Changes in Sef Levels Influence Auditory Brainstem Development and Function

Abraira, Victoria E.; Hyun, N.; Tucker, Andrew F.; Coling, Donald; Brown, M. Christian; Lu, Cindy C.; Hoffman, G. R.; Goodrich, Lisa V.

doi:10.1523/jneurosci.3477-06.2007

Cited by 36 publications

(31 citation statements)

References 62 publications

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“…S1a). Il17rd − / − pups were born in an expected Mendelian ratio and showed no obvious phenotypic abnormalities and this is consistent with previously generated IL-17RD-deficient mice 25 . As expected, Il17rd mRNA expression is abolished in Il17rd − / − mice and replaced by β-Geo expression ( Supplementary Fig.…”

Section: Il-17rd Differentially Regulates Il-17a-responsive Genessupporting

confidence: 91%

Orphan receptor IL-17RD tunes IL-17A signalling and is required for neutrophilia

et al. 2012

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Interleukin-17A, the prototypical member of the interleukin-17 cytokine family, coordinates local tissue inflammation by recruiting neutrophils to sites of infection. Dysregulation of interleukin-17 signalling has been linked to the pathogenesis of inflammatory diseases and autoimmunity. The interleukin-17 receptor family members (A-E) have a broad range of functional effects in immune signalling yet no known role has been described for the remaining orphan receptor, interleukin-17 receptor D, in regulating interleukin-17A-induced signalling pathways. Here we demonstrate that interleukin-17 receptor D can differentially regulate the various pathways employed by interleukin-17A. neutrophil recruitment, in response to in vivo administration of interleukin-17A, is abolished in interleukin-17 receptor D-deficient mice, correlating with reduced interleukin-17A-induced activation of p38 mitogen-activated protein kinase and expression of the neutrophil chemokine mIP-2. In contrast, interleukin-17 receptor D deficiency results in enhanced interleukin-17A-induced activation of nuclear factor-kappa B and interleukin-6 and keratinocyte chemoattractant expression. Interleukin-17 receptor D disrupts the interaction of Act1 and TRAF6 causing differential regulation of nuclear factorkappa B and p38 mitogen-activated protein kinase signalling pathways.

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Section: Il-17rd Differentially Regulates Il-17a-responsive Genessupporting

confidence: 91%

Orphan receptor IL-17RD tunes IL-17A signalling and is required for neutrophilia

et al. 2012

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“…The staining pattern by immunohistochemistry matches the expected distribution of GFAP in mouse auditory brainstem (Abraira et al, 2007). With the use of cultured mouse primary astrocytes, the antibody staining demonstrates a filamentous pattern, consistent with GFAP presence in intermediate filaments.…”

Section: Glial Fibrillary Acidic Protein (Gfap) Antibodysupporting

confidence: 67%

Mapping of endogenous morphine‐like compounds in the adult mouse brain: Evidence of their localization in astrocytes and GABAergic cells

Laux

Muller

Miehe

et al. 2011

J of Comparative Neurology

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Endogenous morphine, morphine-6-glucuronide, and codeine, which are structurally identical to vegetal alkaloids, can be synthesized by mammalian cells from dopamine. However, the role of brain endogenous morphine and its derivative compounds is a matter of debate, and knowledge about its distribution is lacking. In this study, by using a validated antibody, we describe a precise mapping of endogenous morphine-like compounds (morphine and/or its glucuronides and/or codeine) in the mouse brain. First, a mass spectrometry approach confirmed the presence of morphine and codeine in mouse brain, but also, of morphine-6-glucuronide and morphine-3-glucuronide representing two metabolites of morphine. Second, light microscopy allowed us to observe immunopositive cell somas and cytoplasmic processes throughout the mouse brain. Morphine-like immunoreactivity was present in various structures including the hippocampus, olfactory bulb, band of Broca, basal ganglia, and cerebellum. Third, by using confocal microscopy and immunofluroscence co-localization, we characterized cell types containing endogenous opiates. Interestingly, we observed that morphine-like immunoreactivity throughout the encephalon is mainly present in γ-aminobutyric acid (GABA)ergic neurons. Astrocytes were also labeled throughout the entire brain, in the cell body, in the cytoplasmic processes, and in astrocytic feet surrounding blood vessels. Finally, ultrastructural localization of morphine-like immunoreactivity was determined by electron microscopy and showed the presence of morphine-like label in presynaptic terminals in the cerebellum and postsynaptic terminals in the rest of the mouse brain. In conclusion, the presence of endogenous morphine-like compounds in brain regions not usually involved in pain modulation opens the exciting opportunity to extend the role and function of endogenous alkaloids far beyond their analgesic functions.

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“…ABR measurements have proven to be a robust method for analyzing the effects of genetic mutations on hearing in mice, both in mutagenesis screens (Kermany et al, 2006) and in the evaluation of candidate genes (Abraira et al, 2007;Blauwkamp et al, 2007;Polley et al, 2006). In these studies, the candidate genes are transcription factors or morphogens with identified roles in nervous system development.…”

Section: Discussionmentioning

confidence: 99%

Auditory brainstem responses are impaired in EphA4 and ephrin-B2 deficient mice

2008

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The Eph receptor tyrosine kinases and their membrane-anchored ligands, ephrins, are signaling proteins that act as axon guidance molecules during chick auditory brainstem development. We recently showed that Eph proteins also affect patterns of neural activation in the mammalian brainstem. However, functional deficits in the brainstems of mutant mice have not been assessed physiologically. The present study characterizes neural activation in Eph protein deficient mice in the auditory brainstem response (ABR). We recorded the ABR of EphA4 and ephrin-B2 mutant mice, aged postnatal day 18-20, and compared them to wild type controls. The peripheral hearing threshold of EphA4(-/-) mice was 75% higher than that of controls. Waveform amplitudes of peak 1 (P1) were 54% lower in EphA4(-/-) mice than in controls. The peripheral hearing thresholds in ephrin-B2(lacZ/)(+) mice were also elevated, with a mean value 20% higher than that of controls. These ephrin-B2(lacZ/)(+) mice showed a 38% smaller P1 amplitude. Significant differences in latency to waveform peaks were also observed. These elevated thresholds and reduced peak amplitudes provide evidence for hearing deficits in both of these mutant mouse lines, and further emphasize an important role for Eph family proteins in the formation of functional auditory circuitry.

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Changes in Sef Levels Influence Auditory Brainstem Development and Function

Cited by 36 publications

References 62 publications

Orphan receptor IL-17RD tunes IL-17A signalling and is required for neutrophilia

Orphan receptor IL-17RD tunes IL-17A signalling and is required for neutrophilia

Mapping of endogenous morphine‐like compounds in the adult mouse brain: Evidence of their localization in astrocytes and GABAergic cells

Auditory brainstem responses are impaired in EphA4 and ephrin-B2 deficient mice

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