Fibroblast growth factor‐2 immunoreactivity is present in the central and peripheral auditory pathways of adult rats

Silva, Vivian Alessandra; Gomide, V. C.; Chadi, Gerson

doi:10.1002/jmor.10345

Cited by 10 publications

(13 citation statements)

References 38 publications

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“…This possibly explains why otic explants continue to produce neuroblasts for many days, far longer than during normal embryonic development. In rodent embryos, differentiating auditory neurons express Fgf1, Fgf2, Fgf5 and Fgf10 [36], [39]–[42], which could help mediate feedback inhibition. Unfortunately, relevant functional studies are lacking.…”

Section: Discussionmentioning

confidence: 99%

A Spatial and Temporal Gradient of Fgf Differentially Regulates Distinct Stages of Neural Development in the Zebrafish Inner Ear

Vemaraju¹,

Kantarci²,

Padanad³

et al. 2012

PLoS Genet

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Neuroblasts of the statoacoustic ganglion (SAG) initially form in the floor of the otic vesicle during a relatively brief developmental window. They soon delaminate and undergo a protracted phase of proliferation and migration (transit-amplification). Neuroblasts eventually differentiate and extend processes bi-directionally to synapse with hair cells in the inner ear and various targets in the hindbrain. Our studies in zebrafish have shown that Fgf signaling controls multiple phases of this complex developmental process. Moderate levels of Fgf in a gradient emanating from the nascent utricular macula specify SAG neuroblasts in laterally adjacent otic epithelium. At a later stage, differentiating SAG neurons express Fgf5, which serves two functions: First, as SAG neurons accumulate, increasing levels of Fgf exceed an upper threshold that terminates the initial phase of neuroblast specification. Second, elevated Fgf delays differentiation of transit-amplifying cells, balancing the rate of progenitor renewal with neuronal differentiation. Laser-ablation of mature SAG neurons abolishes feedback-inhibition and causes precocious neuronal differentiation. Similar effects are obtained by Fgf5-knockdown or global impairment of Fgf signaling, whereas Fgf misexpression has the opposite effect. Thus Fgf signaling renders SAG development self-regulating, ensuring steady production of an appropriate number of neurons as the larva grows.

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Section: Discussionmentioning

confidence: 99%

A Spatial and Temporal Gradient of Fgf Differentially Regulates Distinct Stages of Neural Development in the Zebrafish Inner Ear

Vemaraju¹,

Kantarci²,

Padanad³

et al. 2012

PLoS Genet

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“…We hypothesize that the perturbation of glial function resulting from loss of Fgfr1 and Fgfr2 results in attenuation of trophic support of neurons by glial cells, leading to significant neuronal loss and pathology of the auditory pathway. Because neurons and nerve fibers, but not myelinating glial cells, produce FGF-1 and FGF-2 in the spiral ganglion and cochlear nucleus (Luo et al, 1993; Pirvola et al, 1995; Riedel et al, 1995; Silva et al, 2005), FGF/FGF receptors provide an efficient means of reciprocal signaling between neurons and glia.…”

Section: Discussionmentioning

confidence: 99%

“…FGF-1 and FGF-2 are expressed by SGN and neurons in the cochlear nucleus (Luo et al, 1993; Pirvola et al, 1995; Riedel et al, 1995; Silva et al, 2005). Schwann cells and oligodendrocytes express Fgfr1, Fgfr2, and Fgfr3 (Bansal et al, 1996, 2003; Grothe and Nikkah, 2001).…”

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confidence: 99%

Inactivation of fibroblast growth factor receptor signaling in myelinating glial cells results in significant loss of adult spiral ganglion neurons accompanied by age‐related hearing impairment

Wang

Furusho

D'Sa

et al. 2009

J of Neuroscience Research

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Hearing loss has been attributed to many factors, including degeneration of sensory neurons in the auditory pathway and demyelination along the cochlear nerve. Fibroblast growth factors (FGFs), which signal through four receptors (Fgfrs), are produced by auditory neurons and play a key role in embryonic development of the cochlea and in neuroprotection against sound-induced injury. However, the role of FGF signaling in the maintenance of normal auditory function in adult and aging mice remains to be elucidated. Furthermore, the contribution of glial cells, which myelinate the cochlear nerves, is poorly understood. To address these questions, we generated transgenic mice in which Fgfr1 and Fgfr2 were specifically inactivated in Schwann cells and oligodendrocytes but not in neurons. Adult mutant mice exhibited late onset of hearing impairment, which progressed markedly with age. The hearing impairment was accompanied by significant loss of myelinated spiral ganglion neurons. The pathology extended into the cochlear nucleus, without apparent loss of myelin or of the deletion-bearing glial cells themselves. This suggests that perturbation of FGF receptor-mediated glial function leads to the attenuation of glial support of neurons, leading to their loss and impairment of auditory functions. Thus, FGF/FGF receptor signaling provides a potentially novel mechanism of maintaining reciprocal interactions between neurons and glia in adult and aging animals. Dysfunction of glial cells and FGF receptor signaling may therefore be implicated in neurodegenerative hearing loss associated with normal aging.

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“…The present paper also demonstrated a delicate NPY labeling in the nucleus of IHC and OHC. In fact, NPY and its Y1 receptor has been described in the cytoplasm and nucleus of endothelial cells, probably related to the regulation of cytosolic and nuclear-free calcium or other autocrine regulatory function (Jacques, Sader, Perreault, Abdel-Samad, & Provost, 2006;Jacques et al, 2003;Silva, Gomide, & Chadi, 2005).…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y in Rat Spiral Ganglion Neurons and Inner Hair Cells of Organ of Corti and Effects of a Nontraumatic Acoustic Stimulation

Gomide

Laureano

Silveira

et al. 2009

International Journal of Neuroscience

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Neuropeptide Y (NPY) is an important neuromodulator found in central and peripheral neurons. NPY was investigated in the peripheral auditory pathway of conventional housed rats and after nontraumatic sound stimulation in order to localize the molecule and also to describe its response to sound stimulus. Rats from the stimulation experiment were housed in monitored sound-proofed rooms. Stimulated animals received sound stimuli (pure tone bursts of 8 kHz, 50 ms duration presented at a rate of 2 per second) at an intensity of 80 dB sound pressure level for 1 hr per day during 7 days. After euthanizing, rat cochleae were processed for one-color immunohistochemistry. The NPY immunoreactivity was detected in inner hair cells (IHC) and also in pillar and Deiters' cells of organ of Corti, and in the spiral ganglion putative type I (> or = 1,009 microm(3)) and type II (< or = 225 microm(3)) neurons. Outer hair cells (OHC) showed light immunoreaction product. Quantitative microdensitometry showed strong and moderate immunoreactions in IHC and spiral ganglion neurons, respectively, without differences among cochlear turns. One week of acoustic stimulation was not able to induce changes in the NPY immunoreactivity intensity in the IHC of cochlea. However, stimulated rats showed an overall increase in the number of putative type I and type II NPY immunoreactive spiral ganglion neurons with strong, moderate, and weak immunolabeling. Localization and responses of NPY to acoustic stimulus suggest an involvement of the neuropeptide in the neuromodulation of afferent transmission in the rat peripheral auditory pathway.

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Fibroblast growth factor‐2 immunoreactivity is present in the central and peripheral auditory pathways of adult rats

Cited by 10 publications

References 38 publications

A Spatial and Temporal Gradient of Fgf Differentially Regulates Distinct Stages of Neural Development in the Zebrafish Inner Ear

A Spatial and Temporal Gradient of Fgf Differentially Regulates Distinct Stages of Neural Development in the Zebrafish Inner Ear

Inactivation of fibroblast growth factor receptor signaling in myelinating glial cells results in significant loss of adult spiral ganglion neurons accompanied by age‐related hearing impairment

Neuropeptide Y in Rat Spiral Ganglion Neurons and Inner Hair Cells of Organ of Corti and Effects of a Nontraumatic Acoustic Stimulation

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