Group I metabotropic glutamate receptors reduce excitotoxic injury and may facilitate neurogenesis

Baskys, Andrius; Bayazitov, Ildar T.; Fang, Liwei; Blaabjerg, Morten; Poulsen, Frantz Rom; Zimmer, Jens

doi:10.1016/j.neuropharm.2005.04.029

Cited by 74 publications

(61 citation statements)

References 47 publications

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“…It is still not clear why mutant Htt protein leads to selective neuronal cell death and why there is a delayed loss of neurons late in life. mGluR1/5 can signal to activate different pathways that can be either protective or exacerbate neuronal cell death (Nicoletti et al, 1996;Bruno et al, 2001;Tang et al, 2003;Baskys et al, 2005). In the present study, we show that mGluR1/5 signaling pathways are altered in the presymptomatic phase of a Hdh Q111/Q111 knock-in mouse model of HD (Fig.…”

Section: Discussionsupporting

confidence: 55%

“…However, other studies have provided evidence that mGluR signaling may be protective. For example, when cortical neuronal cultures are consecutively incubated two times with DHPG, NMDAR-mediated excitotoxicity is attenuated (Bruno et al, 2001;Baskys et al, 2005). The results presented here demonstrate that DHPG-mediated InsP formation is reduced in Hdh Q111/Q111 mice due to an increase in PKC-mediated desensitization of mGluR1/5 in Hdh Q111/Q111 mice.…”

Section: Discussionmentioning

confidence: 64%

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Metabotropic Glutamate Receptor-Mediated Cell Signaling Pathways Are Altered in a Mouse Model of Huntington's Disease

Ribeiro¹,

Paquet²,

Ferreira³

et al. 2010

J. Neurosci.

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Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder caused by a polyglutamine expansion in the huntingtin protein (Httthan in Hdh Q20/Q20 striatum. PKC inhibition not only brings Hdh Q111/Q111 DHPG-stimulated InsP formation to Hdh Q20/Q20 levels, but also causes an increase in neuronal cell death in Hdh Q111/Q111 neurons. However, PKC inhibition does not modify neuronal cell death in Hdh Q20/Q20 neurons, suggesting that PKC-mediated desensitization of mGluR1/5 in Hdh Q111/Q111 mice might be protective in HD. Together, these data indicate that group I mGluR-mediated signaling pathways are altered in HD and that these cell signaling adaptations could be important for striatal neurons survival.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 64%

Metabotropic Glutamate Receptor-Mediated Cell Signaling Pathways Are Altered in a Mouse Model of Huntington's Disease

Ribeiro¹,

Paquet²,

Ferreira³

et al. 2010

J. Neurosci.

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“…Activation of PI-PLC β1 via mGluR5 is critical for the coordinated development of the neocortex [45,95] . Prolonged activation of group I mGluRs reduces neuronal susceptibility to excitotoxic injury, as demonstrated by the results obtained after U-73122 treatment of hippocampal cultures [96] . The reduction is associated with a PI-PLC-dependent depression of excitatory synaptic transmission, thus confirming the PI contribution to neurogenesis.…”

Section: Metabotropic Receptors L-glutamate the Majormentioning

confidence: 77%

Phosphoinositide pathway and the signal transduction network in neural development

Vasco

2012

Neurosci. Bull.

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Abstract:The development of the nervous system is under the strict control of a number of signal transduction pathways, often interconnected. Among them, the phosphoinositide (PI) pathway and the related phospholipase C (PI-PLC) family of enzymes have been attracting much attention. Besides their well-known role in the regulation of intracellular calcium levels, PI-PLC enzymes interact with a number of molecules belonging to further signal transduction pathways, contributing to a specific and complex network in the developing nervous system. In this review, the connections of PI signalling with further transduction pathways acting during neural development are discussed, with special regard to the role of the PI-PLC family of enzymes.

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“…Some investigators have described that an enhancement of PLCβ-1 expression is a necessary downstream signal for the occurrence of mGluR agonist-induced prolonged epileptiform activities (8). Moreover, the generation of rhythmic single cell bursts and the synchronized epileptiform discharges by activation of group I mGluRs are PLCβ-1-dependent in the hippocampal neurons (8,29). With respect to these reports, our findings suggest that enhanced PLCβ-1 expression in the post-ictal SS gerbil hippocampus may be a compensatory response to neuronal hyperexcitability due to abnormal control of excitatory neuronal circuits.…”

Section: Alterations Of Plcβ-1 Immunoreactivity In the Ss Gerbil Hippmentioning

confidence: 99%

Altered PLCβ-1 expression in the gerbil hippocampal complex following spontaneous seizure

Lee

Oh²,

Chung³

et al. 2011

BMB Reports

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Although the phospholipase C (PLC)β-1 isoform is associated with spontaneous seizure and distinctively expressed in the telencephalon, the distribution of PLCβ-1 expression in the epileptic gerbil hippocampus remains controversial. Therefore, we determined whether PLCβ-1 is associated with spontaneous seizure in an animal model of genetic epilepsy. In the present study, PLCβ-1 immunoreactivity was down-regulated in seizure-sensitive (SS) gerbils more than in seizure-resistant (SR) gerbils. The expression of PLCβ-1 within calretinin (CR)-positive neurons was rarely detected within the dentate hilar region of SS gerbils. PLCβ-1 immunoreactivity in the hippocampus was significantly elevated as compared to that in pre-seizure SS gerbil 3 h post-ictal. These findings suggest that alterations in PLCβ-1 immunoreactivity in the SS gerbil hippocampus may be closely related to the epileptic state of the gerbil brain and transiently elevated PLCβ-1 protein levels following seizure episodes. Such alterations may be compensatory responses in the SS gerbil hippocampus. [BMB reports 2011; 44(9) : 566-571]

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Group I metabotropic glutamate receptors reduce excitotoxic injury and may facilitate neurogenesis

Cited by 74 publications

References 47 publications

Metabotropic Glutamate Receptor-Mediated Cell Signaling Pathways Are Altered in a Mouse Model of Huntington's Disease

Metabotropic Glutamate Receptor-Mediated Cell Signaling Pathways Are Altered in a Mouse Model of Huntington's Disease

Phosphoinositide pathway and the signal transduction network in neural development

Altered PLCβ-1 expression in the gerbil hippocampal complex following spontaneous seizure

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