The Effects of Ions, Metabolic Inhibitors, and Colchicine on Luteinizing Hormone-Releasing Hormone Release from Superfused Rat Hypothalami*

Hartter, Daryl E.; Ramírez, Victor D.

doi:10.1210/endo-107-2-375

Cited by 57 publications

(17 citation statements)

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“…However, the observation of progressively smalleramplitude GnRH pulses after the short-term (0-72 min) removal of Ca2' suggests that intracellular Ca2+ stores (or residual extracellular Ca2W) can transiently maintain episodic GnRH release. This is in agreement with the observation that K+-induced GnRH release was initially delayed and finally blocked by the removal of extracellular Ca2W in superfused rat hypothalami (24). Further studies will be necessary to determine the role of intracellular and extracellular Ca2" in the pulsatile release of GnRH.…”

Section: Discussionsupporting

confidence: 89%

Generation and synchronization of gonadotropin-releasing hormone (GnRH) pulses: intrinsic properties of the GT1-1 GnRH neuronal cell line.

Escalera

Choi

Weiner

1992

Proc. Natl. Acad. Sci. U.S.A.

235

130

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The immortalized neuronal cell line GT1-1 was used to investigate the endogenous pattern of GnRH release. The GT1-1 cell line was derived from a GnRHsecreting tumor in a transgenic mouse induced by genetically targeted expression of the potent simian virus 40 oncogene encoding tumor antigen. Cells attached to coverslips were superfused in Sykes-Moore chambers with Locke's medium, Ca2+-free Locke's medium, or Opti-MEM (another defined medium) for 2 hr, and samples were collected at 4-min intervals. Release of GnRH in 17 of 18 superfusion chambers was seen to be pulsatile when data were analyzed by cluster analysis. No significant differences were observed whether only one or both of the coverslips forming the chamber were coated with cells. Pulses exhibited a mean interpulse interval of 25.8 ± 1.5 min, a mean duration of 18.8 ± 1.4 min, and a mean amplitude of 150.5 + 6.0% above preceding nadir.

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Section: Discussionsupporting

confidence: 89%

Generation and synchronization of gonadotropin-releasing hormone (GnRH) pulses: intrinsic properties of the GT1-1 GnRH neuronal cell line.

Escalera

Choi

Weiner

1992

Proc. Natl. Acad. Sci. U.S.A.

235

130

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“…It is generally accepted that neurosecretion is a Ca2+-dependent process [34], The dependency of hypothalamic GnRH release on extracellular calcium has been demon strated in vitro [3][4][5]35]. We have previously shown that 56 mM K+-induced GnRH secretion from GT| cells is dependent on extracellular Ca2+ [14].…”

Section: Discussionmentioning

confidence: 99%

Signaling Pathways Involved in GnRH Secretion in GT<sub>1</sub> Cells

Escalera¹,

Choi²,

Weiner³

1995

Neuroendocrinology

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The GT₁ GnRH neuronal cell lines exhibit highly differentiated properties of GnRH neurons. We have used GT_1–1 cells to study the role of the cyclic AMP/ protein kinase A, cyclic GMP/protein kinase G and Ca²⁺/protein kinase C signaling pathways in the regulation of GnRH secretion. Superfusion of GT_1–1 cells with the cyclic AMP analog 8-Br-cyclic AMP (0.5 and 2.5 mM) or the adenylate cyclase activator forskolin (1 and 10 µM) for 100 min increased the amplitude of GnRH secretion 2- to 35-fold. The cyclic GMP analog 8-Br-cyclic GMP (2.5 mM) also stimulated the amplitude of GnRH release from superfused GT_1-1 cells, although to a much lesser extent (1.5- to 3-fold). The amplitude of GnRH pulses was also stimulated (5- to 50-fold) by the protein kinase C activator TPA (1 µM). Increasing intracellular Ca²⁺ with an iono-phore (ionomycin, 1 µM) or by the Ca²⁺ channel activator Bay K 8644 (10 µM) also stimulated GnRH release, while secretion was markedly decreased and spontaneous pulsatility abolished by the L-type Ca²⁺ channel blocker methoxyverapamil (10 µM). These results demonstrate that in GT₁ cells the protein kinase A, protein kinase G and protein kinase C pathways are functionally coupled to regulation of GnRH secretion. Furthermore, pulsatile GnRH secretion is coupled to the entry of extracellular Ca²⁺ via L-type Ca²⁺ channels.

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“…Previous studies have demonstrated that colchicine inhibits secretion in a number of tissues including the fl-cell of the pancreas (20), thyroid (47), anterior pituitary (31), parotid (30), lacrimal glands (11), hypothalamus (15), and the liver (10) . In this latter organ, colchicine has been shown to inhibit the release of VLDL (41), albumin, and other plasma proteins (39) .…”

Section: Discussionmentioning

confidence: 99%

“…Colchicine has been shown to inhibit the secretory process in liver (2,10,(39)(40)(41) and other tissues (15,20,21,30,31,47) . It has been shown to have a disorganizing effect on Golgi structure in certain tissues (44) and to inhibit endocytosis in chondrocytes (33), fibroblasts (45), and macrophages (44).…”

mentioning

confidence: 99%

Effect of colchicine on the uptake of prolactin and insulin into Golgi fractions of rat liver.

Posner¹,

Verma²,

Patel³

et al. 1982

The Journal of Cell Biology

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In previous studies we have shown that 125I-labeled prolactin is taken up by a receptor-dependent process and concentrated in an intact form in Golgi elements from female rat liver (J. Biol. Chem., 1979, 254:209-214). In this study we have examined the effect of colchicine on this uptake process into Golgi elements. Colchicine [25 mumol (10 mg)/100 gm body wt] was injected intraperitoneally in adult female rats, and hepatic Golgi fractions were prepared at 1, 2, and 3 h postinjection. The enzyme recoveries and morphological appearance of fractions from colchicine-treated and control (alcohol alone) animals were similar. At times greater than 1 h after colchicine there was a marked (greater than 60%) inhibition of uptake of 125I-ovine prolactin (125I-oPRL) into Golgi light and intermediate fractions but no inhibition of uptake into Golgi heavy and plasmalemma elements. At times from 2 to 45 min postinjection, 125I-oPRL was extracted from Golgi elements and found to be largely intact as judged by rebinding to receptors. The inhibitory effect of colchicine was seen at doses ranging from 0.25 mumol to 25 mumol/100 g body wt. Vincristine also inhibited 125I-oPRL uptake into the Golgi light and intermediate fractions but lumicolchicine had no inhibitory effect. There was a smaller effect of colchicine both at early (1 h) and later (3 h) times on the extent and pattern of 125I-insulin uptake. Colchicine treatment did not produce a significant change in lactogen receptor levels in the Golgi fractions. These results demonstrate that colchicine treatment inhibited the transfer of prolactin into Golgi vesicular elements. The much smaller effect on insulin uptake suggests that there may be differences in the manner in which the two hormones are handled in the course of internalization.

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The Effects of Ions, Metabolic Inhibitors, and Colchicine on Luteinizing Hormone-Releasing Hormone Release from Superfused Rat Hypothalami*

Cited by 57 publications

References 0 publications

Generation and synchronization of gonadotropin-releasing hormone (GnRH) pulses: intrinsic properties of the GT1-1 GnRH neuronal cell line.

Generation and synchronization of gonadotropin-releasing hormone (GnRH) pulses: intrinsic properties of the GT1-1 GnRH neuronal cell line.

Signaling Pathways Involved in GnRH Secretion in GT<sub>1</sub> Cells

Effect of colchicine on the uptake of prolactin and insulin into Golgi fractions of rat liver.

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