Potassium channel blockers tetraethylammonium and 4-aminopyridine fail to prevent microglial activation induced by elevated potassium concentration

H. Ábrahám, A. Losonczy, G. Czéh, Gy Lázár

Research output: Contribution to journalArticle

Abstract

The effect of potassium channel blockers tetraethylammonium and 4-aminopyridine was examined on the elevated K+ concentration-induced microglial activation on rat hippocampal slice preparations. Microglial cells were detected by irmnunohistochemistry with a monoclonal antibody (OX 42) raised against a type 3 complement receptor. During activation the morphology of the microglial cells changes and the staining intensity increases. The degree of microglial activation was determined by measuring the integrated optical density of the cells. Tetraethylammonium and 4-aminopyridine failed to reduce the elevated K+ concentration-induced microglial activation. Both potassium channel blockers, when applied on the hippocampal slices without K+, caused significantly increased microglial activation as compared to the control slices. In order to check whether the functional alteration of the neuronal population induced by 4-aminopyridine caused the activation of the microglial cells, Schaffer collaterals were cut to block spreading of epileptiform hyperactivity of the CA3 pyramidal cells to the CA1 region. No significant differences were found in microglial activation between the CA3 and CA1 regions, indicating that the effect of 4-aminopyridine on microglial cells is independent of the epileptiform activity caused by the drug.

Original languageEnglish
Pages (from-to)63-78
Number of pages16
JournalActa Biologica Hungarica
Volume54
Issue number1
DOIs
Publication statusPublished - 2003

Fingerprint

Potassium Channel Blockers
4-aminopyridine
4-Aminopyridine
Tetraethylammonium
potassium channels
Potassium
potassium
Chemical activation
antibody
drug
Macrophage-1 Antigen
cells
Pyramidal Cells
Hippocampus
Cell Count
Monoclonal Antibodies
Staining and Labeling
Density (optical)
absorbance
effect

Keywords

  • Electrophysiology
  • Epileptiform activity
  • Glial cells
  • OX-42

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)

Cite this

Potassium channel blockers tetraethylammonium and 4-aminopyridine fail to prevent microglial activation induced by elevated potassium concentration. / Ábrahám, H.; Losonczy, A.; Czéh, G.; Lázár, Gy.

In: Acta Biologica Hungarica, Vol. 54, No. 1, 2003, p. 63-78.

Research output: Contribution to journalArticle

@article{25565b230069401889148e4a4fd79a8e,
title = "Potassium channel blockers tetraethylammonium and 4-aminopyridine fail to prevent microglial activation induced by elevated potassium concentration",
abstract = "The effect of potassium channel blockers tetraethylammonium and 4-aminopyridine was examined on the elevated K+ concentration-induced microglial activation on rat hippocampal slice preparations. Microglial cells were detected by irmnunohistochemistry with a monoclonal antibody (OX 42) raised against a type 3 complement receptor. During activation the morphology of the microglial cells changes and the staining intensity increases. The degree of microglial activation was determined by measuring the integrated optical density of the cells. Tetraethylammonium and 4-aminopyridine failed to reduce the elevated K+ concentration-induced microglial activation. Both potassium channel blockers, when applied on the hippocampal slices without K+, caused significantly increased microglial activation as compared to the control slices. In order to check whether the functional alteration of the neuronal population induced by 4-aminopyridine caused the activation of the microglial cells, Schaffer collaterals were cut to block spreading of epileptiform hyperactivity of the CA3 pyramidal cells to the CA1 region. No significant differences were found in microglial activation between the CA3 and CA1 regions, indicating that the effect of 4-aminopyridine on microglial cells is independent of the epileptiform activity caused by the drug.",
keywords = "Electrophysiology, Epileptiform activity, Glial cells, OX-42",
author = "H. {\'A}brah{\'a}m and A. Losonczy and G. Cz{\'e}h and Gy L{\'a}z{\'a}r",
year = "2003",
doi = "10.1556/ABiol.54.2003.1.7",
language = "English",
volume = "54",
pages = "63--78",
journal = "Acta Biologica Hungarica",
issn = "0236-5383",
publisher = "Akademiai Kiado",
number = "1",

}

TY - JOUR

T1 - Potassium channel blockers tetraethylammonium and 4-aminopyridine fail to prevent microglial activation induced by elevated potassium concentration

AU - Ábrahám, H.

AU - Losonczy, A.

AU - Czéh, G.

AU - Lázár, Gy

PY - 2003

Y1 - 2003

N2 - The effect of potassium channel blockers tetraethylammonium and 4-aminopyridine was examined on the elevated K+ concentration-induced microglial activation on rat hippocampal slice preparations. Microglial cells were detected by irmnunohistochemistry with a monoclonal antibody (OX 42) raised against a type 3 complement receptor. During activation the morphology of the microglial cells changes and the staining intensity increases. The degree of microglial activation was determined by measuring the integrated optical density of the cells. Tetraethylammonium and 4-aminopyridine failed to reduce the elevated K+ concentration-induced microglial activation. Both potassium channel blockers, when applied on the hippocampal slices without K+, caused significantly increased microglial activation as compared to the control slices. In order to check whether the functional alteration of the neuronal population induced by 4-aminopyridine caused the activation of the microglial cells, Schaffer collaterals were cut to block spreading of epileptiform hyperactivity of the CA3 pyramidal cells to the CA1 region. No significant differences were found in microglial activation between the CA3 and CA1 regions, indicating that the effect of 4-aminopyridine on microglial cells is independent of the epileptiform activity caused by the drug.

AB - The effect of potassium channel blockers tetraethylammonium and 4-aminopyridine was examined on the elevated K+ concentration-induced microglial activation on rat hippocampal slice preparations. Microglial cells were detected by irmnunohistochemistry with a monoclonal antibody (OX 42) raised against a type 3 complement receptor. During activation the morphology of the microglial cells changes and the staining intensity increases. The degree of microglial activation was determined by measuring the integrated optical density of the cells. Tetraethylammonium and 4-aminopyridine failed to reduce the elevated K+ concentration-induced microglial activation. Both potassium channel blockers, when applied on the hippocampal slices without K+, caused significantly increased microglial activation as compared to the control slices. In order to check whether the functional alteration of the neuronal population induced by 4-aminopyridine caused the activation of the microglial cells, Schaffer collaterals were cut to block spreading of epileptiform hyperactivity of the CA3 pyramidal cells to the CA1 region. No significant differences were found in microglial activation between the CA3 and CA1 regions, indicating that the effect of 4-aminopyridine on microglial cells is independent of the epileptiform activity caused by the drug.

KW - Electrophysiology

KW - Epileptiform activity

KW - Glial cells

KW - OX-42

UR - http://www.scopus.com/inward/record.url?scp=0037234494&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037234494&partnerID=8YFLogxK

U2 - 10.1556/ABiol.54.2003.1.7

DO - 10.1556/ABiol.54.2003.1.7

M3 - Article

C2 - 12712959

AN - SCOPUS:0037234494

VL - 54

SP - 63

EP - 78

JO - Acta Biologica Hungarica

JF - Acta Biologica Hungarica

SN - 0236-5383

IS - 1

ER -