Structured Review

Jackson Immuno kv1 3
K + -channel expression in acutely isolated microglia. (a) <t>Kv1.3</t> current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
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1) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

2) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

3) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

4) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

5) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

6) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

7) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

8) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

9) Product Images from "The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke"

Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

Journal: Journal of Cerebral Blood Flow & Metabolism

doi: 10.1177/0271678X15611434

K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
Figure Legend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

Techniques Used: Expressing, Isolation, Injection

KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.
Figure Legend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

Techniques Used: Staining, Expressing, Marker

10) Product Images from "Targeting Effector Memory T Cells with the Small Molecule Kv1.3 Blocker PAP-1 Suppresses Allergic Contact Dermatitis"

Article Title: Targeting Effector Memory T Cells with the Small Molecule Kv1.3 Blocker PAP-1 Suppresses Allergic Contact Dermatitis

Journal:

doi: 10.1038/sj.jid.5700717

Ear infiltrating cells in ACD are CD8 + , CD45RC − , and Kv1.3 +
Figure Legend Snippet: Ear infiltrating cells in ACD are CD8 + , CD45RC − , and Kv1.3 +

Techniques Used:

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    K + -channel expression in acutely isolated microglia. (a) <t>Kv1.3</t> current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.
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    K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

    doi: 10.1177/0271678X15611434

    Figure Lengend Snippet: K + -channel expression in acutely isolated microglia. (a) Kv1.3 current density increases in microglia from the infarct area after MCAO (28.8 ± 2.0 pA/pF, n = 19) and microglia isolated from the hippocampus following intracerebroventricular LPS injection (22.9 ± 16.6 pA/pF, n = 13) compared to microglia from wild-type control brains (5.0 ± 3.9 pA/pF, n = 16) or microglia from the contralateral side after MCAO (5.7 ± 4.4 pA/pF, n = 18). (b) Example current traces showing Kv1.3's characteristic use-dependence and sensitivity to the Kv1.3 blockers PAP-1 and ShK-L5. (c) Microglia from the contralateral (50.2 ± 35.4 pS/pF, n = 18) and ipsilateral side after MCAO (71.6 ± 34.9 pS/pF, n = 21), as well as microglia isolated from the hippocampus following intracerebroventricular LPS injection (84.0 ± 42.4 pS/pF, n = 13) show higher KCa3.1 current densities than microglia from wild-type control brains (29.7 ± 15.2 pS/pF, n = 16). (d) Example KCa3.1 current traces elicited by a ramp protocol showing the current's sensitive to 1 µM of the KCa3.1-selective blocker TRAM-34. (e) Microglia from both the contralateral side (7.8 ± 5.8 pA/pF, n = 18) and the infarct area (15.1 ± 10.2 pA/pF, n = 21) after MCAO show increased Kir current densities compared to those from wild-type (2.4 ± 2.4 pA/pF, n = 16) or LPS-injected brains (1.9 ± 2.9 pA/pF, n = 13). (f) Representative current traces showing a large Kir current, which was observable in some MCAO microglia, but not in microglia isolated from the hippocampus following intracerebroventricular LPS injection. Data are presented as mean ± S.D. Statistical significance was determined by Student's t -test.

    Article Snippet: However, our study is the first to investigate calcium-activated K+ channels in adult microglia and to identify both the Kv and the KCa channel through their biophysical and pharmacological properties as Kv1.3 and KCa3.1.

    Techniques: Expressing, Isolation, Injection

    KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke

    doi: 10.1177/0271678X15611434

    Figure Lengend Snippet: KCa3.1 and Kv1.3 are expressed on microglia/macrophages in human infarcts. (a) KCa3.1 staining in a 2–3-week-old infarct. KCa3.1 expression is localized to macrophages/microglia (M) and vascular endothelial (E) cells. (b) Fluorescent staining for a microglia/macrophage marker (MAC387) and KCa3.1. (c) Kv1.3 staining in a 14-day old-infarct. (d) Fluorescent staining for a microglia/macrophage marker (MAC387) and Kv1.3. All images are from 5-μm thick paraffin sections.

    Article Snippet: However, our study is the first to investigate calcium-activated K+ channels in adult microglia and to identify both the Kv and the KCa channel through their biophysical and pharmacological properties as Kv1.3 and KCa3.1.

    Techniques: Staining, Expressing, Marker