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  Demonstration of an inwardly rectifying K+ current component modulated by thyrotropin-releasing hormone and caffeine in GH3 rat anterior pituitary cells

Barros, F., del Camino, D., Pardo, L. A., Palomero, T., Giráldez, T., & de la Peña, P. (1997). Demonstration of an inwardly rectifying K+ current component modulated by thyrotropin-releasing hormone and caffeine in GH3 rat anterior pituitary cells. Pflugers Archiv European Journal of Physiology, 435(1), 119-129. doi:10.1007/s004240050491.

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Barros, F., Author
del Camino, D., Author
Pardo, L. A.1, Author           
Palomero, T., Author
Giráldez, T., Author
de la Peña, P., Author
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1Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173656              

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 Abstract: Reduction of an inwardly rectifying K+ current by thyrotropin-releasing hormone (TRH) and caffeine has been considered to be an important determinant of electrical activity increases in GH3 rat anterior pituitary cells. However, the existence of an inwardly rectifying K+ current component was recently regarded as a misidentification of an M-like outward current, proposed to be the TRH target in pituitary cells, including GH3 cells. In this report, an inwardly rectifying component of K+ current is indeed demonstrated in perforated-patch voltage-clamped GH3 cells. The degree of rectification varied from cell to cell, but both TRH and caffeine specifically blocked a fraction of current with strong rectification in the hyperpolarizing direction. Use of ramp pulses to continuously modify the membrane potential demonstrated a prominent blockade even in cells with no current reduction at voltages at which M-currents are active. Depolarization steps to positive voltages at the maximum of the inward current induced a caffeine-sensitive instantaneous outward current followed by a single exponential decay. The magnitude of this current was modified in a biphasic way according to the duration of the previous hyperpolarization step. The kinetic characteristics of the current are compatible with the possibility that removal from inactivation of a fast-inactivating delayed rectifier causes the hyperpolarization-induced current. Furthermore, the inwardly rectifying current was blocked by astemizole, a potent and selective inhibitor of human ether-a-go-go -related gene (HERG) K+ channels. Along with other pharmacological and kinetic evidence, this indicates that the secretagogue-regulated current is probably mediated by a HERG-like K+ channel. Addition of astemizole to current-clamped cells induced clear increases in the frequency of action potential production. Thus, an inwardly-rectifying K+ current and not an M-like outward current seems to be involved in TRH and caffeine modulation of electrical activity in GH3 cells.

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 Dates: 1997-11
 Publication Status: Published in print
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 Rev. Type: Peer
 Identifiers: DOI: 10.1007/s004240050491
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Title: Pflugers Archiv European Journal of Physiology
Source Genre: Journal
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Pages: - Volume / Issue: 435 (1) Sequence Number: - Start / End Page: 119 - 129 Identifier: -