Altered K+ Channel Expression in the Hypertrophied and Failing Heart

2001 ◽  
pp. 773-783 ◽  
Author(s):  
Koichi Takimoto ◽  
Edwin S. Levitan
Keyword(s):  
K Channel ◽  
Failing Heart ◽  
Channel Expression

Ion channels in spinal cord astrocytes in vitro. I. Transient expression of high levels of Na+ and K+ channels

1992 ◽  
Vol 68 (4) ◽  
pp. 985-1000 ◽  
Author(s):  
H. Sontheimer ◽  
J. A. Black ◽  
B. R. Ransom ◽  
S. G. Waxman
Keyword(s):  
Spinal Cord ◽  
Membrane Potentials ◽  
Resting Potential ◽  
K Channel ◽  
Na Channels ◽  
Patch Clamp Recording ◽  
K Channels ◽  
Na Currents ◽  
Channel Expression

1. Na+ and K+ channel expression was studied in cultured astrocytes derived from P--0 rat spinal cord using whole cell patch-clamp recording techniques. Two subtypes of astrocytes, pancake and stellate, were differentiated morphologically. Both astrocyte types showed Na+ channels and up to three forms of K+ channels at certain stages of in vitro development. 2. Both astrocyte types showed pronounced K+ currents immediately after plating. Stellate but not pancake astrocytes additionally showed tetrodotoxin (TTX)-sensitive inward Na+ currents, which displayed properties similar to neuronal Na+ currents. 3. Within 4-5 days in vitro (DIV), pancake astrocytes lost K(+)-current expression almost completely, but acquired Na+ currents in high densities (estimated channel density approximately 2-8 channels/microns2). Na+ channel expression in these astrocytes is approximately 10- to 100-fold higher than previously reported for glial cells. Concomitant with the loss of K+ channels, pancake astrocytes showed significantly depolarized membrane potentials (-28.1 +/- 15.4 mV, mean +/- SD), compared with stellate astrocytes (-62.5 +/- 11.9 mV, mean +/- SD). 4. Pancake astrocytes were capable of generating action-potential (AP)-like responses under current clamp, when clamp potential was more negative than resting potential. Both depolarizing and hyperpolarizing current injections elicited overshooting responses, provided that cells were current clamped to membrane potentials more negative than -70 mV. Anode-break spikes were evoked by large hyperpolarizations (less than -150 mV). AP-like responses in these hyperpolarized astrocytes showed a time course similar to neuronal APs under conditions of low K+ conductance. 5. In stellate astrocytes, AP-like responses were not observed, because the K+ conductance always exceeded Na+ conductance by at least a factor of 3. Thus stellate spinal cord astrocyte membranes are stabilized close to EK as previously reported for hippocampal astrocytes. 6. It is concluded that spinal cord pancake astrocytes are capable of synthesizing Na+ channels at densities that can, under some conditions, support electrogenesis. In vivo, however, AP-like responses are unlikely to occur because the cells' resting potential is too depolarized to allow current activation. Thus the absence of electrogenesis in astrocytes may be explained by two mechanisms: 1) a low Na-to-K conductance ratio, as in stellate spinal cord astrocytes and in other previously studied astrocyte preparations; or, 2) as described in detail in the companion paper, a mismatch between the h infinity curve and resting potential, which results in Na+ current inactivation in spinal cord pancake astrocytes.

scholarly journals TWIK-Related Spinal Cord K+Channel Expression Is Increased in the Spinal Dorsal Horn after Spinal Nerve Ligation

2015 ◽  
Vol 56 (5) ◽  
pp. 1307 ◽  
Author(s):  
Hee Youn Hwang ◽  
Enji Zhang ◽  
Sangil Park ◽  
Woosuk Chung ◽  
Sunyeul Lee ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Spinal Nerve ◽  
Spinal Nerve Ligation ◽  
K Channel ◽  
Spinal Dorsal ◽  
Channel Expression

Molecular Methods for Evaluation of K+Channel Expression and Distribution in the Heart

2001 ◽  
pp. 103-118
Author(s):  
Michael J. Morales ◽  
Mulugu V. Brahmajothi ◽  
Donald L. Campbell ◽  
Harold C. Strauss
Keyword(s):  
Molecular Methods ◽  
K Channel ◽  
Channel Expression

scholarly journals Subfamily-Specific Posttranscriptional Mechanism Underlies K+ Channel Expression in a Developing Neuronal Blastomere

1999 ◽  
Vol 19 (16) ◽  
pp. 6874-6886 ◽  
Author(s):  
Fumihito Ono ◽  
You Katsuyama ◽  
Kouichi Nakajo ◽  
Yasushi Okamura
Keyword(s):  
K Channel ◽  
Channel Expression

scholarly journals The systemic inflammatory response is involved in the regulation of K+channel expression in brain via TNF-α-dependent and -independent pathways

FEBS Letters ◽  
2004 ◽  
Vol 572 (1-3) ◽  
pp. 189-194 ◽  
Author(s):  
Rubén Vicente ◽  
Mireia Coma ◽  
Silvia Busquets ◽  
Rodrigo Moore-Carrasco ◽  
Francisco J López-Soriano ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Systemic Inflammatory Response ◽  
K Channel ◽  
Tnf Α ◽  
Channel Expression

Moving on up: auxin-induced K+ channel expression regulates gravitropism

2000 ◽  
Vol 5 (3) ◽  
pp. 85-86 ◽  
Author(s):  
Malcolm J Bennett ◽  
Jeremy Roberts ◽  
Klaus Palme
Keyword(s):  
K Channel ◽  
Channel Expression

Effects of K+ Channel Blockers on Developing Rat Myelinated CNS Axons: Identification of Four Types of K+Channels

2002 ◽  
Vol 87 (3) ◽  
pp. 1376-1385 ◽  
Author(s):  
Jerome Devaux ◽  
Maurice Gola ◽  
Guy Jacquet ◽  
Marcel Crest
Keyword(s):  
Optic Nerve ◽  
Refractory Period ◽  
K Channel ◽  
Channel Blockers ◽  
Optic Nerves ◽  
Kv Channel ◽  
Kv Channels ◽  
Compound Action Potentials ◽  
Channel Expression ◽  
The One

Four blockers of voltage-gated potassium channels (Kv channels) were tested on the compound action potentials (CAPs) of rat optic nerves in an attempt to determine the regulation of Kv channel expression during the process of myelination. Before myelination occurred, 4-aminopyridine (4-AP) increased the amplitude, duration, and refractory period of the CAPs. On the basis of their pharmacological sensitivity, 4-AP-sensitive channels were divided in two groups, the one sensitive to kaliotoxin (KTX), dendrotoxin-I (DTX-I), and 4-AP, and the other sensitive only to 4-AP. In addition, tetraethylammonium chloride (TEA) applied alone broadened the CAPs. At the onset of myelination, DTX-I induced a more pronounced effect than KTX; this indicates that a fourth group of channels sensitive to 4-AP and DTX-I but insensitive to KTX had developed. The effects of KTX and DTX-I gradually disappeared during the period of myelination. Electron microscope findings showed that the disappearance of these effects was correlated with the ongoing process of myelination. This was confirmed by the fact that DTX-I and KTX enlarged the CAPs of demyelinated adult optic nerves. These results show that KTX- and DTX-sensitive channels are sequestrated in paranodal regions. During the process of myelination, KTX had less pronounced effects than DTX-I on demyelinated nerves, which suggests that the density of the KTX-sensitive channels decreased during this process. By contrast, 4-AP increased the amplitude, duration, and refractory period of the CAPs at all the ages tested and to a greater extent than KTX and DTX-I. The effects of TEA alone also gradually disappeared during this period. However, effects of TEA on CAPs were observed when this substance was applied after 4-AP to the adult optic nerve; this shows that TEA-sensitive channels are not masked by the myelin sheath. In conclusion, the process of myelination seems to play an important part in the regulation and setting of Kv channels in optic nerve axons.

Comparison of aldosterone- and RU-28362-induced apical Na+ and K+ conductances in rat distal colon

1994 ◽  
Vol 267 (3) ◽  
pp. G485-G493 ◽  
Author(s):  
R. B. Lomax ◽  
G. I. Sandle
Keyword(s):  
Distal Colon ◽  
Distal Segment ◽  
K Channel ◽  
Rat Colon ◽  
Na Channel ◽  
Channel Blockers ◽  
Mineralocorticoid Antagonist ◽  
Channel Expression ◽  
K Secretion ◽  
Crypt Cells

In mammalian distal colon, aldosterone induces electrogenic Na+ absorption and electrogenic K+ secretion, whereas the sole transport effect of specific glucocorticoid agonists is thought to be stimulation of electroneutral NaCl absorption. In this study, intracellular microelectrodes and Na(+)- and K(+)-channel blockers were used to compare the effects of aldosterone and RU-28362 (a specific glucocorticoid agonist) on apical Na+ and K+ conductances in surface cells and upper crypt cells in the most distal colonic segment from adrenalectomized rats. In control animals, surface cells and crypt cells were devoid of apical Na+ and K+ conductances. In aldosterone-treated animals (70 micrograms.100 g body wt-1.day-1 for 7 days), Na+ conductances were induced in 88% of surface cells but only 40% of crypt cells, and the distribution of K+ conductances was similar (82% of surface cells and 50% of crypt cells). The same dose of RU-28362 also induced Na+ conductances in 82% of surface cells and 50% of crypt cells, which tended to be smaller than those induced by aldosterone. RU-28362, in contrast to aldosterone, had no effect on apical K+ conductance in surface cells or crypt cells. Concurrent treatment with the mineralocorticoid antagonist RU-28318 (3.5 mg.100 g body wt-1.day-1 for 7 days) inhibited Na(+)-channel expression in aldosterone-treated animals but had no effect in RU-28362-treated animals. We conclude that in the most distal segment of rat colon, aldosterone acts via mineralocorticoid receptors to induce apical Na+ and K+ conductances, which are only fully expressed in the surface cell population.(ABSTRACT TRUNCATED AT 250 WORDS)

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