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Rat Cochlea (rat + cochlea)
Selected AbstractsThe ultrastructural distribution of prestin in outer hair cells: a post-embedding immunogold investigation of low-frequency and high-frequency regions of the rat cochleaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2010Shanthini Mahendrasingam Abstract Outer hair cells (OHCs) of the mammalian cochlea besides being sensory receptors also generate force to amplify sound-induced displacements of the basilar membrane thus enhancing auditory sensitivity and frequency selectivity. This force generation is attributable to the voltage-dependent contractility of the OHCs underpinned by the motile protein, prestin. Prestin is located in the basolateral wall of OHCs and is thought to alter its conformation in response to changes in membrane potential. The precise ultrastructural distribution of prestin was determined using post-embedding immunogold labelling and the density of the labelling was compared in low-frequency and high-frequency regions of the cochlea. The labelling was confined to the basolateral plasma membrane in hearing rats but declined towards the base of the cells below the nucleus. In pre-hearing animals, prestin labelling was lower in the membrane and also occurred in the cytoplasm, presumably reflecting its production during development. The densities of labelling in low-frequency and high-frequency regions of the cochlea were similar. Non-linear capacitance, thought to reflect charge movements during conformational changes in prestin, was measured in OHCs in isolated cochlear coils of hearing animals. The OHC non-linear capacitance in the same regions assayed in the immunolabelling was also similar in both the apex and base, with charge densities of 10 000/,m2 expressed relative to the lateral membrane area. The results suggest that prestin density, and by implication force production, is similar in low-frequency and high-frequency OHCs. [source] Developmental regulation of neuron-specific P2X3 receptor expression in the rat cochleaTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 2 2005Lin-Chien Huang Abstract ATP-gated ion channels assembled from P2X3 receptor (P2X3R) subunits contribute to neurotransmission and neurotrophic signaling, associated with neurite development and synaptogenesis, particularly in peripheral sensory neurons. Here, P2X3R expression was characterized in the rat cochlea from embryonic day 16 (E16) to adult (P49,56), using RT-PCR and immunohistochemistry. P2X3R mRNA was strongly expressed in the cochlea prior to birth, declined to a minimal level at P14, and was absent in adult tissue. P2X3R protein expression was confined to spiral ganglion neurons (SGN) within Rosenthal's canal of the cochlea. At E16, immunolabeling was detected in the SGN neurites, but not the distal neurite projection within the developing sensory epithelium (greater epithelial ridge). From E18, the immunolabeling was observed in the peripheral neurites innervating the inner hair cells but was reduced by P6. However, from P2,8, immunolabeling of the SGN neurites extended to include the outer spiral bundle fiber tract beneath the outer hair cells. This labeling of type II SGN afferent fiber declined after P8. By P14, all synaptic terminal immunolabeling in the organ of Corti was absent, and SGN cell body labeling was minimal. In adult cochlear tissue, P2X3R immunolabeling was not detected. Noise exposure did not induce P2X3R expression in the adult cochlea. These data indicate that ATP-gated ion channels incorporating P2X3R subunit expression are specifically targeted to the afferent terminals just prior to the onset of hearing, and likely contribute to the neurotrophic signaling which establishes functional auditory neurotransmission. J. Comp. Neurol. 484:133,143, 2005. © 2005 Wiley-Liss, Inc. [source] Somatostatin and gentamicin-induced auditory hair cell lossTHE LARYNGOSCOPE, Issue 5 2009Antje Caelers PhD Abstract Objective/Hypothesis: Hair cells of the mammalian auditory system do not regenerate, and therefore their loss leads to irreversible hearing loss. Aminoglycosides, among other substances, can irreversibly damage hair cells. Somatostatin, a peptide with hormone/neurotransmitter properties, has neuroprotective effects by binding to its receptor. In this study, we tested whether somatostatin can protect hair cells from gentamicin-induced damage in vitro. Study Design: This study confirmed the expression of somatostatin receptor mRNA within the cochlea and analyzed the effect of somatostatin on gentamicin-induced hair cell damage and death in vitro. Methods: Expression of somatostatin receptor mRNA in the rat cochlea was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). Protection of auditory hair cells from gentamicin was tested using two different concentrations (1 ,M and 5 ,M, respectively) of somatostatin. Results: We detected somatostatin receptor-1 and -2 mRNA and in the organ of Corti (OC), spiral ganglion, and stria vascularis by RT-PCR. Moreover, we could see significantly less hair cell loss in the OCs that were pretreated with either 1 ,M or 5 ,M of somatostatin as compared with samples treated with gentamicin alone. Conclusions: Decreased hair cell loss in somatostatin-treated samples that had been exposed to gentamicin provides evidence for a protective effect of somatostatin in aminoglycoside-induced hair cell death in vitro. [source] |