Calcium Signaling Systems

Stojilković, Stanko S.

doi:10.1002/cphy.cp070109

Cited by 3 publications

(4 citation statements)

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“…These results indicate that ET-1 induces a rapid Ca 2ϩ mobilization from intracellular stores, followed by a sustained Ca 2ϩ influx of a limiting capacity. In this respect, the action of ET-1 in quiescent somatotrophs does not differ from those observed in nonexcitable cells (Stojilkovic, 1998).…”

Section: Effects Of Endothelin and Somatostatin On [Ca 2؉ ] I In Somamentioning

confidence: 64%

“…Because many different ionic channels act in concert to control AP firing, this pathway is referred to as the membrane potential (V m )-dependent pathway for C a 2ϩ signaling (Stojilkovic, 1998). Several of the ionic channels contributing to the V m pathway in somatotrophs have been identified.…”

Section: Abstract: Somatotrophs; Growth Hormone; Calcium; Endothelinmentioning

confidence: 99%

“…The specificity in the operation of Ca 2ϩ -mobilizing receptors in excitable cells is in the need for the synchronization of voltage-gated Ca 2ϩ influx with Ca 2ϩ mobilization (Stojilkovic, 1998). For example, in pituitary lactotrophs and GT1 neurons the activation of thyrotropin-releasing hormone (TRH) and gonadotropinreleasing hormone (GnRH) receptors, respectively, generates biphasic changes in V m and [Ca 2ϩ ] i .…”

Section: Abstract: Somatotrophs; Growth Hormone; Calcium; Endothelinmentioning

confidence: 99%

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Expression of Ca²⁺-Mobilizing Endothelin_AReceptors and Their Role in the Control of Ca²⁺Influx and Growth Hormone Secretion in Pituitary Somatotrophs

et al. 1999

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The expression and coupling of endothelin (ET) receptors were studied in rat pituitary somatotrophs. These cells exhibited periods of spontaneous action potential firing that generated high-amplitude fluctuations in cytosolic calcium concentration ([Ca 2ϩ ] i ). The message and the specific binding sites for ET A , but not ET B , receptors were found in mixed pituitary cells and in highly purified somatotrophs. The activation of these receptors by ET-1 led to an increase in inositol 1,4,5-trisphosphate production and the associated rise in [Ca 2ϩ ] i and growth hormone (GH) secretion. The Ca 2ϩ -mobilizing action of ET-1 lasted for 2-3 min and was followed by an inhibition of action potential-driven Ca 2ϩ influx and GH secretion to below the basal levels. As in somatostatin-treated cells, the ET-1-induced inhibition of spontaneous electrical activity and Ca 2ϩ influx was accompanied by the inhibition of adenylyl cyclase and by the stimulation of inward rectifier potassium current. In contrast to somatostatin, ET-1 did not inhibit voltage-gated Ca 2ϩ channels. During prolonged agonist stimulation a gradual recovery of Ca 2ϩ influx and GH secretion occurred. In somatotrophs treated with pertussis toxin overnight, the ET-1-induced Ca 2ϩ -mobilizing phase was preserved, but it was followed immediately by facilitated Ca 2ϩ influx and GH secretion. Both somatostatin-and ET-1-induced inhibitions of adenylyl cyclase activity were abolished in pertussis toxin-treated cells. These results indicate that the transient cross-coupling of Ca 2ϩ -mobilizing ET A receptors to the G i /G o pathway in somatotrophs provides an effective mechanism to change the rhythm of [Ca 2ϩ ] i signaling and GH secretion during continuous agonist stimulation. Key words: somatotrophs; growth hormone; calcium; endothelin; somatostatin; electrical activityAction potential (AP)-driven C a 2ϩ influx through voltage-gated calcium channels (VGCC s) is operative in various endocrine and neuroendocrine cells, including pituitary somatotrophs. Because many different ionic channels act in concert to control AP firing, this pathway is referred to as the membrane potential (V m )-dependent pathway for C a 2ϩ signaling (Stojilkovic, 1998). Several of the ionic channels contributing to the V m pathway in somatotrophs have been identified. These include VGCCs, voltage-gated sodium channels, pacemaker and ATP-gated cationic channels, and several types of potassium channels, including inwardly rectif ying potassium channels (K ir ) (Lewis et al., 1988;Sims et al., 1991;Brake et al., 1994;Koshimizu et al., 1998). Although resting somatotrophs have a fluctuating V m , Kwiecien and colleagues (1997) have found that these pacemaker fluctuations were unable to initiate spontaneous APs in a majority of cultured somatotrophs. Consequently, they suggested that somatotrophs behave as "conditional pacemakers," because the activation of adenylyl cyclase-coupled receptors is required for AP generation. However, others have observed spontaneous APs (Sims et al., 1991) a...

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Section: Effects Of Endothelin and Somatostatin On [Ca 2؉ ] I In Somamentioning

confidence: 64%

Section: Abstract: Somatotrophs; Growth Hormone; Calcium; Endothelinmentioning

confidence: 99%

Section: Abstract: Somatotrophs; Growth Hormone; Calcium; Endothelinmentioning

confidence: 99%

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Expression of Ca²⁺-Mobilizing Endothelin_AReceptors and Their Role in the Control of Ca²⁺Influx and Growth Hormone Secretion in Pituitary Somatotrophs

et al. 1999

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“…Testicular GnRH receptors have been reported in several species, including humans (87,88). In rats, GnRH affects Ca 2+ mobilisation (89) as well as steroidogenesis in Leydig cells (90). This reported direct effect of GnRH on steroidogenesis is especially noteworthy for the present study because, although testosterone implants returned testosterone concentrations to the normal range in castrated rats, the elevation in testosterone was lower in deslorelin‐treated intact rats.…”

Section: Discussionmentioning

confidence: 99%

Predominant Suppression of Follicle‐Stimulating Hormone β‐Immunoreactivity after Long‐Term Treatment of Intact and Castrate Adult Male Rats with the Gonadotrophin‐Releasing Hormone Agonist Deslorelin

Smith

Cheryl

Edwards

et al. 2012

J Neuroendocrinology

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GnRH agonists are used to treat gonadal steroid-dependent disorders in humans and contracept animals. These agonists are thought to work by desensitizing gonadotropes to GnRH, thereby suppressing FSH and LH secretion. It is not known whether changes occur in the cellular composition of the pituitary gland following chronic GnRH agonist exposure. Adult male Sprague-Dawley rats were treated with a sham, deslorelin, or deslorelin plus testosterone implant for 41.0±0.6 days. In a second experiment, rats were castrated and treated with deslorelin and/or testosterone. Pituitary sections were labeled immunocytochemically for FSHβ and LHβ, or αGSU. Deslorelin suppressed testis weight by two thirds and reduced plasma FSH and LH in intact rats. Deslorelin decreased the percentage of gonadotropes but the effect was specific to the FSHβ-ir cells. Testosterone did not reverse the deslorelin-induced reduction in the overall gonadotrope population. However, in the presence of testosterone, the proportion of gonadotropes that was FSHβ-ir increased in the remaining gonadotropes. There was no effect of treatment on the total LHβ-ir cell population although the loss of FSHβ in bi-hormonal cells increased the proportion of mono-hormonal LHβ-ir gonadotropes. The castration-induced plasma LH and FSH increases were suppressed by deslorelin, testosterone or both. Castration increased both LH-ir and FSH-ir without increasing the overall gonadotrope population; thus increasing the proportion of bi-hormonal cells. Deslorelin suppressed these increases. Testosterone increased FSH-ir in deslorelin-treated castrate rats. Deslorelin did not affect αGSU immunoreactivity, suggesting that the gonadotrope population per se is not eliminated by deslorelin but the ability of gonadotropes to synthesize FSHβ is compromised. We hypothesize that the FSH dominant suppression may be central to the long-term contraceptive efficacy of deslorelin in the male.

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Hypothalamic control of gonadotropin secretion

McCann

Karanth

Mastronardi

et al. 2002

Progress in Brain Research

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Calcium Signaling Systems

Cited by 3 publications

References 501 publications

Expression of Ca²⁺-Mobilizing Endothelin_AReceptors and Their Role in the Control of Ca²⁺Influx and Growth Hormone Secretion in Pituitary Somatotrophs

Expression of Ca²⁺-Mobilizing Endothelin_AReceptors and Their Role in the Control of Ca²⁺Influx and Growth Hormone Secretion in Pituitary Somatotrophs

Predominant Suppression of Follicle‐Stimulating Hormone β‐Immunoreactivity after Long‐Term Treatment of Intact and Castrate Adult Male Rats with the Gonadotrophin‐Releasing Hormone Agonist Deslorelin

Hypothalamic control of gonadotropin secretion

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Calcium Signaling Systems

Cited by 3 publications

References 501 publications

Expression of Ca2+-Mobilizing EndothelinAReceptors and Their Role in the Control of Ca2+Influx and Growth Hormone Secretion in Pituitary Somatotrophs

Expression of Ca2+-Mobilizing EndothelinAReceptors and Their Role in the Control of Ca2+Influx and Growth Hormone Secretion in Pituitary Somatotrophs

Predominant Suppression of Follicle‐Stimulating Hormone β‐Immunoreactivity after Long‐Term Treatment of Intact and Castrate Adult Male Rats with the Gonadotrophin‐Releasing Hormone Agonist Deslorelin

Hypothalamic control of gonadotropin secretion

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Expression of Ca²⁺-Mobilizing Endothelin_AReceptors and Their Role in the Control of Ca²⁺Influx and Growth Hormone Secretion in Pituitary Somatotrophs

Expression of Ca²⁺-Mobilizing Endothelin_AReceptors and Their Role in the Control of Ca²⁺Influx and Growth Hormone Secretion in Pituitary Somatotrophs