Metabotropic Glutamate Receptors mGluR1α and mGluR2/3 Display Dynamic Expression Patterns in Developing Rat Striatum

Jokel, Eve S.; Garduno, E.R.; Ariano, Marjorie A.; Levine, Michael S.

doi:10.1159/000048690

Cited by 12 publications

(15 citation statements)

References 31 publications

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“…The neuropilar localization of mGluR1· in the striatum during development was also observed by Jokel et al [2001] in the rat brain. The postsynaptic localization of this receptor in the striatum suggested by these authors is further supported by a previous work of our laboratory showing that mGluR1·-LI remained unchanged after axonal transport blockade [Berger et al, 2001].…”

Section: Basal Gangliamentioning

confidence: 61%

Differential Localization of Metabotropic Glutamate Receptors during Postnatal Development

2002

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The localization of metabotropic glutamate receptors (mGluRs) during development has been associated with brain maturation and plasticity. The developmental immunohistochemical analysis of mGluR1α, mGluR2/3 and mGluR4a expression was performed in the cerebral cortex, hippocampus and basal ganglia at postnatal days (P) 4, 8, 12, 35 and 60. In early stages (P4 and P8) mGluR1α-like immunoreactivity (mGluR1α-LI) was detected in cell bodies and fibers of the frontal cortex, hippocampus and globus pallidus. At P35 and P60, the staining was observed in pyramidal cells and fibers in the deepest layers of the cortex and in stratum oriens of the hippocampus, while a lower labeling was observed in fibers of the globus pallidus. No immunostaining was observed in substantia nigra pars reticulata until P12, when a dense network of fiber staining was detected through the adult stages (P35, P60). mGluR2/3-LI was present from the second week of development in fibers and cell bodies of the stratum lacunosum moleculare of the CA1–CA3 and striatum; this staining pattern persisted until adult stages. mGluR4a-LI was observed at P12 in neuronal bodies of the cortex, in pyramidal cells of the hippocampus and in neuronal cells of the striatum. At P35 and P60, a strong signal was observed in a reduced number of labeled cells of the cerebral cortex, in fibers of the stratum oriens of CA1 and in long processes of substantia nigra pars reticulata. Our results indicate that there are significant changes in the protein expression of mGluR subunits through postnatal development. These differences may play a significant role in the establishment of proper synaptic circuitry in early postnatal life, as well as contributing to the maintenance, stabilization, and plasticity of the rat forebrain, particularly through the participation of mGluR1α and mGluR4a.

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Section: Basal Gangliamentioning

confidence: 61%

Differential Localization of Metabotropic Glutamate Receptors during Postnatal Development

2002

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“…mGlu 2/3 receptors are localized to corticostriatal axon terminals that synapse in the ventral striatum, and their activation causes long-term depression of excitatory synaptic transmission (Robbe et al, 2002). These receptors have also been localized to glial processes, but are absent from postsynaptic dendrites and neuronal cell bodies in the striatum (Jokel et al, 2001;Robbe et al, 2002). We found that LY379268 blocked PCP-and MK-801-induced locomotion in both control and DD mice.…”

Section: Discussionmentioning

confidence: 99%

Dopamine is not Required for the Hyperlocomotor Response to NMDA Receptor Antagonists

Chartoff

Heusner

Palmiter

2005

Neuropsychopharmacol

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N-methyl-D-aspartate (NMDA) receptor antagonists can elicit symptoms in humans that resemble those seen in schizophrenic patients. Rodents manifest locomotor and stereotypic behaviors when treated with NMDA receptor antagonists such as phencyclidine (PCP) or dizocilpine maleate (MK-801); these behaviors are usually associated with an activated dopamine system. However, recent evidence suggests that increased glutamatergic transmission mediates the effects of these NMDA receptor antagonists. The role of dopamine in PCP-and MK-801-induced behavior (eg hyperlocomotion) remains unclear. We used dopamine-deficient (DD) mice in which tyrosine hydroxylase is selectively inactivated in dopaminergic neurons to determine whether dopamine is required for the locomotor and molecular effects of PCP and MK-801. DD mice showed a similar increase in locomotor activity and c-fos mRNA induction in the striatum in response to these NMDA receptor antagonists as control mice. Restoration of dopamine signaling in DD mice enhanced their locomotor response to PCP and MK-801. Administration of LY379268, a group II metabotropic glutamate receptor agonist that inhibits glutamate release, blocked PCP-and MK-801-induced hyperlocomotion in both DD and control mice. These results suggest that glutamate, rather than dopamine, is required for the locomotor and molecular effects of NMDA receptor antagonists, but that glutamate and dopamine can act cooperatively.

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“…Notably, neurons grown in culture for less than a week failed to respond to DHPG (not shown). This was unsurprising because group I mGluR expression is developmentally regulated, and is not expected to be highly expressed before postnatal day 7 (Jokel et al, 2001). Fortuitously, many striatal neurons isolated from P0-3 rats did respond to DHPG when allowed to grow in culture for 2 weeks (Fig.…”

Section: Functional Interaction Of Mglur1 and Mglur5mentioning

confidence: 99%

Cooperative Signaling between Homodimers of Metabotropic Glutamate Receptors 1 and 5

Sevastyanova

Kammermeier

2014

Mol Pharmacol

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Metabotropic glutamate receptors (mGluRs) function as dimers. Recent work suggests that mGluR1 and mGluR5 may physically interact, but the nature and functional consequences of this relationship have not been addressed. In this study, the functional and pharmacological consequences of this interaction were investigated. Using heterologous expression of mGluR cDNA in rat sympathetic neurons from the superior cervical ganglion and inhibition of the native calcium currents as an assay for receptor activation, a functional interdependence between mGluR1 and mGluR5 was demonstrated. In neurons coexpressing these receptors, combining a selective mGluR1 competitive antagonist with either an mGluR1-or mGluR5-selective negative allosteric modulator[2-methyl-6-(phenylethynyl)pyridine hydrochloride], respectively, strongly occluded signaling by both receptors to an approximately equal degree. By contrast, in cells coexpressing mGluR1 and mGluR2, combining the same mGluR1 competitive inhibitor with an mGluR1 or mGluR2 NAM yielded partial and full inhibition of the response, respectively, as expected for independently acting receptors. In neurons expressing mGluR1 and mGluR5, the selective NAMs each strongly inhibited the response to glutamate, suggesting that these receptors do not interact as heterodimers, which would not be inhibited by selective NAMs. Finally, evidence for a similar mGluR1/mGluR5 functional dependence is shown in medium spiny striatal neurons.Together, these data demonstrate cooperative signaling between mGluR1 and mGluR5 in a manner inconsistent with heterodimerization, and thus suggest an interaction between homodimers.

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Metabotropic Glutamate Receptors mGluR1α and mGluR2/3 Display Dynamic Expression Patterns in Developing Rat Striatum

Cited by 12 publications

References 31 publications

Differential Localization of Metabotropic Glutamate Receptors during Postnatal Development

Differential Localization of Metabotropic Glutamate Receptors during Postnatal Development

Dopamine is not Required for the Hyperlocomotor Response to NMDA Receptor Antagonists

Cooperative Signaling between Homodimers of Metabotropic Glutamate Receptors 1 and 5

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