The developmental expression of K+ channels in retinal glial cells is associated with a decrease of osmotic cell swelling

Glia ◽  
2006 ◽  
Vol 54 (5) ◽  
pp. 411-423 ◽  
Author(s):  
Antje Wurm ◽  
Thomas Pannicke ◽  
Ianors Iandiev ◽  
Peter Wiedemann ◽  
Andreas Reichenbach ◽  
...  
Keyword(s):  
Glial Cells ◽  
Developmental Expression ◽  
Cell Swelling ◽  
K Channels

scholarly journals Cell swelling activates cloned Ca2+-activated K+ channels: a role for the F-actin cytoskeleton

2003 ◽  
Vol 1615 (1-2) ◽  
pp. 115-125 ◽  
Author(s):  
Nanna K Jorgensen ◽  
Stine F Pedersen ◽  
Hanne B Rasmussen ◽  
Morten Grunnet ◽  
Dan A Klaerke ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Cell Swelling ◽  
K Channels

Developmental Expression of Rat Insulin-Like Growth Factor Binding Protein-2 by Astrocytic Glial Cells in Culture*

Endocrinology ◽  
1991 ◽  
Vol 129 (2) ◽  
pp. 1066-1074 ◽  
Author(s):  
JOHN A. OLSON ◽  
KATHLEEN T. SHIVERICK ◽  
SUSAN OGILVIE ◽  
WILLIAM C. BUHI ◽  
MOHAN K. RAIZADA
Keyword(s):  
Growth Factor ◽  
Glial Cells ◽  
Binding Protein ◽  
Developmental Expression ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Cells In Culture

Three distinct types of voltage-dependent K+ channels are expressed by M�ller (glial) cells of the rabbit retina

1994 ◽  
Vol 426 (1-2) ◽  
pp. 51-60 ◽  
Author(s):  
T. Ivo Chao ◽  
Andr� Henke ◽  
Winfried Reichelt ◽  
Wolfgang Eberhardt ◽  
Sigrid Reinhardt-Maelicke ◽  
...  
Keyword(s):  
Glial Cells ◽  
Rabbit Retina ◽  
K Channels ◽  
Voltage Dependent

scholarly journals Heteromultimeric Delayed-Rectifier K+Channels in Schwann Cells: Developmental Expression and Role in Cell Proliferation

1998 ◽  
Vol 18 (24) ◽  
pp. 10398-10408 ◽  
Author(s):  
Alexander Sobko ◽  
Asher Peretz ◽  
Orian Shirihai ◽  
Sarah Etkin ◽  
Vera Cherepanova ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Schwann Cells ◽  
Developmental Expression ◽  
Delayed Rectifier ◽  
K Channels

scholarly journals Developmental expression of voltage-sensitive K+ channels in mouse skeletal muscle and C2 C12 cells

FEBS Letters ◽  
1992 ◽  
Vol 310 (2) ◽  
pp. 162-166 ◽  
Author(s):  
Florian Lesage ◽  
Bernard Attali ◽  
Michel Lazdunski ◽  
Jacques Barhanin
Keyword(s):  
Skeletal Muscle ◽  
Developmental Expression ◽  
K Channels ◽  
Mouse Skeletal Muscle

scholarly journals Opioid Receptor Protein Expression During Development of the Rat Brainstem

2021 ◽  
Author(s):  
◽  
Bronwyn Maree Kivell
Keyword(s):  
Confocal Microscopy ◽  
Opioid Receptor ◽  
Glial Cells ◽  
Opioid Receptors ◽  
Cultured Cells ◽  
Expression Patterns ◽  
Receptor Expression ◽  
Developmental Expression ◽  
Receptor Protein ◽  
Western Blots

<p>Few satisfactory protocols exist for primary culture of postnatal brainstem neurons, and commonly used procedures often give poor survival rates in older foetal (>E16) and early postnatal brainstem cultures. The present study describes the first reliable method for establishing stable in vitro cultures of foetal and postnatal brainstem neurons up to six days postnatal age in a defined, serum-free culture medium. This novel culture method was used to study opioid receptor expression and distribution in developing brainstem cells. Opioids play an important role in brainstem functions, being involved in respiratory and cardiovascular modulation and pain control (Olsen et al., 1995; Olson et al., 1997; Vaccarino et al., 1999; Vaccarino and Kastin, 2001). These brainstem functions are particularly important for survival at birth, and opioid receptor distribution patterns and sensitivities to opioid ligands change during development. Using cultured cells and frozen sections of brainstem tissue, mu (MOR) and delta (DOR) opioid receptor localisation in neuronal and glial cells at different stages of foetal and postnatal development in the rat were examined by immunocytochemistry and confocal microscopy. Bipolar and multipolar neurons showed similar immunoreactivities; whereas, glial cells were more lightly stained than neurons. Developmentally advanced stages were more intensely stained for MOR (P<0.006, Mann-Whitney test); whereas, DOR immunoreactivity did not change during development. These developmental expression patterns observed in culture for MOR were similar to those obtained from Western blots of electrophoreses brainstem lysates. DOR, however, decreased in expression in brainstem lysates with increased developmental age, even though there was no difference in DOR expression in cultured cells. MOR and DOR were colocalised in specific brainstem regions and in the cerebellum of foetal and postnatal animals, although the distribution of both opioid receptors in the foetal brain was more diffuse than in the older animals. The intracellular distributions of MOR and DOR were investigated by confocal microscopy. In addition to plasma membrane staining, a population of internalised cytoplasmic receptors was present in neurons. MOR was down-regulated after exposure of either cultured brainstem cells or transfected or non-transfected SH-SY5Y neuroblastoma cells to the MOR agonist DAMGO. From the above investigation, it was concluded that opioid receptors are developmentally regulated during maturation of the brainstem of the rat, and that primary cell culture, immunocytochemistry, and immunoblotting of cell lysates are suitable techniques for investigating opioid systems in the foetal, postnatal, and adult rat.</p>

scholarly journals Juxtaparanodal clustering of Shaker-like K+ channels in myelinated axons depends on Caspr2 and TAG-1

2003 ◽  
Vol 162 (6) ◽  
pp. 1149-1160 ◽  
Author(s):  
Sebastian Poliak ◽  
Daniela Salomon ◽  
Hadas Elhanany ◽  
Helena Sabanay ◽  
Brent Kiernan ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Ion Channels ◽  
Gene Targeting ◽  
Glial Cells ◽  
Adhesion Molecule ◽  
Myelin Sheath ◽  
Cell Adhesion Molecule ◽  
Myelinated Axons ◽  
Axonal Membrane ◽  
K Channels

In myelinated axons, K+ channels are concealed under the myelin sheath in the juxtaparanodal region, where they are associated with Caspr2, a member of the neurexin superfamily. Deletion of Caspr2 in mice by gene targeting revealed that it is required to maintain K+ channels at this location. Furthermore, we show that the localization of Caspr2 and clustering of K+ channels at the juxtaparanodal region depends on the presence of TAG-1, an immunoglobulin-like cell adhesion molecule that binds Caspr2. These results demonstrate that Caspr2 and TAG-1 form a scaffold that is necessary to maintain K+ channels at the juxtaparanodal region, suggesting that axon–glia interactions mediated by these proteins allow myelinating glial cells to organize ion channels in the underlying axonal membrane.

Swelling-activated K fluxes in vascular endothelial cells: volume regulation via K-Cl cotransport and K channels

1993 ◽  
Vol 265 (3) ◽  
pp. C763-C769 ◽  
Author(s):  
P. B. Perry ◽  
W. C. O'Neill
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Regulatory Volume Decrease ◽  
Cell Swelling ◽  
Ionophore A23187 ◽  
Vascular Endothelial ◽  
Aortic Endothelial Cells ◽  
K Channels ◽  
Volume Decrease ◽  
Aortic Endothelial

K efflux pathways responsible for regulatory volume decrease (RVD) were examined in bovine aortic endothelial cells. Hypotonic swelling produced a rapid and reversible threefold increase in bumetanide-insensitive 86Rb efflux. Swelling-activated 86Rb efflux was inhibited 43% when Cl was replaced with NO3, and this Cl-dependent efflux was inhibited by 1 mM furosemide. Neither Cl replacement nor furosemide inhibited the efflux stimulated by a Ca ionophore (A23187) in isotonic medium. Swelling-activated 86Rb efflux was also inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonate but not by dinitrostilbenedisulfonate. Cell swelling induced a volume-regulatory K loss that was incomplete in hypotonic medium but complete and more rapid when bumetanide was added or when cells were swollen isosmotically. K loss in the presence of bumetanide was partially blocked by furosemide. We conclude that two separate swelling-activated K fluxes mediate RVD in aortic endothelial cells: a Cl-dependent, furosemide-sensitive, but bumetanide-insensitive flux that is consistent with K-Cl cotransport, and a Cl-independent efflux that presumably is mediated by K channels.

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