Endogenous somatostatin receptors mobilize calcium from inositol 1,4,5-trisphosphate-sensitive stores in NG108-15 cells

Duck Joo Rhie, Jong Ho Sung, U. Sin Ha, Hee Jung Kim, Do Sik Min, Sang June Hahn, Myung Suk Kim, Yang Hyeok Jo, Shin Hee Yoon

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Somatostatin receptors are members of the G-protein-coupled receptor superfamily and exert their principal effects by coupling to inhibitory G-proteins. We used fura-2-based digital calcium imaging and assayed for [3H]inositol phosphates (IPs) to study the effects of somatostatin on intracellular calcium signaling in neuroblastomaXglioma NG108-15 cells. Both somatostatin-14 and octreotide induced concentration-dependent increases in intracellular Ca2+ concentration ([Ca2+]i). Thirty-four percent of the cells responded to treatment with 100 nM somatostatin-14. Somatostatin-induced responses were not blocked by the removal of extracellular calcium; instead, they were abolished by pretreatment with 100 nM thapsigargin, an agent that depletes and prevents refilling of intracellular Ca2+ stores. Pretreatment with the inositol 1,4,5-trisphosphate (IP3) receptor antagonist xestospongin C (10 μM) for 20 min inhibited markedly the somatostatin-induced response. Somatostatin (100 nM) increased [3H]IPs formation. U73122 (1 μM), an inhibitor of phospholipase C (PLC), completely blocked the somatostatin-induced [Ca2+]i increases and the formation of [3H]IPs. Pretreatment with pertussis toxin (PTX, 200 ng/ml) for 24 h blocked the somatostatin-induced responses. Thus, we conclude that activation of endogenous somatostatin receptors in NG108-15 cells induces the release of calcium from IP3-sensitive intracellular stores through PTX-sensitive G-protein-coupled PLC.

Original languageEnglish
Pages (from-to)120-128
Number of pages9
JournalBrain Research
Volume975
Issue number1-2
DOIs
Publication statusPublished - 2003 Jun 13

Fingerprint

Somatostatin Receptors
Inositol 1,4,5-Trisphosphate
Somatostatin
Calcium
Inositol Phosphates
Type C Phospholipases
GTP-Binding Proteins
Inositol 1,4,5-Trisphosphate Receptors
Thapsigargin
Calcium Signaling
Octreotide
Fura-2
Pertussis Toxin
G-Protein-Coupled Receptors

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

Rhie, Duck Joo ; Sung, Jong Ho ; Ha, U. Sin ; Kim, Hee Jung ; Min, Do Sik ; Hahn, Sang June ; Kim, Myung Suk ; Jo, Yang Hyeok ; Yoon, Shin Hee. / Endogenous somatostatin receptors mobilize calcium from inositol 1,4,5-trisphosphate-sensitive stores in NG108-15 cells. In: Brain Research. 2003 ; Vol. 975, No. 1-2. pp. 120-128.
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Endogenous somatostatin receptors mobilize calcium from inositol 1,4,5-trisphosphate-sensitive stores in NG108-15 cells. / Rhie, Duck Joo; Sung, Jong Ho; Ha, U. Sin; Kim, Hee Jung; Min, Do Sik; Hahn, Sang June; Kim, Myung Suk; Jo, Yang Hyeok; Yoon, Shin Hee.

In: Brain Research, Vol. 975, No. 1-2, 13.06.2003, p. 120-128.

Research output: Contribution to journalArticle

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AU - Rhie, Duck Joo

AU - Sung, Jong Ho

AU - Ha, U. Sin

AU - Kim, Hee Jung

AU - Min, Do Sik

AU - Hahn, Sang June

AU - Kim, Myung Suk

AU - Jo, Yang Hyeok

AU - Yoon, Shin Hee

PY - 2003/6/13

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N2 - Somatostatin receptors are members of the G-protein-coupled receptor superfamily and exert their principal effects by coupling to inhibitory G-proteins. We used fura-2-based digital calcium imaging and assayed for [3H]inositol phosphates (IPs) to study the effects of somatostatin on intracellular calcium signaling in neuroblastomaXglioma NG108-15 cells. Both somatostatin-14 and octreotide induced concentration-dependent increases in intracellular Ca2+ concentration ([Ca2+]i). Thirty-four percent of the cells responded to treatment with 100 nM somatostatin-14. Somatostatin-induced responses were not blocked by the removal of extracellular calcium; instead, they were abolished by pretreatment with 100 nM thapsigargin, an agent that depletes and prevents refilling of intracellular Ca2+ stores. Pretreatment with the inositol 1,4,5-trisphosphate (IP3) receptor antagonist xestospongin C (10 μM) for 20 min inhibited markedly the somatostatin-induced response. Somatostatin (100 nM) increased [3H]IPs formation. U73122 (1 μM), an inhibitor of phospholipase C (PLC), completely blocked the somatostatin-induced [Ca2+]i increases and the formation of [3H]IPs. Pretreatment with pertussis toxin (PTX, 200 ng/ml) for 24 h blocked the somatostatin-induced responses. Thus, we conclude that activation of endogenous somatostatin receptors in NG108-15 cells induces the release of calcium from IP3-sensitive intracellular stores through PTX-sensitive G-protein-coupled PLC.

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