Corticotropin releasing hormone inhibits an inwardly rectifying potassium current in rat corticotropes

Kuryshev, Yuri A.; Haak, Lee; Childs, Gwen V.; Ritchie, A K

doi:10.1111/j.1469-7793.1997.265bk.x

Cited by 46 publications

(83 citation statements)

References 38 publications

(58 reference statements)

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“…In accordance with literature data in other pituitary cell types (Kuryshev et al, 1997), 5 mM Cs ϩ reduced the K ϩ current in lactotrophs (Fig. 8, A and B).…”

Section: Characterization Of Ksupporting

confidence: 79%

“…Two channels expressed in pituitary lactotrophs could mediate the ET-1-induced and Cs ϩ -sensitive hyperpolarizing current: K ir channels (Einhorn et al, 1991;Kuryshev et al, 1997) and/or ether-a go-go-related gene (erg)-like K ϩ channels (Schafer et al, 1999;Schledermann et al, 2001). Both channels are activated by hyperpolarizing pulses, exhibit inward rectification, and can be blocked by Cs ϩ .…”

Section: Characterization Of Kmentioning

confidence: 99%

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Ca²⁺-Mobilizing Endothelin-A Receptors Inhibit Voltage-Gated Ca²⁺ Influx through G_i/oSignaling Pathway in Pituitary Lactotrophs

Tomić

Goor

et al. 2002

Mol Pharmacol

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In excitable cells, receptor-induced Ca 2ϩ release from intracellular stores is usually accompanied by sustained depolarization of cells and facilitated voltage-gated Ca 2ϩ influx (VGCI). In quiescent pituitary lactotrophs, however, endothelin-1 (ET-1) induced rapid Ca 2ϩ release without triggering Ca 2ϩ influx. Furthermore, in spontaneously firing and depolarized lactotrophs, the Ca 2ϩ -mobilizing action of ET-1 was followed by inhibition of spontaneous VGCI caused by prolonged cell hyperpolarization and abolition of action potential-driven Ca 2ϩ influx. Agonistinduced depolarization of cells and enhancement of VGCI upon Ca 2ϩ mobilization was established in both quiescent and firing lactotrophs treated overnight with pertussis toxin (PTX). Activation of adenylyl cyclase by forskolin and addition of cellpermeable 8-bromo-cAMP did not affect ET-1-induced sustained inhibition of VGCI, suggesting that the cAMP-protein kinase A signaling pathway does not mediate the inhibitory action of ET-1 on VGCI. Consistent with the role of PTX-sensitive K ϩ channels in ET-1-induced hyperpolarization of control cells, but not PTX-treated cells, ET-1 decreased the cell input resistance and activated a 5 mM Cs ϩ -sensitive K ϩ current. In the presence of Cs ϩ , ET-1 stimulated VGCI in a manner comparable with that observed in PTX-treated cells, whereas E-4031, a specific blocker of ether-a-go-go-related gene-like K ϩ channels, was ineffective. Similar effects of PTX and Cs ϩ were also observed in GH 3 immortalized cells transiently expressing ET A receptors. These results indicate that signaling of ET A receptors through the G i/o pathway in lactotrophs and the subsequent activation of inward rectifier K ϩ channels provide an effective and adenylyl cyclase-independent mechanism for a prolonged uncoupling of Ca 2ϩ mobilization and influx pathways.

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“…In accordance with literature data in other pituitary cell types (Kuryshev et al, 1997), 5 mM Cs ϩ reduced the K ϩ current in lactotrophs (Fig. 8, A and B).…”

Section: Characterization Of Ksupporting

confidence: 79%

Section: Characterization Of Kmentioning

confidence: 99%

Ca²⁺-Mobilizing Endothelin-A Receptors Inhibit Voltage-Gated Ca²⁺ Influx through G_i/oSignaling Pathway in Pituitary Lactotrophs

Tomić

Goor

et al. 2002

Mol Pharmacol

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“…The blockade of I K(IR) did not prevent the effect of CRH on LC neurons although barium readily blocked the inward rectification. Collectively, these data suggest that CRH modulates LC neuron activity via a different potassium conductance than has been suggested for corticotropes and neurons in the hippocampus and amygdala (Siggins et al, 1985;Aldenhoff, 1986;Rainnie et al, 1992;Kuryshev et al, 1997).…”

Section: Potential Mechanism Of Crh Action: Potassium Conductancesmentioning

confidence: 87%

Corticotropin-Releasing Hormone Directly Activates Noradrenergic Neurons of the Locus Ceruleus RecordedIn Vitro

Jedema¹,

Grace²

2004

J. Neurosci.

153

126

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The neuropeptide corticotropin-releasing hormone (CRH) activates locus ceruleus (LC) neurons, thereby increasing norepinephrine levels throughout the CNS. Despite anatomical and physiological evidence for CRH innervation of the LC, the mechanism of CRH-evoked activation of LC neurons is unknown. Moreover, given the apparent absence of mRNA for CRH receptors in LC neurons, the exact location of action of CRH within the cerulear region is debated. Using in vitro intracellular recordings from rat brainstem, we examined whether CRH exerts a direct effect on LC neurons and which ionic currents are likely affected by CRH. We demonstrate that CRH dose-dependently increases the firing rate of LC neurons through a direct (TTX-and cadmium-insensitive) mechanism by decreasing a potassium conductance. The CRH-evoked activation of LC neurons is, at least in part, mediated by CRH 1 receptors and a cAMP-dependent second messenger system. These data provide additional support that CRH functions as an excitatory neurotransmitter in the LC and the hypothesis that dysfunction of the CRH peptidergic and noradrenergic systems observed in patients with mood and anxiety disorders are functionally related.

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“…In contrast, cultured gonadotrophs exclusively exhibit axonal type APs that are associated with small-amplitude Ca 2ϩ transients and low basal gonadotropin release (van Goor et al 2001b). Corticotrophs also fire axonal type of APs spontaneously (Kuryshev et al 1997).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of Spontaneous and Receptor-Controlled Electrical Activity in Pituitary Somatotrophs: Experiments and Theory

Tsaneva-Atanasova

Sherman²,

Goor³

et al. 2007

Journal of Neurophysiology

135

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. Cultured pituitary somatotrophs release growth hormone in response to spontaneous Ca 2ϩ entry through voltage-gated calcium channels (VGCCs) that is governed by plateau-bursting electrical activity and is regulated by several neurohormones, including GH-releasing hormone (GHRH) and somatostatin. Here we combine experiments and theory to clarify the mechanisms underlying spontaneous and receptor-controlled electrical activity. Experiments support a role of a Na ϩ -conducting and tetrodotoxin-insensitive channel in controlling spontaneous and GHRH-stimulated pacemaking, the latter in a cAMP-dependent manner; an opposing role of spontaneously active inwardly rectifying K ϩ (K ir ) channels and G-protein-regulated K ir channels in somatostatin-mediated inhibition of pacemaking; as well as a role of VGCCs in spiking and large conductance (BK-type) Ca 2ϩ -activated K ϩ channels in plateau bursting. The mathematical model is compatible with a wide variety of experimental data involving pharmacology and extracellular ion substitution and supports the importance of constitutively active tetrodotoxin-insensitive Na ϩ and K ir channels in maintaining spontaneous pacemaking in pituitary somatotrophs. The model also suggests that these channels are involved in the up-and downregulation of electrical activity by GHRH and somatostatin. In the model, the plateau bursting is controlled by two functional populations of BK channels, characterized by distance from the VGCCs. The rapid activation of the proximal BK channels is critical for the establishment of the plateau, whereas slow recruitment of the distal BK channels terminates the plateau. I N T R O D U C T I O NIn the absence of hypothalamic factors in vitro, the membrane potential (V m ) of secretory anterior pituitary cells in culture is not stable but oscillates from the baseline potential of about -60 mV. When V m oscillations reach the threshold level, pituitary cells fire action potentials (APs). This is a common feature of all secretory anterior pituitary cell types and is observed in 15-80% of cells, depending on the cell type and preparation Stojilkovic and Catt 1992). The majority of cultured somatotrophs and lactotrophs frequently exhibit broader V m oscillations in the form of a depolarizing plateau with bursts of APs superimposed. These spikes are small in amplitude and usually do not reach 0 mV (Kwiecien et al. 1997;Sims et al. 1991;van Goor et al. 2001a). Such complex plateau bursting activity is periodic and results in an oscillatory increase in intracellular Ca 2ϩ concentration ([Ca 2ϩ

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Corticotropin releasing hormone inhibits an inwardly rectifying potassium current in rat corticotropes

Cited by 46 publications

References 38 publications

Ca²⁺-Mobilizing Endothelin-A Receptors Inhibit Voltage-Gated Ca²⁺ Influx through G_i/oSignaling Pathway in Pituitary Lactotrophs

Ca²⁺-Mobilizing Endothelin-A Receptors Inhibit Voltage-Gated Ca²⁺ Influx through G_i/oSignaling Pathway in Pituitary Lactotrophs

Corticotropin-Releasing Hormone Directly Activates Noradrenergic Neurons of the Locus Ceruleus RecordedIn Vitro

Mechanism of Spontaneous and Receptor-Controlled Electrical Activity in Pituitary Somatotrophs: Experiments and Theory

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Corticotropin releasing hormone inhibits an inwardly rectifying potassium current in rat corticotropes

Cited by 46 publications

References 38 publications

Ca2+-Mobilizing Endothelin-A Receptors Inhibit Voltage-Gated Ca2+ Influx through Gi/oSignaling Pathway in Pituitary Lactotrophs

Ca2+-Mobilizing Endothelin-A Receptors Inhibit Voltage-Gated Ca2+ Influx through Gi/oSignaling Pathway in Pituitary Lactotrophs

Corticotropin-Releasing Hormone Directly Activates Noradrenergic Neurons of the Locus Ceruleus RecordedIn Vitro

Mechanism of Spontaneous and Receptor-Controlled Electrical Activity in Pituitary Somatotrophs: Experiments and Theory

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Product

Resources

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Ca²⁺-Mobilizing Endothelin-A Receptors Inhibit Voltage-Gated Ca²⁺ Influx through G_i/oSignaling Pathway in Pituitary Lactotrophs

Ca²⁺-Mobilizing Endothelin-A Receptors Inhibit Voltage-Gated Ca²⁺ Influx through G_i/oSignaling Pathway in Pituitary Lactotrophs