Calcium currents in dissociated cochlear neurons from the chick embryo and their modification by neurotrophin-3

Jimenez, C. Paradinas; Giráldez, Fernando; Represa, Juan; García-Díaz, J. Fernando

doi:10.1016/s0306-4522(96)00505-2

Cited by 29 publications

(25 citation statements)

References 53 publications

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“…This would suggest that mechanisms other than selective survival account for the robust alterations that were observed in the present study. Because we had noted previously changes in voltage-gated ion channel density with immunocytochemical studies (Adamson et al, 2002a), we assume that part of the mechanism involves altered gene expression that underlies changes in current density (Levine et al, 1995;Jimenez et al, 1997;Baldelli et al, 2000). However, from the time courses that we chose to evaluate in the present study, we cannot rule out that more immediate modifications may also be involved, such as those revealed for glutamate receptors (Levine et al, 1998;Arvanov et al, 2000;Balkowiec et al, 2000) as well as in some types of voltage-gated ion channels (Kafitz et al, 1999;Tucker and Fadool, 2002).…”

Section: Discussionmentioning

confidence: 89%

Complex Regulation of Spiral Ganglion Neuron Firing Patterns by Neurotrophin-3

Zhou

Liu²,

Davis³

2005

J. Neurosci.

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Auditory information is conveyed into the CNS via the spiral ganglion neurons, cells that possess distinctive electrophysiological properties that vary according to their cochlear innervation. Neurons from the base of the cochlea fire action potentials with shorter latencies and durations with more rapid accommodation than apical neurons (Adamson et al., 2002b). Interestingly, these features are altered by exposure to brain-derived neurotrophic factor and neurotrophin-3 (NT-3), suggesting that the electrophysiological diversity is not preprogrammed into the neurons but instead results from extrinsic regulation. In support of this, gradients of neurotrophins exist in the cochlea that could account for the apex-base differences in firing. To understand the determinants of spiral ganglion function, we characterized the NT-3 concentration dependence and mode of action on spiral ganglion neurons. Whole-cell current-clamp recordings were made from mouse basal spiral ganglion neurons (postnatal day 5) exposed to different concentrations of NT-3 for 3 d in vitro. Measurements of accommodation, latency, onset time course, and action potential latency revealed a nonmonotonic dependence on NT-3 concentration, with a peak effect occurring at 10 ng/ml. Addition of NT-3 at different time points showed that neurotrophin exposure altered the firing features of existing neurons rather than supporting differential survival. These experiments establish that the electrophysiological phenotype of spiral ganglion neurons depends critically on the precise concentration of NT-3 and that the functional organization of this component of the peripheral auditory system results from a complex interplay between multiple kinds of neurotrophins and their cognate receptors.

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Section: Discussionmentioning

confidence: 89%

Complex Regulation of Spiral Ganglion Neuron Firing Patterns by Neurotrophin-3

Zhou

Liu²,

Davis³

2005

J. Neurosci.

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“…We identified only one Ca 2+ channel gene, coding for the low voltage-gated, T-type, a1G subunit (CACNA1G), in both human and mouse libraries. I CaT is found briefly during different stages of development in the cochlear ganglion and hair cells of the chick (Jimenez et al 1997;Sokolowski 2006;Levic et al submitted). Both human and mouse libraries used in the present study are from fetal and late neonatal stages, respectively, suggesting a reason for detection in these libraries.…”

Section: K+ Channelsmentioning

confidence: 99%

“…Both human and mouse libraries used in the present study are from fetal and late neonatal stages, respectively, suggesting a reason for detection in these libraries. Ca 2+ channel subunits a1A (P/Q type) and a1B (L and N type) were found in a rat vestibular library (Roche et al 2005), while P and Q types were reported in recordings from chick embryonic cochlear ganglion cells (Jimenez et al 1997). Other Ca 2+ channel subunits, for which there was no strong and consistent amplification, such a1S, b2, and g, were never found in any of the available inner ear cDNA libraries, nor detected by microarray experiments.…”

Section: K+ Channelsmentioning

confidence: 99%

Ion Channel Gene Expression in the Inner Ear

Gabashvili

Sokolowski

Morton

et al. 2007

JARO

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The ion channel genome is still being defined despite numerous publications on the subject. The ion channel transcriptome is even more difficult to assess. Using high-throughput computational tools, we surveyed all available inner ear cDNA libraries to identify genes coding for ion channels. We mapped over 100,000 expressed sequence tags (ESTs) derived from human cochlea, mouse organ of Corti, mouse and zebrafish inner ear, and rat vestibular end organs to Homo sapiens, Mus musculus, Danio rerio, and Rattus norvegicus genomes. A survey of EST data alone reveals that at least a third of the ion channel genome is expressed in the inner ear, with highest expression occurring in hair cell-enriched mouse organ of Corti and rat vestibule. Our data and comparisons with other experimental techniques that measure gene expression show that every method has its limitations and does not per se provide a complete coverage of the inner ear ion channelome. In addition, the data show that most genes produce alternative transcripts with the same spectrum across multiple organisms, no ion channel gene variants are unique to the inner ear, and many splice variants have yet to be annotated. Our high-throughput approach offers a qualitative computational and experimental analysis of ion channel genes in inner ear cDNA collections. A lack of data and incomplete gene annotations prevent both rigorous statistical analyses and comparisons of entire ion channelomes derived from different tissues and organisms.

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“…In addition to the concomitant trkB and trkC protein expression in the cochlea and cochlear ganglion demonstrated by the present study, previous studies of the avian auditory periphery have documented the presence of BDNF Hallböök and Fritzsch, 1997;Pirvola et al, 1997), NT-3 (Pirvola et al, 1997), and trkB (Hallböök and Fritzsch, 1997;Pirvola et al, 1997) mRNA in the basilar papilla and BDNF (Bernd et al, 1994), NT-3 (Bernd et al, 1994), trkB (Déchant et al, 1993;Bernd et al, 1994;Hallböök and Fritzsch, 1997;Pirvola et al, 1997), and trkC (Bernd et al, 1994;Pirvola et al, 1997) mRNA in the cochlear ganglion. Furthermore, in vitro studies of the developing cochlear ganglion have shown active effects of BDNF Represa et al, 1993;Hossain et al, 1997;Pirvola et al, 1997;Sokolowski, 1997) and NT-3 (Avila et al, 1993;Represa et al, 1993;Jimènez et al, 1997;Pirvola et al, 1997;San José et al, 1997;Sokolowski, 1997) on cell proliferation, cell survival, and neurite outgrowth. Our study is the first to demonstrate neurotrophin tyrosine kinase receptors in the central auditory system of birds; we find a pattern of spatial and temporal overlap of trkB and trkC expression in auditory brainstem nuclei that is even more pronounced and pro- Fig.…”

Section: Overlapping Expression Of Neurotrophins/trks In Avian Auditomentioning

confidence: 99%

“…Since the discovery of the first neurotrophin, nerve growth factor (NGF), three other neurotrophins (brainderived neurotrophic factor (BDNF), neurotrophin-4/5 (NT-4/5), and neurotrophin-3 (NT-3) have been discovered, and our understanding of neurotrophins has broadened sufficiently such that we are beginning to identify the numerous aspects of neuronal development, maintenance, and repair that neurotrophins can mediate. These varied aspects include cell differentiation (reviewed in Chao, 1992;, ion channel expression (Jimènez et al, 1997), neuronal plasticity (Lindholm et al, 1994), and cell death (Carter et al, 1996;Frade et al, 1996;Bredesen and Rabizadeh, 1997;for review: Frade and Barde, 1998). Moreover, the presence of neurotrophins and their receptors has been demonstrated in the adult brain (Friedman et al, 1991;Wu et al, 1996;Conner et al, 1997;Yan et al, 1997), suggesting that neurotrophins are necessary both for the initiation and for the maintenance of synaptic circuitry.…”

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confidence: 99%

Ontogenetic expression of trk neurotrophin receptors in the chick auditory system

et al. 1999

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Neurotrophins and their cognate receptors are critical to normal nervous system development. Trk receptors are high-affinity receptors for nerve-growth factor (trkA), brain-derived neurotrophic factor and neurotrophin-4/5 (trkB), and neurotrophin-3 (trkC). We examine the expression of these three neurotrophin tyrosine kinase receptors in the chick auditory system throughout most of development. Trks were localized in the auditory brainstem, the cochlear ganglion, and the basilar papilla of chicks from embryonic (E) day 5 to E21, by using antibodies and standard immunocytochemical methods. TrkB mRNA was localized in brainstem nuclei by in situ hybridization.TrkB and trkC are highly expressed in the embryonic auditory brainstem, and their patterns of expression are both spatially and temporally dynamic. During early brainstem development, trkB and trkC are localized in the neuronal cell bodies and in the surrounding neuropil of nucleus magnocellularis (NM) and nucleus laminaris (NL). During later development, trkC is expressed in the cell bodies of NM and NL, whereas trkB is expressed in the nerve calyces surrounding NM neurons and in the ventral, but not the dorsal, dendrites of NL. In the periphery, trkB and trkC are located in the cochlear ganglion neurons and in peripheral fibers innervating the basilar papilla and synapsing at the base of hair cells.The protracted expression of trks seen in our materials is consistent with the hypothesis that the neurotrophins/tyrosine kinase receptors play one or several roles in the development of auditory circuitry. In particular, the polarized expression of trkB in NL is coincident with refinement of NM terminal arborizations on NL.

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Calcium currents in dissociated cochlear neurons from the chick embryo and their modification by neurotrophin-3

Cited by 29 publications

References 53 publications

Complex Regulation of Spiral Ganglion Neuron Firing Patterns by Neurotrophin-3

Complex Regulation of Spiral Ganglion Neuron Firing Patterns by Neurotrophin-3

Ion Channel Gene Expression in the Inner Ear

Ontogenetic expression of trk neurotrophin receptors in the chick auditory system

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