Activation of CCK-B receptors elevates cytosolic Ca2+ levels in a pituitary cell line

Kuwahara, Toshikazu; Nagase, Hajime; Takamiya, Mari; Yoshizaki, H; Kudoh, Tsutomu; Nakano, Atsuko; Arisawa, Mikio

doi:10.1016/0196-9781(93)90117-y

Cited by 14 publications

(10 citation statements)

References 27 publications

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“…This spike and plateau pattern also is produced by activation of CCK-B receptors in a variety of other preparations, including pituitary cells (24), pancreatic duct cells (47), lymphocytes (31), pancreatic tumor cells (41), small cell lung cancer cells (48), and gastric D cells (13). In these responses the spike of calcium arises from intracellular stores and the plateau comes from extracellular sources.…”

Section: General Characteristics Of the Cck-8-induced Calcium Responsmentioning

confidence: 99%

“…CCK induces an increase in cytosolic calcium in a variety of different cells; however, the nature of the CCK-induced calcium signal varies depending on the preparation under study and concentration of CCK used. These CCK-induced calcium signals range from an oscillating signal independent of extracellular calcium (52,57), to a single spike of calcium from intracellular sources (19), to a spike and plateau pattern with the spike from intracellular sources and the plateau from extracellular sources (13,24,31,34,41,44,47,48), to a single spike of calcium that is totally dependent on extracellular calcium (35).…”

Section: General Characteristics Of the Cck-8-induced Calcium Responsmentioning

confidence: 99%

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Cholecystokinin increases cytosolic calcium in a subpopulation of cultured vagal afferent neurons

Simasko

Wiens

Karpiel

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: General Characteristics Of the Cck-8-induced Calcium Responsmentioning

confidence: 99%

Section: General Characteristics Of the Cck-8-induced Calcium Responsmentioning

confidence: 99%

Cholecystokinin increases cytosolic calcium in a subpopulation of cultured vagal afferent neurons

Simasko

Wiens

Karpiel

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…These cells produce prolactin (as well as growth hormone) and their secretory activity is controlled by neuropeptides as thyrotropin-releasing hormone, vasoactive intestinal peptide and cholecystokinin, which act as activators of prolactin secretion in vivo [11, 12]. It is also known that similar mechanisms (i.e.…”

Section: Introductionmentioning

confidence: 99%

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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“…Both receptors couple to G-proteins (Wank et al, 1994), and their relative distributions in the CNS and peripheral nervous system correlate well with CCK immunoreactivity (Dockray, 1987;Hays et al, 1980;Innis and Snyder, 1980). Cholecystokinin receptors have been shown to interact with several different cellular transduction systems in central and peripheral tissues, including the activation of phospholipase C (Kuwahara et al, 1993;Lee et al, 1993;Wu and Wang, 1996b), the modulation of potassium and calcium channels (Boden and Hill, 1988;Buckett and Saint, 1989;Miyoshi et al, 1991;Branchereau et al, 1993;Cox et al, 1995;Liu et al, 1995), and activation of nonselective cation channels (Dodd and Kelly, 1981;Jarvis et al, 1992).…”

mentioning

confidence: 99%

Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

Miller¹,

Hoffer²,

Svoboda³

et al. 1997

J. Neurosci.

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Cholecystokinin (CCK) is found co-localized with the inhibitory neurotransmitter GABA in interneurons of the hippocampus. Also, CCK receptors are found in abundance in this brain region. The possibility that CCK alters interneuron activity was examined using whole-cell current-and voltage-clamp recordings from visualized interneurons in the stratum radiatum of area CA1 in rat hippocampal slices. The effect of CCK on GABA-mediated IPSCs was also determined in pyramidal neurons. The sulfated octapeptide CCK-8S increased action potential frequency or generated inward currents in the majority of interneurons. These effects of CCK persisted in the presence of tetrodotoxin and cadmium, suggesting that they were direct. Current-voltage plots revealed that CCK-8S inhibited a conductance that was linear across command potentials and reversed near the equilibrium potential for K ϩ ions. The K ϩ channel blocker tetraethylammonium (10 mM) generated inward currents similar to those initiated by CCK, and it occluded the effect of the peptide. BaCl 2 (1 mM) and 4-aminopyridine (2 mM) did not alter the effect of CCK. The CCK B receptor antagonist PD-135,158 completely blocked the inward currents generated by CCK-8S. CCK also resulted in an increase in spontaneous action potential-dependent IPSC frequency, but no changes in action potential-independent miniature IPSCs or evoked IPSCs in pyramidal neurons. These results provide evidence that CCK can depolarize hippocampal interneurons through the inhibition of a resting K ϩ conductance, leading to increased tonic inhibition of pyramidal neurons. This action of CCK may contribute to its anticonvulsant properties, as observed in limbic seizure models.

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Activation of CCK-B receptors elevates cytosolic Ca2+ levels in a pituitary cell line

Cited by 14 publications

References 27 publications

Cholecystokinin increases cytosolic calcium in a subpopulation of cultured vagal afferent neurons

Cholecystokinin increases cytosolic calcium in a subpopulation of cultured vagal afferent neurons

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

Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

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Activation of CCK-B receptors elevates cytosolic Ca2+ levels in a pituitary cell line

Cited by 14 publications

References 27 publications

Cholecystokinin increases cytosolic calcium in a subpopulation of cultured vagal afferent neurons

Cholecystokinin increases cytosolic calcium in a subpopulation of cultured vagal afferent neurons

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

Cholecystokinin Increases GABA Release by Inhibiting a Resting K+Conductance in Hippocampal Interneurons

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Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons