Differential regulation of β-arrestin 1 and β-arrestin 2 gene expression in rat brain by morphine

Fan, Xionglin; Zhang, J.S; Zhang, X.Q; Wen, Yangping; Ma, Lan

doi:10.1016/s0306-4522(02)00930-2

Cited by 60 publications

(47 citation statements)

References 37 publications

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“…mice, MOR desensitization was prevented when ERK1/2 was inhibited in conjunction with the disruption of GRK2 function to prevent ␤arr recruitment. Because LC neurons also express ␤arr-1 (Fan et al, 2003), it is possible that MOR desensitization is mediated through ␤arr-1 when ␤arr-2 is deleted. However, the present results suggest that ␤arr-1 does not substitute for ␤arr-2 in LC neurons from ␤arr-2 k.o.…”

Section: Discussionmentioning

confidence: 99%

“…One challenge for isolating mechanisms of desensitization in native neurons may be redundancy in molecular mechanisms mediating GPCR regulation. For example, LC neurons express GRKs 2, 3, 5 (weak), and 6 (Arriza et al, 1992) as well as ␤arr-1 (Fan et al, 2003), which could conceivably substitute for GRK2 and ␤arr-2 when their functions are disrupted.…”

Section: Introductionmentioning

confidence: 99%

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Two Distinct Mechanisms Mediate Acute μ-Opioid Receptor Desensitization in Native Neurons

Dang

Napier²,

Christie³

2009

J. Neurosci.

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Sustained stimulation of G-protein coupled receptors (GPCRs) leads to rapid loss of receptor function (acute desensitization). For manyGPCRs including the -opioid receptor (MOR), an accepted mechanism for acute desensitization is through G-protein coupled receptor kinase (GRKs) mediated phosphorylation of the receptor, which facilitates the binding of ␤-arrestins (␤arrs) to the receptor and then promotes endocytosis. However, the mechanism(s) that mediate acute desensitization have not yet been well defined in native neurons. This study used whole-cell patch clamp recording of G-protein coupled inward-rectifying potassium (GIRK) currents to assay MOR function and identify mechanisms of acute MOR desensitization in locus ceruleus (LC) neurons. The rate and extent of MOR desensitization were unaffected by ␤arr-2 knock-out. Disruption of GRK2 function via inhibitory peptide introduced directly into neurons also failed to affect desensitization in wild type or ␤arr-2 knock-outs. Inhibition of ERK1/2 activation alone had little effect on acute desensitization. However, when both GRK2-␤arr-2 and ERK1/2 functions were disrupted simultaneously, desensitization of MOR was nearly abolished. Together, these results suggest that acute desensitization of MOR in native LC neurons is determined by at least two molecular pathways, one involving GRK2 and ␤arr-2, and a parallel pathway mediated by activated ERK1/2.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Two Distinct Mechanisms Mediate Acute μ-Opioid Receptor Desensitization in Native Neurons

Dang

Napier²,

Christie³

2009

J. Neurosci.

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“…The modulation of transcription factors (CREB, DFosB) after chronic morphine treatment has been described (Lane Ladd et al, 1997;Maldonado et al, 1996). Several heat-shock proteins (hsp70, hsp40, hsp27 and hsp105) are upregulated in the frontal cortex of rats chronically treated with morphine (Ammon et al, 2003;Fan et al, 2002Fan et al, , 2003Loguinov et al, 2001;Nestler et al, 2001). Our results showing an increase in the mRNA level of Arc and no change in that of actin are consistent with the results of Ammon et al The present results also confirm the increase in dynamin protein level previously showed in the striatum of mice chronically treated with morphine (Noble et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Acute morphine administration induces modification of the expression of genes involved in processes as diverse as signal transduction coupled to m opioid receptors (Fan et al, 2002(Fan et al, , 2003Kaewsuk et al, 2001;Przewlocka et al, 1994), transcription factors (ErdtmannVourliotis et al, 1998;Kelz et al, 1999), and calcium binding proteins (Tirumalai and Howells, 1994). Interestingly, an analysis of the gene expression profile following a single injection of morphine revealed that one of the major groups of altered genes in the rat medial striatum consisted of cytoskeleton-related proteins (Loguinov et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Marie-Claire

Courtin

Roques

et al. 2004

Neuropsychopharmacol

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It has been previously suggested that morphine can regulate the expression and function of some proteins of the cytoskeleton. In the present study, we used real-time quantitative polymerase chain reaction to examine the effects of chronic morphine administration, in rat striatum, on 14 proteins involved in microtubule polymerization and stabilization, intracellular trafficking, and serving as markers of neuronal growth and degeneration. Chronic morphine treatment led to modulation of the mRNA level of seven of the 14 genes tested. Glial fibrillary acidic protein (Gfap) and activity-regulated cytoskeleton-associated protein (Arc) mRNA were upregulated, while growth associated protein (Gap43), clathrin heavy chain (Cltc), a-tubulin, Tau, and stathmin were downregulated. In order to determine if the regulation of an mRNA correlates with a modulation of the expression of the corresponding protein, immunoblot analyses were performed. With the exception of Gap43, the levels of Cltc, Gfap, Tau, stathmin, and a-tubulin proteins were found to be in good agreement with those from mRNA quantification. These results demonstrate that neuroadaptation to chronic morphine administration in rat striatum implies modifications of the expression pattern of several genes and proteins of the cytoskeleton and cytoskeletonassociated components.

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“…They also function as scaffolding/signaling molecules to recruit Src, MAP kinases, MDM2, I B␣, and Akt, and are involved in mediating cross-talk to other signal pathways. ␤-arrestins play a critical role in a wide variety of physiological and pathophysiological cellular processes (1) Although ubiquitously expressed, ␤-arrestins are found in high abundance in the immune and central nervous systems (2,3). The critical roles for ␤-arrestins in innate immune responses and autoimmunity have been demonstrated in many studies.…”

mentioning

confidence: 99%

Regulation of amygdalar PKA by β-arrestin-2/phosphodiesterase-4 complex is critical for fear conditioning

Liu

et al. 2009

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

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␤-arrestins, key regulators of receptor signaling, are highly expressed in the central nervous system, but their roles in brain physiology are largely unknown. Here we show that ␤-arrestin-2 is critically involved in the formation of associative fear memory and amygdalar synaptic plasticity. In response to fear conditioning, ␤-arrestin-2 translocates to amygdalar membrane where it interacts with PDE-4, a cAMP-degrading enzyme, to inhibit PKA activation. Arrb2 ؊/؊ mice exhibit impaired conditioned fear memory and long-term potentiation at the lateral amygdalar synapses. Moreover, expression of the ␤-arrestin-2 in the lateral amygdala of Arrb2 ؊/؊ mice, but not its mutant form that is incapable of binding PDE-4, restores basal PKA activity and rescues conditioned fear memory. Taken together, our data demonstrate that the feedback regulation of amygdalar PKA activation by ␤-arrestin-2 and PDE-4 complex is critical for the formation of conditioned fear memory.

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Differential regulation of β-arrestin 1 and β-arrestin 2 gene expression in rat brain by morphine

Cited by 60 publications

References 37 publications

Two Distinct Mechanisms Mediate Acute μ-Opioid Receptor Desensitization in Native Neurons

Two Distinct Mechanisms Mediate Acute μ-Opioid Receptor Desensitization in Native Neurons

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Regulation of amygdalar PKA by β-arrestin-2/phosphodiesterase-4 complex is critical for fear conditioning

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