G(o)‐2 protein mediates the reduction in Ca2+ currents by somatostatin in cultured ovine somatotrophs.

Chen, Chen; Clarke, I. J.

doi:10.1113/jphysiol.1996.sp021193

Cited by 34 publications

(19 citation statements)

References 19 publications

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“…Furthermore, either because the cells were fragile or because the cells divide, we were unable to do antisense experiments. Gï is known to mediate Ca¥ current inhibition by SRIF in endocrine cells (Kleuss et al 1991;Chen & Clarke, 1996). The subtype of SRIF receptor that mediates the activation of the inward rectifier K¤ channel in AtT-20 cells is unknown.…”

Section: Discussion Srif Response In Locus Coeruleus Neuronesmentioning

confidence: 99%

“…In GH× cells (another cell line from the anterior pituitary), SRIF-induced inhibition of Ca¥ currents is mediated by Gï (Kleuss et al 1991). In ovine somatotrophs (Chen & Clarke, 1996) and in AtT-20 cells (Law & Reisine, 1992) SRIF receptors couple to Gï. Further, Gi1 couples to adenylyl cyclase (Tallent & Reisine, 1992).…”

Section: Specificity Of G Protein á_subunitsmentioning

confidence: 99%

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Different G proteins mediate somatostatin‐induced inward rectifier K⁺ currents in murine brain and endocrine cells

Takano

Yasufuku‐Takano

Kozasa

et al. 1997

The Journal of Physiology

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Somatostatin (somatotrophin release-inhibiting factor, SRIF), a fourteen amino acid peptide, was discovered in the hypothalamus (Brazeau et al. 1973). This peptide was shown to inhibit the secretion of growth hormone in the hypophysis (Brazeau et al. 1973). Later, SRIF was shown to be widely distributed in the brain, and it is now known to be an important neurotransmitter in the brain. The locus coeruleus, a pair of small nuclei located in the brainstem, consists of tightly packed noradrenergic neurones which project to virtually the entire brain and spinal cord. Hence, this nucleus, as the main supplier of noradrenaline in the brain, plays a vital role in brain function. SRIF inhibits locus coeruleus neurones by activating an inward rectifier K¤ current, and this SRIF effect is mediated through a pertussis toxin (PTX)-sensitive G protein (Inoue, Nakajima & Nakajima, 1988). However, the type (or types) of PTX-sensitive G protein (Gi1, Gi2, Gi3 or Gï) involved in this SRIF effect has yet to be determined. In AtT-20 cells (a mouse pituitary tumour cell line) and in human pituitary tumour cells, SRIF activates an inward rectifier K¤ current, and this SRIF effect is also mediated by a PTX-sensitive G protein (Yamashita, Shibuya & Ogata, 1988;Pennefather, Heisler & MacDonald, 1988;Kozasa, Kaziro, Ohtsuka, Grigg, Nakajima & Nakajima, 1996). In AtT-20 cells as well, it has not yet been determined which one of several PTX-sensitive G proteins is involved in the SRIF effect. The objective of this paper is to identify the G protein that mediates the SRIF effect on inward rectifier K¤ currents in locus coeruleus neurones and in 1. Types of G proteins (G protein á_subunit subtypes) which mediate the activation of inward rectifier K¤ currents by somatostatin (somatotrophin release-inhibiting factor, SRIF) were determined in cultured locus coeruleus neurones from newborn rats and in AtT-20 cells (a mouse pituitary cell line). 2. The whole-cell patch clamp technique was used together with injection of antibodies against pertussis toxin (PTX)-sensitive G protein á_subunits or with injection of antisense (or sense) oligonucleotides against these G proteins. 3. In locus coeruleus neurones, the SRIF-induced activation of inward rectifier K¤ currents was inhibited by anti-Gái1ÏGái2 antibody injection, but not by anti-Gái3 or by anti-GáïÏGái3 antibody injection, suggesting that the SRIF response is mediated through Gái1 andÏor Gái2. 4. The SRIF-induced activation of the inward rectifier was suppressed in locus coeruleus neurones after injection of antisense oligonucleotides against Gái2, but not by injection of sense oligonucleotides against Gái2. Injection of antisense (or sense) oligonucleotides against Gái1, Gái3 and Gáï(common) had no effect. These results suggest that Gái2 is involved in this SRIF response. 5. In AtT-20 cells, the SRIF-induced activation of inward rectifier K¤ currents was suppressed by injection of anti-Gái3 antibody, but not by injection of anti-Gái1ÏGái2 antibody. 6. The above results indicate that Gé medi...

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Section: Discussion Srif Response In Locus Coeruleus Neuronesmentioning

confidence: 99%

Section: Specificity Of G Protein á_subunitsmentioning

confidence: 99%

Different G proteins mediate somatostatin‐induced inward rectifier K⁺ currents in murine brain and endocrine cells

Takano

Yasufuku‐Takano

Kozasa

et al. 1997

The Journal of Physiology

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“…Grishina and Berlot, 2000). Differences in receptor recognition, leading to the selective activation of either G o1 or G o2 regulating the same downstream effector system, were documented (Kleuss et al, 1991;Chen and Clarke, 1996). The selective loss of retinal bipolar ON cell activation by glutamic acid from retinal photoreceptor cells in mice lacking G␣ o1 (Dhingra et al, 2000), but not in mice lacking G␣ o2 (Dhingra et al, 2002), has Chloride dependence of VGLUT activity in deletion mutants of G␣ o1 , G␣ o2 , G␣ q , and G␣ 11 .…”

Section: G␣ O2 As a Modulator Of Vesicular Transmitter Transporter Acmentioning

confidence: 99%

Gα_o2Regulates Vesicular Glutamate Transporter Activity by Changing Its Chloride Dependence

Winter¹,

Brunk²,

Walther³

et al. 2005

J. Neurosci.

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Classical neurotransmitters, including monoamines, acetylcholine, glutamate, GABA, and glycine, are loaded into synaptic vesicles by means of specific transporters. Vesicular monoamine transporters are under negative regulation by ␣ subunits of trimeric G-proteins, including G␣ o2 and G␣ q . Furthermore, glutamate uptake, mediated by vesicular glutamate transporters (VGLUTs), is decreased by the nonhydrolysable GTP-analog guanylylimidodiphosphate. Using mutant mice lacking various G␣ subunits, including G␣ o1 , G␣ o2 , G␣ q , and G␣ 11 , and a G␣ o2 -specific monoclonal antibody, we now show that VGLUTs are exclusively regulated by G␣ o2 . G-protein activation does not affect the electrochemical proton gradient serving as driving force for neurotransmitter uptake; rather, G␣ o2 exerts its action by specifically affecting the chloride dependence of VGLUTs. All VGLUTs show maximal activity at ϳ5 mM chloride. Activated G␣ o2 shifts this maximum to lower chloride concentrations. In contrast, glutamate uptake by vesicles isolated from G␣ o2 Ϫ/Ϫ mice have completely lost chloride activation. Thus, G␣ o2 acts on a putative regulatory chloride binding domain that appears to modulate transport activity of vesicular glutamate transporters.

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“…Gi1 and Gi3, because of their much lower expression levels are likely to be acting for the most part via their ␣ subunits, whereas receptors activating Go or Gi2 are likely to elicit immediate effects primarily via G␤␥ (Go) or via both G␤␥ and G␣ (Gi2). Indeed, receptors recognize this difference and appear to exhibit very high degrees of specificity toward the ␣ subunit of the G protein(s) they activate, including distinguishing between G␣o1 and G␣o2 splice variants (30,31). This high degree of specificity extends also to the recognition of the G12 and G13 class of G proteins that regulate cytoskeletal aspects of cell function.…”

Section: ϩmentioning

confidence: 99%

Most central nervous system D2 dopamine receptors are coupled to their effectors by Go

Jiang

Spicher

Boulay

et al. 2001

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

123

117

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We reported previously that Go-deficient mice develop severe neurological defects that include hyperalgesia, a generalized tremor, lack of coordination, and a turning syndrome somewhat reminiscent of unilateral lesions of the dopaminergic nigro-striatal pathway. By using frozen coronal sections of serially sectioned brains of normal and Go-deficient mice, we studied the ability of several G protein coupled receptors to promote binding of GTP␥S to G proteins and the ability of GTP to promote a shift in the affinity of D2 dopamine receptor for its physiologic agonist dopamine. We found a generalized, but not abolished reduction in agoniststimulated binding of GTP␥S to frozen brain sections, with no significant left-right differences. Unexpectedly, the ability of GTP to regulate the binding affinity of dopamine to D2 receptors (as seen in in situ [ 35 S]sulpiride displacement curves) that was robust in control mice, was absent in Go-deficient mice. The data suggest that most of the effects of the Gi͞Go-coupled D2 receptors in the central nervous system are mediated by Go instead of Gi1, Gi2, or Gi3. In agreement with this, the effect of GTP on dopamine binding to D2 receptors in double Gi1 plus Gi2-and Gi1 plus Gi3-deficient mice was essentially unaffected.G protein ͉ knockout mice ͉ homologous recombination ͉ GTP shift ͉ sulpiride

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G(o)‐2 protein mediates the reduction in Ca2+ currents by somatostatin in cultured ovine somatotrophs.

Cited by 34 publications

References 19 publications

Different G proteins mediate somatostatin‐induced inward rectifier K⁺ currents in murine brain and endocrine cells

Different G proteins mediate somatostatin‐induced inward rectifier K⁺ currents in murine brain and endocrine cells

Gα_o2Regulates Vesicular Glutamate Transporter Activity by Changing Its Chloride Dependence

Most central nervous system D2 dopamine receptors are coupled to their effectors by Go

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G(o)‐2 protein mediates the reduction in Ca2+ currents by somatostatin in cultured ovine somatotrophs.

Cited by 34 publications

References 19 publications

Different G proteins mediate somatostatin‐induced inward rectifier K+ currents in murine brain and endocrine cells

Different G proteins mediate somatostatin‐induced inward rectifier K+ currents in murine brain and endocrine cells

Gαo2Regulates Vesicular Glutamate Transporter Activity by Changing Its Chloride Dependence

Most central nervous system D2 dopamine receptors are coupled to their effectors by Go

Contact Info

Product

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Different G proteins mediate somatostatin‐induced inward rectifier K⁺ currents in murine brain and endocrine cells

Different G proteins mediate somatostatin‐induced inward rectifier K⁺ currents in murine brain and endocrine cells

Gα_o2Regulates Vesicular Glutamate Transporter Activity by Changing Its Chloride Dependence