Potential role of BFGF and retinoic acid in the regeneration of chicken cochlear hair cells

1996 ◽  
Vol 94 (1-2) ◽  
pp. 1-13 ◽  
Author(s):  
Kenneth H. Lee ◽  
Douglas A. Cotanche
Keyword(s):  
Retinoic Acid ◽  
Hair Cells ◽  
Potential Role ◽  
Cochlear Hair Cells

scholarly journals Triphenyl phosphate-induced developmental toxicity in zebrafish: Potential role of the retinoic acid receptor

2015 ◽  
Vol 161 ◽  
pp. 221-230 ◽  
Author(s):  
Gregory M. Isales ◽  
Rachel A. Hipszer ◽  
Tara D. Raftery ◽  
Albert Chen ◽  
Heather M. Stapleton ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Potential Role ◽  
Retinoic Acid Receptor ◽  
Developmental Toxicity ◽  
Triphenyl Phosphate ◽  
Acid Receptor

scholarly journals Elmod3 knockout leads to progressive hearing loss and abnormalities in cochlear hair cell stereocilia

2019 ◽  
Vol 28 (24) ◽  
pp. 4103-4112 ◽  
Author(s):  
Wu Li ◽  
Yong Feng ◽  
Anhai Chen ◽  
Taoxi Li ◽  
Sida Huang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Actin Cytoskeleton ◽  
Hearing Impairment ◽  
Hair Cells ◽  
Organ Of Corti ◽  
Vestibular Function ◽  
Outer Hair Cells ◽  
Auditory Function ◽  
Cochlear Hair Cells

Abstract ELMOD3, an ARL2 GTPase-activating protein, is implicated in causing hearing impairment in humans. However, the specific role of ELMOD3 in auditory function is still far from being elucidated. In the present study, we used the CRISPR/Cas9 technology to establish an Elmod3 knockout mice line in the C57BL/6 background (hereinafter referred to as Elmod3−/− mice) and investigated the role of Elmod3 in the cochlea and auditory function. Elmod3−/− mice started to exhibit hearing loss from 2 months of age, and the deafness progressed with aging, while the vestibular function of Elmod3−/− mice was normal. We also observed that Elmod3−/− mice showed thinning and receding hair cells in the organ of Corti and much lower expression of F-actin cytoskeleton in the cochlea compared with wild-type mice. The deafness associated with the mutation may be caused by cochlear hair cells dysfunction, which manifests with shortening and fusion of inner hair cells stereocilia and progressive degeneration of outer hair cells stereocilia. Our finding associates Elmod3 deficiencies with stereocilia dysmorphologies and reveals that they might play roles in the actin cytoskeleton dynamics in cochlear hair cells, and thus relate to hearing impairment.

scholarly journals Role of Myosin VI in the Differentiation of Cochlear Hair Cells

1999 ◽  
Vol 214 (2) ◽  
pp. 331-341 ◽  
Author(s):  
Tim Self ◽  
Tama Sobe ◽  
Neal G. Copeland ◽  
Nancy A. Jenkins ◽  
Karen B. Avraham ◽  
...  
Keyword(s):  
Hair Cells ◽  
Myosin Vi ◽  
Cochlear Hair Cells

The role of peroxiredoxin III in the ototoxic drug-induced mitochondrial apoptosis of cochlear hair cells

2008 ◽  
Vol 128 (9) ◽  
pp. 944-951 ◽  
Author(s):  
Ho Seok Choi ◽  
Kwang Joo Park ◽  
Sung Chul Hwang ◽  
Hun Yi Park ◽  
Young Sun Kim ◽  
...  
Keyword(s):  
Hair Cells ◽  
Mitochondrial Apoptosis ◽  
Drug Induced ◽  
Cochlear Hair Cells ◽  
Ototoxic Drug

scholarly journals Role and Mechanism of Vitamin A Metabolism in the Pathophysiology of Parkinson’s Disease

2021 ◽  
pp. 1-22
Author(s):  
Anaıs Marie ◽  
Morgane Darricau ◽  
Katia Touyarot ◽  
Louise C. Parr-Brownlie ◽  
Clémentine Bosch-Bouju
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Retinoic Acid ◽  
Vitamin A ◽  
Dopaminergic Neurons ◽  
Potential Role ◽  
Therapeutic Potential ◽  
Vitamin A Metabolism ◽  
Health And Wellbeing

Evidence shows that altered retinoic acid signaling may contribute to the pathogenesis and pathophysiology of Parkinson’s disease (PD). Retinoic acid is the bioactive derivative of the lipophilic vitamin A. Vitamin A is involved in several important homeostatic processes, such as cell differentiation, antioxidant activity, inflammation and neuronal plasticity. The role of vitamin A and its derivatives in the pathogenesis and pathophysiology of neurodegenerative diseases, and their potential as therapeutics, has drawn attention for more than 10 years. However, the literature sits in disparate fields. Vitamin A could act at the crossroad of multiple environmental and genetic factors of PD. The purpose of this review is to outline what is known about the role of vitamin A metabolism in the pathogenesis and pathophysiology of PD. We examine key biological systems and mechanisms that are under the control of vitamin A and its derivatives, which are (or could be) exploited for therapeutic potential in PD: the survival of dopaminergic neurons, oxidative stress, neuroinflammation, circadian rhythms, homeostasis of the enteric nervous system, and hormonal systems. We focus on the pivotal role of ALDH1A1, an enzyme expressed by dopaminergic neurons for the detoxification of these neurons, which is under the control of retinoic acid. By providing an integrated summary, this review will guide future studies on the potential role of vitamin A in the management of symptoms, health and wellbeing for PD patients.

scholarly journals TRPV5, TRPV6, TRPM6, and TRPM7 do not contribute to hair-cell mechanotransduction

2017 ◽  
Author(s):  
Clive P. Morgan ◽  
Hongyu Zhao ◽  
Meredith LeMasurier ◽  
Wei Xiong ◽  
Bifeng Pan ◽  
...  
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Auditory Function ◽  
Cochlear Hair Cells ◽  
Cochlear Hair Cell ◽  
Cysteine Substitution ◽  
Tip Link ◽  
Transient Receptor ◽  
Receptor Channel

AbstractThe hair-cell mechanotransduction channel remains unidentified. We tested whether four transient receptor channel (TRP) family members, TRPV5, TRPV6, TRPM6, and TRPM7, participated in transduction. Using cysteine-substitution mouse knock-ins and methanethiosulfonate reagents selective for those alleles, we found that inhibition of TRPV5 or TRPV6 had no effect on transduction in mouse cochlear hair cells. TRPM6 and TRPM7 each interacted with the tip-link component PCDH15 in cultured eukaryotic cells, which suggested they could participate in transduction. Cochlear hair cell transduction was insensitive to shRNA knockdown ofTrpm6orTrpm7, however, and was not affected by manipulations of Mg2+, which normally perturbs TRPM6 and TRPM7. To definitively examine the role of these two channels in transduction, we showed that deletion of either or both of their genes selectively in hair cells had no effect on auditory function. We suggest that TRPV5, TRPV6, TRPM6, and TRPM7 are unlikely to be the pore-forming subunit of the hair-cell transduction channel.

scholarly journals 5-HT and GABA Modulate Intrinsic Excitability of Type I Interneurons in Hermissenda

2009 ◽  
Vol 102 (5) ◽  
pp. 2825-2833 ◽  
Author(s):  
Nan Ge Jin ◽  
Lian-Ming Tian ◽  
Terry Crow
Keyword(s):  
Hair Cells ◽  
Spike Activity ◽  
Potential Role ◽  
Neuronal Excitability ◽  
Intrinsic Excitability ◽  
Resting Membrane Potential ◽  
Type I ◽  
Outward Currents

The sensory neurons (photoreceptors) in the visual system of Hermissenda are one site of plasticity produced by Pavlovian conditioning. A second site of plasticity produced by conditioning is the type I interneurons in the cerebropleural ganglia. Both photoreceptors and statocyst hair cells of the graviceptive system form monosynaptic connections with identified type I interneurons. Two proposed neurotransmitters in the graviceptive system, serotonin (5-HT) and γ-aminobutyric acid (GABA), have been shown to modify synaptic strength and intrinsic neuronal excitability in identified photoreceptors. However, the potential role of 5-HT and GABA in plasticity of type I interneurons has not been investigated. Here we show that 5-HT increased the peak amplitude of light-evoked complex excitatory postsynaptic potentials (EPSPs), enhanced intrinsic excitability, and increased spike activity of identified type Ie(A) interneurons. In contrast, 5-HT decreased spike activity and intrinsic excitability of type Ie(B) interneurons. The classification of two categories of type Ie interneurons was also supported by the observation that 5-HT produced opposite effects on whole cell steady-state outward currents in type Ie interneurons. Serotonin produced a reduction in the amplitude of light-evoked complex inhibitory PSPs (IPSPs), increased spontaneous spike activity, decreased intrinsic excitability, and depolarized the resting membrane potential of identified type Ii interneurons. In contrast to the effects of 5-HT, GABA produced inhibition in both types of Ie interneurons and type Ii interneurons. These results show that 5-HT and GABA can modulate the intrinsic excitability of type I interneurons independent of the presynaptic effects of the same transmitters on excitability and synaptic efficacy of photoreceptors.

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