Catecholamine‐independent transient expression of tyrosine hydroxylase in primary auditory neurons is coincident with the onset of hearing in the rat cochlea

Trigueiros-Cunha, Nuno; Renard, Nathalie; Humbert, Ghyslaine; Tavares, M. A.; Eybalin, Michel

doi:10.1046/j.1460-9568.2003.02989.x

Cited by 17 publications

(15 citation statements)

References 80 publications

(142 reference statements)

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“…Previously, TH expression also was reported to occur transiently during postnatal maturation of type I cochlear afferents in rats, but specifically not in type II (peripherin-positive) afferents (Trigueiros-Cunha et al 2003). However, Th 2A-CreER -driven reporter expression was found in type II afferents, and not type I afferents in the present study.…”

Section: Discussioncontrasting

confidence: 66%

“…Unexpectedly however, Th 2a-CreER cochleas also showed a pattern of reporter protein expression reminiscent of type II afferent morphology. Previous immunohistochemical studies in mice (Darrow et al 2006), rats (Trigueiros-Cunha et al 2003), and guinea pig (Eybalin et al 1993) reported that tyrosine hydroxylase is expressed by the lateral efferents originating near the lateral superior olive (LSO) and in type I cochlear afferents, rather than the type II-like pattern observed here. Thus, we compared TH-2A-CreER-positive neurons with immunolabeling of type I afferent and efferent neurons of the cochlea.…”

Section: Introductionmentioning

confidence: 41%

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Tyrosine Hydroxylase Expression in Type II Cochlear Afferents in Mice

Vyas

Zimmerman

et al. 2016

JARO

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Acoustic information propagates from the ear to the brain via spiral ganglion neurons that innervate hair cells in the cochlea. These afferents include unmyelinated type II fibers that constitute 5 % of the total, the majority being myelinated type I neurons. Lack of specific genetic markers of type II afferents in the cochlea has been a roadblock in studying their functional role. Unexpectedly, type II afferents were visualized by reporter proteins induced by tyrosine hydroxylase (TH)-driven Cre recombinase. The present study was designed to determine whether TH-driven Cre recombinase (TH-2A-CreER) provides a selective and reliable tool for identification and genetic manipulation of type II rather than type I cochlear afferents. The BTH-2A-CreER neurons^radiated from the spiral lamina, crossed the tunnel of Corti, turned towards the base of the cochlea, and traveled beneath the rows of outer hair cells. Neither the processes nor the somata of TH-2A-CreER neurons were labeled by antibodies that specifically labeled type I afferents and medial efferents.TH-2A-CreER-positive processes partially co-labeled with antibodies to peripherin, a known marker of type II afferents. Individual TH-2A-CreER neurons gave off short branches contacting 7-25 outer hair cells (OHCs). Only a fraction of TH-2A-CreER boutons were associated with CtBP2-immunopositive ribbons. These results show that TH-2A-CreER provides a selective marker for type II versus type I afferents and can be used to describe the morphology and arborization pattern of type II cochlear afferents in the mouse cochlea.

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Section: Discussioncontrasting

confidence: 66%

Section: Introductionmentioning

confidence: 41%

Tyrosine Hydroxylase Expression in Type II Cochlear Afferents in Mice

Vyas

Zimmerman

et al. 2016

JARO

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“…In a previous study using chromatin condensation and electrophoretic laddering of DNA as criteria to identify cell death, apoptosis was concluded to be the probable explanation for transient expression of neuropeptide Y in the developing hamster paraventricular area (Botchkina et al, 1996). In other reports that utilized TUNEL, cell death was rejected as the cause of transient histamine immunoreactivity in the developing rat raphe nucleus (Kinnunen et al, 1998) and as an explanation for transient TH immunostaining in developing rat primary auditory neurons (Trigueiros-Cunha et al, 2003). We observed neither DNA fragmentation detected with TUNEL nor active caspase 3 immunostaining in cortical TH-IR neurons at any age, making cell death an unlikely explanation for the reduction in TH-IR cell profile number seen during postnatal development.…”

Section: Discussionmentioning

confidence: 99%

“…In the developing rat autonomic nervous system, for example, sympathetic neurons that innervate sweat glands (Landis and Keefe, 1983;Francis and Landis, 1999) and periosteum (Asmus et al, 2000) down-regulate catecholaminergic traits, including TH production, in response to cholinergic-inducing signals derived from the target tissue. In rat primary auditory neurons, transient TH production is concurrent with the development of hearing (Trigueiros-Cunha et al, 2003). When grown in culture, embryonic rat and human cerebral cortical cells, which do not produce TH in vivo, are capable of TH expression (Iacovitti et al, 1987;Theofilopoulos et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Neurochemical characterization of tyrosine hydroxylase-immunoreactive interneurons in the developing rat cerebral cortex

et al. 2008

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Understanding the development of cortical interneuron phenotypic diversity is critical because interneuron dysfunction has been implicated in several neurodevelopmental disorders. Here, tyrosine hydroxylase (TH)-immunoreactive neurons in the developing and adult rat cortex were characterized in light of findings regarding interneuron neurochemistry and development. Cortical THimmunoreactive neurons were first observed two weeks postnatally and peaked in number three weeks after birth. At subsequent ages, the number of these cell profiles was gradually reduced, and they were seen less frequently in adults. No DNA fragmentation or active caspase 3 was observed in cortical TH cells at any age examined, eliminating cell death as an explanation for the decrease in cell number. Although cortical TH cells reportedly fail to produce subsequent catecholaminergic enzymes, we found that the majority of these cells at all ages contained phosphorylated TH, suggesting that the enzyme may be active and producing L-DOPA as an end-product. Morphological criteria and colocalization of some TH cells with glutamic acid decarboxylase suggests that these cells are interneurons. Previously, parvalbumin, somatostatin, and calretinin were demonstrated in nonoverlapping subsets of interneurons. Cortical TH neurons colocalized with calretinin but not with parvalbumin or somatostatin. These findings suggest that the transitory increase in TH cell number is not due to cell death but possibly due to alterations in the amount of detectable TH present in these cells, and that at least some cortical TH-producing interneurons belong to the calretinin-containing subset of interneurons that originate developmentally in the caudal ganglionic eminence.

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“…Fourteen-micrometer-thick sections were cut with a Reichert-Jung 2800 cryostat microtome and stored at Ϫ20°C until use. The immunohistochemical procedures were similar to those described previously (27). The sections were rinsed (3-5 min) in PBS, preincubated 1 h in 30% normal goat serum with 0.3% Triton X-100, and incubated overnight at 4°C with FXYD6 (1:500), Na,K-ATPase ␣1-subunit (1:100), and parvalbumin (Swants, 1:750) antibodies diluted in PBS with 1% normal goat serum.…”

Section: Methodsmentioning

confidence: 99%

FXYD6 Is a Novel Regulator of Na,K-ATPase Expressed in the Inner Ear

Delprat

Schaer

Roy

et al. 2007

Journal of Biological Chemistry

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The exquisite sensitivity of the cochlea, which mediates the transduction of sound waves into nerve impulses, depends on the endolymph ionic composition and the endocochlear potential. A key protein in the maintenance of the electrochemical composition of the endolymph is the Na,K-ATPase. In this study, we have looked for the presence in the rat inner ear of members of the FXYD protein family, recently identified as tissue-specific modulators of Na,K-ATPase. Only FXYD6 is detected at the protein level. FXYD6 is expressed in various epithelial cells bordering the endolymph space and in the auditory neurons. FXYD6 co-localizes with Na,K-ATPase in the stria vascularis and can be co-immunoprecipitated with Na,K-ATPase. After expression in Xenopus oocytes, FXYD6 associates with Na,K-ATPase ␣1-␤1 and ␣1-␤2 isozymes, which are preferentially expressed in different regions of the inner ear and also with gastric and non-gastric H,K-ATPases. The apparent K ؉ and Na ؉ affinities of ␣1-␤1 and ␣1-␤2 isozymes are different. Association of FXYD6 with Na,K-ATPase ␣1-␤1 isozymes slightly decreases their apparent K ؉ affinity and significantly decreases their apparent Na ؉ affinity. On the other hand, association with ␣1-␤2 isozymes increases their apparent K ؉ and Na ؉ affinity. The effects of FXYD6 on the apparent Na ؉ affinity of Na,KATPase and the voltage dependence of its K ؉ effect are distinct from other FXYD proteins. In conclusion, this study defines the last FXYD protein of unknown function as a modulator of Na,K-ATPase. Among FXYD protein, FXYD6 is unique in its expression in the inner ear, suggesting a role in endolymph composition.

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Catecholamine‐independent transient expression of tyrosine hydroxylase in primary auditory neurons is coincident with the onset of hearing in the rat cochlea

Cited by 17 publications

References 80 publications

Tyrosine Hydroxylase Expression in Type II Cochlear Afferents in Mice

Tyrosine Hydroxylase Expression in Type II Cochlear Afferents in Mice

Neurochemical characterization of tyrosine hydroxylase-immunoreactive interneurons in the developing rat cerebral cortex

FXYD6 Is a Novel Regulator of Na,K-ATPase Expressed in the Inner Ear

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