 nM for K<sub>Ca</sub>2.1; 250 pM for K<sub>Ca</sub>2.2), apamin(8 nM for K<sub>Ca</sub>2.1; 60-200 pM for K<sub>Ca</sub>2.2; 10 nM for K<sub>Ca</sub>2.3), tamapin(42 nM for K<sub>Ca</sub>2.1; 24 pM for K<sub>Ca</sub>2.2)
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EBIO(630 µM), NS309(30 nM)
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K<sub>Ca</sub>3.1
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KCNT1
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IK<sub>Ca</sub>1
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calmodulin
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細胞内Ca<sup>2+</sup>濃度上昇による活性化
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書く
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charybdotoxin(5 nM), iberiotoxin(1.7 nM), TEA(24 mM), ketoconazol(30 µM), econazole(12 µM)
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EBIO, NS309(10 nM)
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K<sub>Ca</sub>4.1, 4.2
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KCNT2
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Slack, Slo2.2; Slick, Slo2.1
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細胞内Na<sup>+</sup>濃度上昇による活性化
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書く
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TEA, quinidine
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K<sub>Ca</sub>5.1
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KCNU1
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Slo3
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細胞内Ca<sup>2+</sup>濃度上昇による活性化
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書く
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TEA
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|rowspan=8 | [[Inward-rectifier potassium ion channel|Inwardly rectifying]] <br /> 2[[transmembrane helix|T]] & 1[[pore-forming loop|P]]
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K<sub>ir</sub>2.1-2.4
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KCNJ2,12,4,14
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IRK
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常時活性
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静止膜電位形成への関与、心臓におけるIK1電流(Kir2.1/Kir2.2)
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Ba<sup>2+</sup>, Cs<sup>+</sup>, 細胞内Mg<sup>2+</sup>, 細胞内polyamines
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K<sub>ir</sub>3.1-3.4
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KCNJ3,6,9,5
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GIRK
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Gbgによる活性化、代謝型受容体依存的な膜興奮性抑制
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神経細胞における遅延性の抑制性シナプス後電位の形成(Kir3.1/Kir3.2)、心臓における徐脈の分子機構(Kir3.1/Kir3.4)
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Ba<sup>2+</sup>, Cs<sup>+</sup>, terpiapin
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Gbg、細胞内Na<sup>+</sup>、PIP<sub>2</sub>、GPCR活性化薬(三量体G蛋白質シグナルを介して)
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K<sub>ir</sub>4.1-4.2
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KCNJ10,15
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KAB-2, BIR(K)10
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常時活性
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脳内におけるグリア細胞によるカリウムバッファリング機構、内耳や腎臓におけるカリウム恒常性
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Ba<sup>2+</sup>, Cs<sup>+</sup>, 細胞内Mg<sup>2+</sup>, 細胞内polyamines
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K<sub>ir</sub>5.1
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KCNJ16
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BIR9
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常時活性
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pHセンシング機構
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Ba<sup>2+</sup>, Cs<sup>+</sup>, 細胞内H<sup>+</sup>
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K<sub>ir</sub>6.1
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KCNJ8
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uKATP-1
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SUR2B(血管平滑筋)
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細胞内ヌクレオチドによる活性化
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血管平滑筋の緊張度調節
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Ba<sup>2+</sup>, Cs<sup>+</sup>,  スルホニル尿素剤(SURに結合することによる)
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カリウムチャネル開口薬(diazoxide, pinacidil, nicorandilなど、SURに結合することによる)
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K<sub>ir</sub>6.2
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KCNJ11
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BIR
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SUR1(膵臓b細胞), SUR2A(心筋細胞), SUR2B(血管平滑筋)
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細胞内ATPによる抑制
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膵臓b細胞からのインスリン分泌、脳内における酸素・グルコースセンサー機能、心臓、脳における虚血に対する細胞保護作用
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Ba<sup>2+</sup>, Cs<sup>+</sup>,  スルホニル尿素剤(SURに結合することによる)
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カリウムチャネル開口薬(diazoxide, pinacidil, nicorandilなど、SURに結合することによる)
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K<sub>ir</sub>7.1
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KCNJ13
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常時活性
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Ba<sup>2+</sup>, Cs<sup>+</sup>(他のKirファミリーに比べて感受性は低い)
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|rowspan=18 | [[Tandem pore domain potassium channel|Tandem pore domain]] <br /> 4[[transmembrane helix|T]] & 2[[pore-forming loop|P]]
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K<sub>2P</sub>1.1
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KCNK1
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TWIK-1
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常時活性、GHK整流性
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静止膜電位形成への関与
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K<sub>2P</sub>2.1
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KCNK2
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TREK-1
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常時活性、GHK整流性
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静止膜電位形成への関与
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アラキドン酸(10 mM)、揮発性吸入麻酔薬(halothane, isofluorane)など
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K<sub>2P</sub>3.1
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KCNK3
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TASK-1
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常時活性、GHK整流性
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静止膜電位形成への関与
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細胞外酸性化(pH7.3)
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揮発性吸入麻酔薬(halothane, isofluorane)など
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K<sub>2P</sub>4.1
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KCNK4
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TRAAK
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常時活性、GHK整流性
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静止膜電位形成への関与
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K<sub>2P</sub>5.1
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KCNK5
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TASK-2
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常時活性、GHK整流性
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静止膜電位形成への関与
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細胞外酸性化(pH6.5)
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K<sub>2P</sub>6.1
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KCNK6
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TWIK-2
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常時活性、GHK整流性
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静止膜電位形成への関与
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K<sub>2P</sub>7.1
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KCNK7
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(KCNK8)
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常時活性
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静止膜電位形成への関与
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K<sub>2P</sub>8.1
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K<sub>2P</sub>9.1
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KCNK9
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TASK-3
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常時活性、GHK整流性
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静止膜電位形成への関与
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細胞外酸性化(pH6.5)、ruthenium red (700 nM)
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K<sub>2P</sub>10.1
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KCNK10
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TREK-2
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常時活性、GHK整流性
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静止膜電位形成への関与
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K<sub>2P</sub>11.1
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K<sub>2P</sub>12.1
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KCNK12
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THIK-2
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K<sub>2P</sub>13.1
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KCNK13
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THIK-1
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常時活性、GHK整流性
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静止膜電位形成への関与
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アラキドン酸(0.98 mM)
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K<sub>2P</sub>14.1
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K<sub>2P</sub>15.1
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KCNK15
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TASK-5
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機能的なチャネル発現の報告なし
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K<sub>2P</sub>16.1
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KCNK16
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TALK-1
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K<sub>2P</sub>17.1
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KCNK17
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TASK-4
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常時活性、GHK整流性
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静止膜電位形成への関与
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K<sub>2P</sub>18.1
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KCNK18
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TRESK-1/TRESK-2
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常時活性、GHK整流性
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静止膜電位形成への関与
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|rowspan=19 | [[Voltage-gated potassium channel|Voltage-gated]] <br /> 6[[transmembrane helix|T]] & 1[[pore-forming loop|P]]
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Kv1.1-1.3
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KCNA1-3
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|rowspan=6 |Shaker-related
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Kvb
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脱分極によって活性化、遅延性整流性
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神経細胞、骨格筋細胞における興奮性の制御(遅延性整流性カリウム電流 Kv1.2)
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4-Aminopyridine(< mM), TEA(0.3 mM)(Kv1.1)
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Kv1.4
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KCNA4
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Kvb
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脱分極によって活性化、早い不活性化(A-type)
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A-type電流、神経細胞における脱分極後過分極AHP
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4-Aminopyridine(13 µM), TEA(>100 mM)
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Kv1.5
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KCNA5
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Kvb
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脱分極によって活性化、遅延性整流性
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心臓におけるIKur
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quinidine(0.6 µM), propafenone(4.4 µM), 4-Aminopyridine(270 µM), TEA(330 mM)
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Kv1.6
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KCNA6
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Kvb
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脱分極によって活性化、遅延性整流性
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神経細胞における膜電位の制御
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a-dendrotoxin(20 nM), 4-Aminopyridine(1.5 mM), TEA(7 mM)
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Kv1.7
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KCNA7
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脱分極によって活性化、遅延性整流性
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心臓におけるIKur
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flecainide(8 µM), quinidine(15 µM), verapamil(16 µM), amiodarone(35 µM), 4-Aminopyridine(150 µM), TEA(150 mM)
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* 1-EBIO
* NS309
* CyPPA
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|rowspan=3 | [[Inward-rectifier potassium ion channel|Inwardly rectifying]] <br /> 2[[transmembrane helix|T]] & 1[[pore-forming loop|P]]
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* [[ROMK]] (K<sub>ir</sub>1.1)
Kv1.8
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KCNA10
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脱分極によって活性化、遅延性整流性
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腎近位尿細管における膜電位の制御
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Ba<sup>2+</sup>(5 mM), charybdotoxin(100 nM), 4-Aminopyridine(1.5 mM), TEA(50 mM)
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Kv2.1, 2.2
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KCNB1,2
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Shab-related
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Kv5,6,8,9, KChaP
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脱分極によって活性化、遅延性整流性
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* recycling and secretion of potassium in [[nephron]]s
神経細胞、骨格筋細胞における興奮性の制御
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* Nonselective: Ba<sup>2+</sup>, Cs<sup>+</sup>
Hanatoxin(42 nM)(Kv2.1), 細胞内TEA, 細胞外TEA(2.6 mM)(Kv2.2), 4-Aminopyridine(18 mM for Kv2.1; 1.5 mM for Kv2.2)
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* none
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* [[G protein-coupled inwardly-rectifying potassium channel|GPCR regulated]] (K<sub>ir</sub>3.x)
Kv3.1, 3.2
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KCNC1,2
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|rowspan=2 |Shaw-related
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* mediate the inhibitory effect of many [[GPCR]]s
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* [[GPCR]] antagonists
脱分極によって活性化、遅延性整流性
* [[ifenprodil]]<ref name="pmid16123769"><pubmed>16123769</pubmed></ref>
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神経細胞の高頻度発火、fast spiking
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4-Aminopyridine(29 µM for Kv3.1; 0.1 mM for Kv3.2), TEA(0.2 mM for Kv3.1; 0.1 mM for Kv3.2)
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* [[GPCR]] agonists
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* [[ATP-sensitive K+ channels|ATP-sensitive]] (K<sub>ir</sub>6.x)
Kv3.3, 3.4
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* close when [[adenosine triphosphate|ATP]] is high to promote [[insulin]] secretion
KCNC3,4
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* [[glibenclamide]]
* [[tolbutamide]]
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* [[diazoxide]]
脱分極によって活性化、早い不活性化(A-type)
* [[pinacidil]]
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書く
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4-Aminopyridine(1.2 mM for Kv3.3), TEA(0.14 mM for Kv3.3; 0.3 mM for Kv3.4)
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| [[Tandem pore domain potassium channel|Tandem pore domain]] <br /> 4[[transmembrane helix|T]] & 2[[pore-forming loop|P]]
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* TWIK ([[KCNK1|TWIK-1]], [[KCNK6|TWIK-2]], [[KCNK7]])<ref name="pmid20393194">{{cite journal | author = Enyedi P, Czirják G | title = Molecular background of leak K<sup>+</sup> currents: two-pore domain potassium channels | journal = Physiological Reviews | volume = 90 | issue = 2 | pages = 559–605 | year = 2010 | pmid = 20393194 | doi = 10.1152/physrev.00029.2009 }}</ref><ref name="pmid17652773">{{cite journal | author = Lotshaw DP | title = Biophysical, pharmacological, and functional characteristics of cloned and native mammalian two-pore domain K+ channels | journal = Cell Biochemistry and Biophysics | volume = 47 | issue = 2 | pages = 209–56 | year = 2007 | pmid = 17652773 | doi = 10.1007/s12013-007-0007-8 }}</ref>
Kv4.1-4.3
* TREK ([[KCNK2|TREK-1]], [[KCNK10|TREK-2]], [[KCNK4|TRAAK]]<ref name="pmid9628867">{{cite journal | author = Fink M, Lesage F, Duprat F, Heurteaux C, Reyes R, Fosset M, Lazdunski M | title = A neuronal two P domain K+ channel stimulated by arachidonic acid and polyunsaturated fatty acids | journal = The EMBO Journal | volume = 17 | issue = 12 | pages = 3297–308 | year = 1998 | pmid = 9628867 | pmc = 1170668 | doi = 10.1093/emboj/17.12.3297 }}</ref>)<ref name="pmid20393194"/><ref name="pmid17652773"/>
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* TASK ([[KCNK3|TASK-1]], [[KCNK9|TASK-3]], [[KCNK15|TASK-5]])<ref name="pmid20393194"/><ref name="pmid17652773"/>
KCND1-3
* TALK ([[KCNK5|TASK-2]],<ref name="pmid11256078">{{cite journal | author = Goldstein SA, Bockenhauer D, O'Kelly I, Zilberberg N | title = Potassium leak channels and the KCNK family of two-P-domain subunits | journal = Nature Reviews Neuroscience | volume = 2 | issue = 3 | pages = 175–84 | year = 2001 | pmid = 11256078 | doi = 10.1038/35058574 }}</ref> [[KCNK16|TALK-1]], [[KCNK17|TALK-2]])<ref name="pmid20393194"/><ref name="pmid17652773"/>
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* THIK ([[KCNK13|THIK-1]], [[KCNK12|THIK-2]])<ref name="pmid20393194"/><ref name="pmid17652773"/>
Shal-related
* [[KCNK18|TRESK]]<ref name="pmid20393194"/><ref name="pmid17652773"/><ref name="pmid12754259">{{cite journal | author = Sano Y, Inamura K, Miyake A, Mochizuki S, Kitada C, Yokoi H, Nozawa K, Okada H, Matsushime H, Furuichi K | title = A novel two-pore domain K+ channel, TRESK, is localized in the spinal cord | journal = The Journal of Biological Chemistry | volume = 278 | issue = 30 | pages = 27406–12 | year = 2003 | pmid = 12754259 | doi = 10.1074/jbc.M206810200 }}</ref><ref name="pmid14981085">{{cite journal | author = Czirják G, Tóth ZE, Enyedi P | title = The two-pore domain K+ channel, TRESK, is activated by the cytoplasmic calcium signal through calcineurin | journal = The Journal of Biological Chemistry | volume = 279 | issue = 18 | pages = 18550–8 | year = 2004 | pmid = 14981085 | doi = 10.1074/jbc.M312229200 }}</ref>
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KChiP1, KChiPs, DPPX, DPP10(Kv4.2)
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* Contribute to [[resting potential]]
脱分極によって活性化、早い不活性化(A-type)
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* [[bupivacaine]]<ref name="pmid10201682">{{cite journal | doi = 10.1097/00000542-199904000-00024 | author = Kindler CH, Yost CS, Gray AT | title = Local anesthetic inhibition of baseline potassium channels with two pore domains in tandem | journal = Anesthesiology | volume = 90 | issue = 4 | pages = 1092–102 | year = 1999 | pmid = 10201682 }}</ref><ref name="pmid11249964">{{cite journal | author = Meadows HJ, Randall AD | title = Functional characterisation of human TASK-3, an acid-sensitive two-pore domain potassium channel | journal = Neuropharmacology | volume = 40 | issue = 4 | pages = 551–9 | year = 2001 | pmid = 11249964 | doi = 10.1016/S0028-3908(00)00189-1 }}</ref><ref name="pmid12660311">{{cite journal | author = Kindler CH, Paul M, Zou H, Liu C, Winegar BD, Gray AT, Yost CS | title = Amide local anesthetics potently inhibit the human tandem pore domain background K+ channel TASK-2 (KCNK5) | journal = Journal of Pharmacology and Experimental Therapeutics | volume = 306 | issue = 1 | pages = 84–92 | year = 2003 | pmid = 12660311 | doi = 10.1124/jpet.103.049809 }}</ref><ref name="pmid12760993">{{cite journal | author = Punke MA, Licher T, Pongs O, Friederich P | title = Inhibition of human TREK-1 channels by bupivacaine | journal = Anesthesia & Analgesia | volume = 96 | issue = 6 | pages = 1665–73 | year = 2003 | pmid = 12760993 | doi = 10.1213/01.ANE.0000062524.90936.1F }}</ref>
心臓におけるIto(Kv4.2/Kv4.3/KChiP2)、神経細胞の細胞体におけるISA
* [[quinidine]]<ref name="pmid11249964"/><ref name="pmid8605869">{{cite journal | author = Lesage F, Guillemare E, Fink M, Duprat F, Lazdunski M, Romey G, Barhanin J | title = TWIK-1, a ubiquitous human weakly inward rectifying K+ channel with a novel structure | journal = The EMBO Journal | volume = 15 | issue = 5 | pages = 1004–11 | year = 1996 | pmid = 8605869 | pmc = 449995 }}</ref><ref name="pmid9312005">{{cite journal | author = Duprat F, Lesage F, Fink M, Reyes R, Heurteaux C, Lazdunski M | title = TASK, a human background K+ channel to sense external pH variations near physiological pH | journal = The EMBO Journal | volume = 16 | issue = 17 | pages = 5464–71 | year = 1997 | pmid = 9312005 | pmc = 1170177 | doi = 10.1093/emboj/16.17.5464 }}</ref><ref name="pmid9812978">{{cite journal | author = Reyes R, Duprat F, Lesage F, Fink M, Salinas M, Farman N, Lazdunski M | title = Cloning and expression of a novel pH-sensitive two pore domain K+ channel from human kidney | journal = The Journal of Biological Chemistry | volume = 273 | issue = 47 | pages = 30863–9 | year = 1998 | pmid = 9812978 | doi = 10.1074/jbc.273.47.30863 }}</ref><ref name="pmid10784345">{{cite journal | author = Meadows HJ, Benham CD, Cairns W, Gloger I, Jennings C, Medhurst AD, Murdock P, Chapman CG | title = Cloning, localisation and functional expression of the human orthologue of the TREK-1 potassium channel | journal = Pflügers Archiv : European Journal of Physiology | volume = 439 | issue = 6 | pages = 714–22 | year = 2000 | pmid = 10784345 | doi = 10.1007/s004240050997 }}</ref>
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4-Aminopyridine(9 mM for Kv4.1; 5 mM for Kv4.2), TEA(>10 mM for Kv4.1)
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* [[halothane]]<ref name="pmid11249964"/><ref name="pmid10321245">{{cite journal | author = Patel AJ, Honoré E, Lesage F, Fink M, Romey G, Lazdunski M| title = Inhalational anesthetics activate two-pore-domain background K+ channels | journal = Nature Neuroscience | volume = 2 | issue = 5 | pages = 422–6 | year = 1999 | pmid = 10321245 | doi = 10.1038/8084 }}</ref><ref name="pmid10839924">{{cite journal | doi = 10.1097/00000542-200006000-00032 | author = Gray AT, Zhao BB, Kindler CH, Winegar BD, Mazurek MJ, Xu J, Chavez RA, Forsayeth JR, Yost CS | title = Volatile anesthetics activate the human tandem pore domain baseline K+ channel KCNK5 | journal = Anesthesiology | volume = 92 | issue = 6 | pages = 1722–30 | year = 2000 | pmid = 10839924 }}</ref>
|-
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| [[Voltage-gated potassium channel|Voltage-gated]] <br /> 6[[transmembrane helix|T]] & 1[[pore-forming loop|P]]
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* [[hERG]] (K<sub>v</sub>11.1)
Kv5.1
* [[KvLQT1]] (K<sub>v</sub>7.1)
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KCNF1
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modifier
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Kv2 familyのmodifier
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|
|-
|
Kv6.1-6.4
|
KCNG1-4
|
modifiers
|
|
Kv2 familyのmodifiers
|
|
|
|-
|
Kv7.1
|
KCNQ1
|
KVLQT, KQT
|
KCNE1-3
|
脱分極によって活性化、遅延性整流性
|
活動電位の再分極、心臓におけるIKs電流(Kv7.1(KCNQ1)/KCNE1)、LQT1の原因遺伝子
|
Chlomanol 298B(1 µM)(Kv7.1)
|
|-
|
Kv7.2-7.5
|
KCNQ2-5
|
|
|
脱分極によって活性化、遅延性整流性
|
神経細胞におけるM電流(Kv7.2/7.3, Kv7.5)、内耳機能(Kv7.4)
|
|
Retigabine(10 µM for Kv7.2; 0.6 µM for Kv7.3; 1 µM for Kv7.4; 1.4 µM for Kv7.3/Kv7.5)
|-
|
Kv8.1-8.2
|
KCNV1-2
|
modifiers
|
|
Kv2 familyのmodifiers
|
|
|
|-
|
Kv9.1-9.3
|
KCNS1-3
|
modifiers
|
|
Kv2 familyのmodifiers
|
|
|
|-
|
Kv10.1, 10.2
|
KCNH1, 5
|
eag
|
|
脱分極によって活性化、遅延性整流性
|
|
quinidine(1.4 µM for Kv10.4)
|
|-
|
Kv11.1-11.3
|
KCNH2,6,7
|
erg
|
minK, KCNE2(Kv11.1)
|
脱分極によって活性化、早い不活性化機構(C-type)による内向き整流性
|
活動電位の再分極、心臓におけるIKr電流、LQT2の原因遺伝子、薬物誘発性不整脈の分子機構(Kv11.1)
|
astemizol(1 nM for Kv11.1), dofetilide(15-35 nM for Kv11.1), sertindole(3 nM for Kv11.1; 43 nM for Kv11.3)
|
|-
|
Kv12.1-12.3
|
KCNH8,3,4
|
elk
|
|
|
|
* [[action potential]] [[repolarization]]
* limits frequency of action potentials (disturbances cause [[Cardiac dysrhythmia|dysrhythmia]])
|
|
* [[tetraethylammonium]]
* [[4-Aminopyridine|4-aminopyridine]]
* [[dendrotoxin]]s (some types)
|
|
* [[retigabine]] (K<sub>v</sub>7)<ref name=Rogawski>{{cite journal |author=Rogawski MA, Bazil CW |title=New Molecular Targets for Antiepileptic Drugs: α2δ, SV2A, and Kv7/KCNQ/M Potassium Channels |journal=Curr Neurol Neurosci Rep |volume=8 |issue=4 |pages=345–52 |year=2008 |month=July |pmid=18590620 |pmc=2587091 |doi=10.1007/s11910-008-0053-7}}</ref>
|-
|-
|}
|}
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