Okadaic acid and calyculin A enhance the effect of thyrotropin‐releasing hormone on GH3 rat anterior pituitary cells excitability

Delgado, Luis M.; Peña, Pilar de la; Camino, Donato del; Barros, Francisco

doi:10.1016/0014-5793(92)81362-p

Cited by 15 publications

(12 citation statements)

References 29 publications

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“…We have used such a high-Ca 2+ /low-K + solution to potentiate the contribution of voltage-dependent Ca 2+ channels and K + channels. This also allows for a better comparison with electrical parameters previously recorded from these cells [18, 19, 21]. In this case, the depolarizations in physiological low-Ca 2+ /high-K + mostly consisted of single depolarizing spikes showing a delayed repolarizing phase following a relatively negative maximum.…”

Section: Resultsmentioning

confidence: 99%

“…It has been repeatedly reported that the characteristics of the APs are fairly variable between individual GH 3 cells [9, 18, 19, 21]. Typical examples of spontaneous membrane depolarizations (APs) in cells bathed in physiological low-Ca 2+ /high-K + saline are shown in figure 1.…”

Section: Resultsmentioning

confidence: 99%

“…It is important to note that the existence of a subpopulation of cells with reduced BK currents could also explain the detection of cells showing long-lasting APs and/or high-amplitude [Ca 2+ ] i oscillations even when high-Ca 2+ /low-K + medium is used [18, 19, 21]. As a reflection of such a heterogeneity, we performed simultaneous recordings of electrical activity and [Ca 2+ ] i in a sample of 23 Fura-2-loaded cells bathed in high-Ca 2+ /low-K + solution.…”

Section: Resultsmentioning

confidence: 99%

“…Maintenance of GH 3 cells (ATCC-CCL 82.1) and conditions for perforated-patch recordings are described in detail elsewhere [13, 14, 18, 19, 21]. All recordings were performed at room temperature with the perforated-patch variant of the patch-clamp technique using a recording chamber of 0.2–0.3 ml continuously perfused at 0.5– 1.0 ml/min.…”

Section: Methodsmentioning

confidence: 99%

“…Thus, both under basal and stimulated conditions, large cell-to-cell variations in duration and shape of APs and [Ca 2+ ] i transients have been observed [9, 17, 18, 19, 20, 21]. By simultaneously measuring electrical activity and [Ca 2+ ] i levels in perforated-patch current-clamped individual GH 3 cells, we have recently shown that the firing frequency constitutes a primary factor determining the averaged [Ca 2+ ] i , but also that the magnitude of the [Ca 2+ ] i oscillations is highly dependent on the size and duration of the APs [21].…”

Section: Introductionmentioning

confidence: 99%

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Role of BK Potassium Channels Shaping Action Potentials and the Associated [Ca2+]i Oscillations in GH3 Rat Anterior Pituitary Cells

Miranda

Peña²,

Gómez-Varela³

et al. 2003

Neuroendocrinology

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Measurements of electrical activity and intracellular Ca²⁺ levels were performed in perforated-patch clamped GH₃ cells to determine the contribution of large-conductance calcium-activated K⁺ (BK) channels to action potential repolarization and size of the associated Ca²⁺ oscillations. By examining the dependence of action potential (AP) duration on extracellular Ca²⁺ levels in the presence and the absence of the specific BK channel blocker paxilline, it is observed that plateau-like action potentials are associated to low densities of paxilline-sensitive currents. Extracellular Ca²⁺ increases or paxilline additions are not able to largely modify action potential duration in cells showing a reduced expression of BK currents. Furthermore, specific blockade of these currents with paxilline systematically elongates AP duration, but only under conditions in which short APs and/or prominent BK currents recorded under voltage-clamp mode are present in the same cells. Our data indicate that in GH₃ cells, BK channels act primarily ending the action potential and suggest that by contributing to fine-tuning cellular electrical properties and hence intracellular Ca²⁺ variations, BK channels may play an important role on time- and cell-dependent modulation of physiological outputs in adenohypophyseal cells.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Role of BK Potassium Channels Shaping Action Potentials and the Associated [Ca2+]i Oscillations in GH3 Rat Anterior Pituitary Cells

Miranda

Peña²,

Gómez-Varela³

et al. 2003

Neuroendocrinology

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The role of the inwardly rectifying K+ current in resting potential and thyrotropin-releasing-hormone-induced changes in cell excitability of GH3 rat anterior pituitary cells

et al. 1994

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Exposure of GH3 rat anterior pituitary cells to cholera toxin for 2-4 h significantly increased the thyrotropin-releasing-hormone(TRH)-induced inhibition of the inwardly rectifying K+ current studied in patch-perforated voltage-clamped cells. On the other hand, the current reduction became almost totally irreversible after washout of the neuropeptide. Comparison of the effects elicited by the toxin with those of 8-(4-chlorophenylthio)-cAMP or forskolin plus isobutylmethylxanthine indicated that, although the irreversibility may be due, at least in part, to elevations of cAMP levels, the enhancement of the TRH-induced inhibition of the current is not mediated by the cyclic nucleotide. Only reductions on the inwardly rectifying K+ current, but not those elicited by TRH on voltage-dependent Ca2+ currents, were increased by the treatment with cholera toxin. In current-clamped cells showing similar rates of firing, the second phase of enhanced action-potential frequency induced by TRH was also significantly potentiated by cholera toxin. Measurements of [Ca2+]i oscillations associated with electrical activity, using video imaging with fura-2-loaded cells, demonstrated that cholera toxin treatment causes a clear reduction of spontaneous [Ca2+]i oscillations. However, this did not prevent the stimulatory effect of TRH on oscillations due to the action potentials. In cholera-toxin-treated cells, the steady-state, voltage dependence of inactivation of the inward rectifier was shifted by nearly 20 mV to more negative values. These data suggest that the inwardly rectifying K+ current plays an important role in maintenance of the resting K+ conductance in GH3 cells. Furthermore, the TRH-induced reductions on this current may be an important factor contributing to the increased cell excitability promoted by the neuropeptide.

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Capacitative Ca2+ entry contributes to the Ca2+ influx induced by thyrotropin-releasing hormone (TRH) in GH3 pituitary cells

Alonso

García‐Sancho

1995

Pflugers Arch.

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Treatment of GH3 cells with either hypothalamic peptide thyrotropin-releasing hormone (TRH), the endomembrane Ca2+-ATPase inhibitor thapsigargin or the Ca2+ ionophore ionomycin mobilized, with different kinetics, essentially all of the Ca2+ pool from the intracellular Ca2+ stores. Any of the above- described treatments induced a sustained increase in intracellular Ca2+ concentration ([Ca2+]i), which was dependent on extracellular Ca2+ and was prevented by Ni2+ but not by dihydropyridines (DHPs), suggesting that it was due to capacitative Ca2+ entry via activation of a plasma membrane pathway which opened upon the emptying of the intracellular Ca2+ stores. The increase of the plasma membrane permeability to Ca2+ correlated negatively with the filling degree of the intracellular Ca2+ stores and was reversed by refilling of the stores. The mechanism of capacitative Ca2+ entry into GH3 cells differed from similar mechanisms described in several types of blood cells in that the pathway was poorly permeable to Mn2+ and not sensitive to cytochrome P450 inhibitors. In GH3 cells, TRH induced a transient [Ca2+]i increase due to Ca2+ release from the stores (phase 1) followed by a sustained [Ca2+]i increase due to Ca2+ entry (phase 2). At the single-cell level, phase 2 was composed of a DHP-insensitive sustained [Ca2+]i increase, due to activation of capacitative Ca2+ entry, superimposed upon which DHP- sensitive [Ca2+]i oscillations took place. The two components of the TRH-induced Ca2+ entry differed also in that [Ca2+]i oscillations remained for several minutes after TRH removal, whereas the sustained [Ca2+]i increase dropped quickly to prestimulatory levels, following the same time course as the refilling of the stores. The drop was prevented when the refilling was inhibited by thapsigargin. It is concluded that, even though the mechanisms of capacitative Ca2+ entry may show differences from cell to cell, it is also present and may contribute to the regulation of physiological functions in excitable cells such as GH3. There, capacitative Ca2+ entry cooperates with voltage-gated Ca2+ channels to generate the [Ca2+]i increase seen during phase 2 of TRH action. This contribution of capacitative Ca2+ entry may be relevant to the enhancement of prolactin secretion induced by TRH.

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Okadaic acid and calyculin A enhance the effect of thyrotropin‐releasing hormone on GH₃ rat anterior pituitary cells excitability

Cited by 15 publications

References 29 publications

Role of BK Potassium Channels Shaping Action Potentials and the Associated [Ca<sup>2+</sup>]<sub>i</sub> Oscillations in GH<sub>3</sub> Rat Anterior Pituitary Cells

Role of BK Potassium Channels Shaping Action Potentials and the Associated [Ca<sup>2+</sup>]<sub>i</sub> Oscillations in GH<sub>3</sub> Rat Anterior Pituitary Cells

The role of the inwardly rectifying K+ current in resting potential and thyrotropin-releasing-hormone-induced changes in cell excitability of GH3 rat anterior pituitary cells

Capacitative Ca2+ entry contributes to the Ca2+ influx induced by thyrotropin-releasing hormone (TRH) in GH3 pituitary cells

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