K(+) currents fail to change in reactive retinal glial cells in a mouse model of glaucoma
Standard
K(+) currents fail to change in reactive retinal glial cells in a mouse model of glaucoma. / Bolz, Sylvia; Schuettauf, Frank; Fries, Julia E; Thaler, Sebastian; Reichenbach, Andreas; Pannicke, Thomas.
In: GRAEF ARCH CLIN EXP, Vol. 246, No. 9, 09.2008, p. 1249-54.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - K(+) currents fail to change in reactive retinal glial cells in a mouse model of glaucoma
AU - Bolz, Sylvia
AU - Schuettauf, Frank
AU - Fries, Julia E
AU - Thaler, Sebastian
AU - Reichenbach, Andreas
AU - Pannicke, Thomas
PY - 2008/9
Y1 - 2008/9
N2 - PURPOSE: To investigate the membrane physiology of Müller glial cells from retinae of DBA/2J mice (which develop ocular hypertension) and of C57BL/6 control mice of different ages.METHODS: Retinae were obtained at the ages of 3, 6, and 12 months from DBA/2J mice and from C57BL/6 controls. Immunohistochemistry was performed using antibodies against glial fibrillary acidic protein (GFAP). Whole-cell membrane currents, membrane potentials and capacitances were recorded from freshly isolated Müller cells.RESULTS: Strong immunostaining for GFAP was found in Müller cells of 12-month-old DBA/2J mice, whereas only astrocytes were immunopositive in C57BL/6 retinae. No significant alterations of membrane currents or potentials of Müller cells from DBA/2J mice as compared to controls were observed at any age; however, the membrane capacitance was increased in Müller cells from DBA/2J mice at the age of 6 months.CONCLUSIONS: Although Müller cells of DBA/2J mice display some symptoms of reactive gliosis, the lack of significant alterations of the membrane physiology confirm previous data demonstrating that these cells undergo a nonproliferative gliosis.
AB - PURPOSE: To investigate the membrane physiology of Müller glial cells from retinae of DBA/2J mice (which develop ocular hypertension) and of C57BL/6 control mice of different ages.METHODS: Retinae were obtained at the ages of 3, 6, and 12 months from DBA/2J mice and from C57BL/6 controls. Immunohistochemistry was performed using antibodies against glial fibrillary acidic protein (GFAP). Whole-cell membrane currents, membrane potentials and capacitances were recorded from freshly isolated Müller cells.RESULTS: Strong immunostaining for GFAP was found in Müller cells of 12-month-old DBA/2J mice, whereas only astrocytes were immunopositive in C57BL/6 retinae. No significant alterations of membrane currents or potentials of Müller cells from DBA/2J mice as compared to controls were observed at any age; however, the membrane capacitance was increased in Müller cells from DBA/2J mice at the age of 6 months.CONCLUSIONS: Although Müller cells of DBA/2J mice display some symptoms of reactive gliosis, the lack of significant alterations of the membrane physiology confirm previous data demonstrating that these cells undergo a nonproliferative gliosis.
KW - Animals
KW - Astrocytes/metabolism
KW - Disease Models, Animal
KW - Female
KW - Fluorescent Antibody Technique, Indirect
KW - Glaucoma/physiopathology
KW - Glial Fibrillary Acidic Protein
KW - Gliosis/physiopathology
KW - Membrane Potentials/physiology
KW - Mice
KW - Mice, Inbred C57BL
KW - Mice, Inbred DBA
KW - Microscopy, Fluorescence
KW - Nerve Tissue Proteins/metabolism
KW - Neuroglia/physiology
KW - Ocular Hypertension/physiopathology
KW - Patch-Clamp Techniques
KW - Potassium Channels/physiology
KW - Retina/physiopathology
KW - Retinal Degeneration/physiopathology
U2 - 10.1007/s00417-008-0872-x
DO - 10.1007/s00417-008-0872-x
M3 - SCORING: Journal article
C2 - 18546005
VL - 246
SP - 1249
EP - 1254
JO - GRAEF ARCH CLIN EXP
JF - GRAEF ARCH CLIN EXP
SN - 0721-832X
IS - 9
ER -
