Differential expression of ryanodine receptors in the rat cochlea

Morton-Jones, Rachel T.; Cannell, Mark B.; Jeyakumar, Loice H.; Fleischer, Sidney; Housley, Gary D.

doi:10.1016/j.neuroscience.2005.09.011

Cited by 25 publications

(18 citation statements)

References 62 publications

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“…Additional evidence that an alternative, TH independent, mechanism contributes to PCB ototoxicity was recently presented (Powers BE, 2009). Interestingly, these effects on cochlear development are produced primarily by non-coplanar PCBs (Kostyniak et al, 2005; Powers, Widholm, Lasky, & Schantz, 2006), and all three RyR isoforms are differentially expressed throughout the organ of Corti, including inner and outer hair cells, and within spiral ganglion neurons (Grant, Slapnick, Kennedy, & Hackney, 2006; Morton-Jones, Cannell, Jeyakumar, Fleischer, & Housley, 2006). RyR1 is the major isoform expressed in the outer hair cells where it is co-localized with nicotinic cholinergic receptors at “synaptic cisterns” resembling triadic junctions that are essential for engaging excitation-contraction coupling in skeletal muscle (Lioudyno et al, 2004).…”

Section: Ryr Macromolecular Complexes: Significance To Pcb-mediatementioning

confidence: 99%

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Pessah

Cherednichenko

Lein

2010

Pharmacology & Therapeutics

213

311

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Chronic low level polychlorinated biphenyls (PCB) exposures remain a significant public health concern since results from epidemiological studies indicate PCB burden is associated with immune system dysfunction, cardiovascular disease, and impairment of the developing nervous system. Of these various adverse health effects, developmental neurotoxicity has emerged as a particularly vulnerable endpoint in PCB toxicity. Arguably the most pervasive biological effects of PCBs could be mediated by their ability to alter the spatial and temporal fidelity of Ca 2+ signals through one or more receptor mediated processes. This review will focus on our current knowledge of the structure and function of ryanodine receptors (RyRs) in muscle and nerve cells and how PCBs and related non-coplanar structures alter these functions. The molecular and cellular mechanisms by which noncoplanar PCBs and related structures alter local and global Ca 2+ signaling properties and the possible short and long-term consequences of these perturbations on neurodevelopment and neurodegeneration are reviewed. Dioxin-like and non-dioxin-like PCBs Occurrence and concerns to public healthPolychlorinated biphenyls (PCBs) are synthetic chlorinated aromatic hydrocarbons that are non-flammable, chemically stable and have high boiling points. In the United States, PCBs were synthesized and marketed primarily as Aroclor® mixtures whose degree of chlorination was identified by a four-digit designation (e.g., 1248, 1254, 1260, etc.), with the first two digits identifying the mixture as PCBs and the last two digits identifying the percent of chlorine used during synthesis. A higher degree of PCB chlorination increases melting point and lipophilicity, whereas lower chlorination increases vapor pressure and water solubility. Similar PCB mixtures were synthesized worldwide and identified under several trade names such as Clophen® and Kanechlor®. PCB mixtures, especially those of intermediate chlorination, such as Aroclor 1248 and Aroclor 1254, were widely used in several industries for their insulation and heat dissipating properties. PCBs were also broadly incorporated into a variety of common products such as pesticide extenders, plastics, varnishes, adhesives, carbonless copy paper, newsprint, fluorescent light ballasts and caulking compounds (Ross, 2004).By 1977, when PCBs were banned, more than 600,000 tons were manufactured in the United States, and global production is estimated at over 1.5 million tons (Breivik, Sweetman, Pacyna, & Jones, 2002). Because of their extensive industrial use and chemical stability, PCBs have Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the conten...

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Section: Ryr Macromolecular Complexes: Significance To Pcb-mediatementioning

confidence: 99%

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Pessah

Cherednichenko

Lein

2010

Pharmacology & Therapeutics

213

311

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“…Also present is a Ca 2þ -leakage channel that determines Ca 2þ efflux from the sacs, and so partly determines resting cisternal Ca 2þ . Type I ryanodine receptors (RyRs; Grant et al, 2006;Morton-Jones et al, 2006) involved in Ca-induced-Ca-release (CICR) have also been found in these sacs (Grant et al, 2006;Lioudyno et al, 2004), suggesting that they are involved in CICR, and therefore act to amplify rather than buffer any transient rise in cytosolic Ca 2þ (due to an inflow through the plasma membrane). The sensitivity of the RyRs-controlled release from the sacs is probably also modulated by intracellular messengers (Berridge et al, 2003), and there may also be sac-to-sac communication called 'Ca 2þ -sparks', where one sac triggers release from others nearby (see Russell and Lukashkin, 2008).…”

Section: Ca 2þ Sequestration Sacs In Ohcsmentioning

confidence: 99%

Ion flow in cochlear hair cells and the regulation of hearing sensitivity

Patuzzi

2011

Hearing Research

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“…Inner hair cells, which express RyR1 and RyR2 [253, 254], modify afferent nerve fiber activity in response to exogenous ryanodine [253]. Calcium release from RyR-gated [255, 256] and inositol 1,4,5-trisphosphate receptor (IP 3 R)-gated [255] stores potentiates exocytosis from vestibular hair cells during prolonged stimulation.…”

Section: Calcium Buffering Sequestration and Release From Internal mentioning

confidence: 99%

The Molecular Architecture of Ribbon Presynaptic Terminals

Zanazzi

Matthews

2009

Mol Neurobiol

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The primary receptor neurons of the auditory, vestibular, and visual systems encode a broad range of sensory information by modulating the tonic release of the neurotransmitter glutamate in response to graded changes in membrane potential. The output synapses of these neurons are marked by structures called synaptic ribbons, which tether a pool of releasable synaptic vesicles at the active zone, where glutamate release occurs in response to calcium influx through L-type channels. Ribbons are composed primarily of the protein, RIBEYE, which is unique to ribbon synapses, but cytomatrix proteins that regulate the vesicle cycle in conventional terminals, such as Piccolo and Bassoon, also are found at ribbons. Conventional and ribbon terminals differ, however, in the size, molecular composition, and mobilization of their synaptic vesicle pools. Calcium-binding proteins and plasmamembrane calcium pumps, together with endomembrane pumps and channels, play important roles in calcium handling at ribbon synapses. Taken together, emerging evidence suggests that several molecular and cellular specializations work in concert to support the sustained exocytosis of glutamate that is a hallmark of ribbon synapses. Consistent with its functional importance, abnormalities in a variety of functional aspects of the ribbon presynaptic terminal underlie several forms of auditory neuropathy and retinopathy.

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Differential expression of ryanodine receptors in the rat cochlea

Cited by 25 publications

References 62 publications

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Ion flow in cochlear hair cells and the regulation of hearing sensitivity

The Molecular Architecture of Ribbon Presynaptic Terminals

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