Distribution of group‐III metabotropic glutamate receptors in the retina

Quraishi, Salma; Gayet, Jacqueline; Morgans, Catherine W.; Duvoisin, Robert M.

doi:10.1002/cne.21274

Cited by 37 publications

(44 citation statements)

References 52 publications

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“…We observed immunolabeling similar to that previously observed in the mouse retina using the same antibody (Quraishi et al, 2007;Xu and Tian, 2007;Puthussery et al, 2010;Hilgen et al, 2011).…”

Section: Anti-calretininsupporting

confidence: 86%

Requirement for the paired‐like homeodomain transcription factor VSX1 in type 3a mouse retinal bipolar cell terminal differentiation

Shi¹,

Jervis²,

Nickerson³

et al. 2011

J of Comparative Neurology

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Retinal bipolar cells make up a class of at least 11 distinct interneurons that have been classified through morphological and molecular approaches. Previous work has shown that the paired-like homeodomain transcription factor Vsx1 is essential for the proper development of a subset of these interneurons. In Vsx1-null mice, bipolar cells are properly specified but exhibit terminal differentiation defects characterized by reduced expression of OFF bipolar cell markers and defects in OFF visual signaling. Here, we further examined the role of Vsx1 in OFF bipolar cells using recently identified cell-type-specific markers. In contrast to its previously characterized expression in type 2 OFF bipolar cells, Vsx1 expression was not detected in type 3 OFF bipolar cells, by either immunohistological or transgenic reporter labeling approaches. This observation was unexpected given previous findings that Cabp5 immunolabeling of type 3 bipolar cell axon terminals is reduced in Vsx1-null mice. However, we observed reduced levels of the type 3a bipolar cell marker hyperpolarization-activated and cyclic nucleotide-gated channel 4 (HCN4) in Vsx1-null mice, which is consistent with a requirement for Vsx1 in type 3 bipolar cell differentiation. In contrast, expression of the type 3b bipolar cell marker regulatory subunit RII-beta of protein kinase A was unchanged. Despite the absence of Vsx1 in mature type 3 bipolar cells, colabeling of Vsx1 and HCN4 was observed at postnatal stages. These findings reveal a role for Vsx1 in type 3a bipolar cells and suggest that Vsx1 function is required transiently in this cell type during the postnatal period.

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Section: Anti-calretininsupporting

confidence: 86%

Requirement for the paired‐like homeodomain transcription factor VSX1 in type 3a mouse retinal bipolar cell terminal differentiation

Shi¹,

Jervis²,

Nickerson³

et al. 2011

J of Comparative Neurology

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“…All group III mGluRs are expressed in the mammalian retina and their distribution has been analyzed in detail (Brandstätter et al 1998;Quraishi et al 2007). In contrast, the expression of band 4.1 proteins in the mammalian retina has not been studied so far.…”

Section: Discussionmentioning

confidence: 99%

Band 4.1 proteins are expressed in the retina and interact with both isoforms of the metabotropic glutamate receptor type 8

Rose

Dütting

Enz

2008

Journal of Neurochemistry

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Abbreviations used: CTD, C-terminal domain; EF1a, elongation factor 1a; GCL, ganglion cell layer; GFP, green fluorescent protein; INL, inner nuclear layer; IPL, inner plexiform layer; MDB, membrane binding domain; mGluR, metabotropic glutamate receptor; ONL, outer nuclear layer; OPL, outer plexiform layer; PICK1, protein interacting with C-kinase; PRS, photoreceptor segments; SAB, spectrin/actin binding domain. AbstractThe function of the CNS depends on the correct regulation of neurotransmitter receptors by interacting proteins. Here, we screened a retinal cDNA library for proteins interacting with the intracellular C-terminus of the metabotropic glutamate receptor isoform 8a (mGluR8a). The band 4.1B protein binds to the C-termini of mGluR8a and mGluR8b, co-localizes with these glutamate receptors in transfected mammalian cells, facilitates their cell surface expression and inhibits the mGluR8 mediated reduction of intracellular cAMP concentrations. In contrast, no interaction with 4.1B was observed for other mGluRs tested. Amino acids encoded by exons 19 and 20 of 4.1B and a stretch of four basic amino acids present in the mGluR8 C-termini mediate the protein interaction. Besides binding to 4.1B, mGluR8 isoforms interact with 4.1G, 4.1N, and 4.1R. Because band 4.1 transcripts undergo extensive alternative splicing, we analyzed the splicing pattern of interacting regions and detected a 4.1B isoform expressed specifically in the retina. Within this tissue, mGluR8 and 4.1B, 4.1G, 4.1N, and 4.1R show a comparable distribution, being expressed in both synaptic layers and in somata of the ganglion cell layer. In summary, our studies identified band 4.1 proteins as new players for the mGluR8 mediated signal transduction.

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“…A previously characterized mouse monoclonal antibody specific for mGluR8 was used (Quraishi et al, 2007). Because the secondary rabbit anti-mouse antibody strongly reacts with endogenous IgGs in the vasculature, it was not possible to assess mGluR8 immunoreactivity in mouse brain.…”

Section: Materials and Methods Mglur8 Immunohistochemistrymentioning

confidence: 99%

mGluR8 Modulates Excitatory Transmission in the Bed Nucleus of the Stria Terminalis in a Stress-Dependent Manner

Gosnell

Silberman

Grueter

et al. 2011

Neuropsychopharmacol

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Metabotropic glutamate receptors (mGluRs) are important modulators of excitatory transmission, and have been implicated in anxiety and stress-related behaviors. Previously, we showed that group III mGluR agonists could depress excitatory synaptic transmission in the bed nucleus of the stria terminalis (BNST), an integral component of the anxiety circuitry. Here, we provide converging evidence indicating that this effect is mediated primarily by mGluR8, is exerted presynaptically, and is modulated by noradrenergic signaling and stress. The effects of the group III mGluR agonist L-AP4 on excitatory transmission are not potentiated by the mGluR4-selective allosteric potentiator PHCCC, but are mimicked by the mGluR8-selective agonist DCPG. Consistent with these results, mGluR8-like immunoreactivity is seen in the BNST, and the actions of L-AP4 on excitatory transmission are absent in slices from mGluR8 knockout (KO) mice. Application of DCPG is associated with an increase in paired-pulse evoked glutamate synaptic currents, and a decrease in spontaneous glutamate synaptic current frequency, consistent with a primarily presynaptic action. mGluR8-mediated suppression of excitatory transmission is disrupted ex vivo by activation of a1 adrenergic receptors (a1 ARs). BNST mGluR8 function is also disrupted by both acute and chronic in vivo exposure to restraint stress, and in brain slices from a2A AR KO mice. These studies show that mGluR8 is an important regulator of excitatory transmission in the BNST, and suggest that this receptor is selectively disrupted by noradrenergic signaling and by both acute and chronic stress.

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Distribution of group‐III metabotropic glutamate receptors in the retina

Cited by 37 publications

References 52 publications

Requirement for the paired‐like homeodomain transcription factor VSX1 in type 3a mouse retinal bipolar cell terminal differentiation

Requirement for the paired‐like homeodomain transcription factor VSX1 in type 3a mouse retinal bipolar cell terminal differentiation

Band 4.1 proteins are expressed in the retina and interact with both isoforms of the metabotropic glutamate receptor type 8

mGluR8 Modulates Excitatory Transmission in the Bed Nucleus of the Stria Terminalis in a Stress-Dependent Manner

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