Synaptic ERK2 phosphorylates and regulates metabotropic glutamate receptor 1 in vitro and in neurons

Yang, Jialong; Kim, Jieun; Sohn, Sumin; Kim, Sung-Hyun; Choe, Eun Sang

doi:10.1016/j.ibror.2019.07.938

Cited by 3 publications

(5 citation statements)

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“…In the present study, repeated nicotine exposure increased pERK binding to mGluR5 and enhanced IP 3 levels, and these increases were reduced by blocking ERK to mGluR5 binding. Consistently, in a previous study, we showed that blockade of ERK2 to mGluR1a binding in rat cerebellum decreased mGluR1a‐mediated increase in IP 3 levels 8 . Taken together, these findings suggest that repeated exposure to nicotine potentiates activated ERK binding to the D‐domain in the CT region of mGluR5 and stimulates the mGluR5‐linked IP 3 pathway in the NAc of adult rats.…”

Section: Discussionsupporting

confidence: 90%

“…These findings suggest that ERK phosphorylation is a prerequisite for mGluR5‐linked IP 3 signaling cascades in adult NAc. Similarly, it was previously concluded, ERK phosphorylation is necessary for the production of IP 3 , which is linked to mGluR1a in rat cerebellum 8 …”

Section: Discussionsupporting

confidence: 67%

“…The mGluR5 is a dominant group I metabotropic glutamate receptor (mGluR1/5) that is expressed in the gamma aminobutyric acid (GABA) medium spiny projection neurons (MSNs) of the NAc, and caudate and putamen, whereas mGluR1 is expressed in the cerebellum 5,6 . Stimulation of mGluR5 phosphorylates extracellular signal‐regulated kinase (ERK), which in turn phosphorylates the receptor itself in a proline‐dependent manner in vitro and in the cerebellum 7,8 . For instance, activated mitogen‐activated protein kinases kinase (MEK), which activates ERK, phosphorylates mGluR5 at its serine residue at position 1126 (mGluR5‐S1126) in HEK293T cells, and inhibition of MEK decreases mGluR5‐S1167 phosphorylation in cultured cortical neurons 9 .…”

Section: Introductionmentioning

confidence: 99%

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Repeated nicotine exposure increases the intracellular interaction between ERK‐mGluR5 in the nucleus accumbens more in adult than adolescent rats

et al. 2020

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Intracellular interactions between protein kinases and metabotropic receptors in the striatum regulate behavioral changes in response to drug exposure. We investigated the difference in the degree of interaction between extracellular signal‐regulated kinase (ERK) and metabotropic glutamate receptor subtype 5 (mGluR5) in the nucleus accumbens (NAc) after repeated exposure to nicotine in adult and adolescent rats. The results showed that repeated exposure to nicotine (0.5 mg/kg/day, s.c.) for seven consecutive days increased ERK phosphorylation more in adults than in adolescents. Furthermore, membrane expression of mGluR5 in gamma‐aminobutyric acid (GABA) medium spiny neurons was higher in adults than adolescents as a result of repeated exposure to nicotine. Blockade of mGluR5 with MPEP (0.5 nmol/side) decreased the repeated nicotine‐induced increase in ERK phosphorylation. Either blockade of mGluR5 or inhibition of ERK with SL327 (150 nmol/side) decreased the repeated nicotine‐induced increase in the level of inositol‐1,4,5‐triphosphate (IP3), a key transducer associated with mGluR5‐coupled signaling cascades. Similarly, interference of binding between activated ERK and mGluR5 by the blocking peptide, Tat‐mGluR5‐i (2 nmol/side), decreased the repeated nicotine‐induced increases in IP3 and locomotor activity in adults. These findings suggest that the intracellular interaction between ERK and mGluR5 in the NAc is stronger in adult than in adolescent rats, which enhances the understanding of age‐associated behavioral changes that occur after repeated exposure to nicotine.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

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Repeated nicotine exposure increases the intracellular interaction between ERK‐mGluR5 in the nucleus accumbens more in adult than adolescent rats

et al. 2020

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“…Eng et al, 2016;Gulia et al, 2017). Second messengeractivated kinases also provide negative feedback regulating cellular responses (iCa 2+ oscillations or receptor desensitization) through phosphorylation of intracellular loops and/or the C terminus (Kawabata et al, 1996;Gereau and Heinemann, 1998;Bhattacharya et al, 2004;Mundell et al, 2004;Kim et al, 2005;Ko et al, 2012;Jin et al, 2013aJin et al, ,b, 2018Raka et al, 2015;Uematsu et al, 2015;Vergouts et al, 2017;Yang et al, 2017;Marks et al, 2018). However, not all functional responses are equally influenced.…”

Section: B Localization and Signal Transductionmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. CXI. Pharmacology, Signaling, and Physiology of Metabotropic Glutamate Receptors

Gregory

Goudet

2020

Pharmacol Rev

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“…Structural studies have proved that ERK1 can bind to mGluR5 in vitro and ERK2 interacts with mGluR1a in rat cerebellum; thus, mGluRs can be phosphorylated and maintain adequate surface expression. 24,25 Molecules that activate ERKs, brain-derived neurotrophic factor, for example, elevate mGluR5 phosphorylation in cultured cortical and striatal neurons. This elevation can be blocked by MEK inhibitor, U0126.…”

Section: Roles Of Erks In Plasticity-related Neuronal Signalingmentioning

confidence: 99%

Presynaptic long-term potentiation requires extracellular signal-regulated kinases in the anterior cingulate cortex

et al. 2020

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Extracellular signal-regulated kinases are widely expressed protein kinases in neurons, which serve as important intracellular signaling molecules for central plasticity such as long-term potentiation. Recent studies demonstrate that there are two major forms of long-term potentiation in cortical areas related to pain: postsynaptic long-term potentiation and presynaptic long-term potentiation. In particular, presynaptic long-term potentiation in the anterior cingulate cortex has been shown to contribute to chronic pain-related anxiety. In this review, we briefly summarized the components and roles of extracellular signal-regulated kinases in neuronal signaling, especially in the presynaptic long-term potentiation of anterior cingulate cortex, and discuss the possible molecular mechanisms and functional implications in pain-related emotional disorders.

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Synaptic ERK2 phosphorylates and regulates metabotropic glutamate receptor 1 in vitro and in neurons

Cited by 3 publications

References 0 publications

Repeated nicotine exposure increases the intracellular interaction between ERK‐mGluR5 in the nucleus accumbens more in adult than adolescent rats

Repeated nicotine exposure increases the intracellular interaction between ERK‐mGluR5 in the nucleus accumbens more in adult than adolescent rats

International Union of Basic and Clinical Pharmacology. CXI. Pharmacology, Signaling, and Physiology of Metabotropic Glutamate Receptors

Presynaptic long-term potentiation requires extracellular signal-regulated kinases in the anterior cingulate cortex

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