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Titolo:
CHEMICAL SYNAPTIC TRANSMISSION IN THE COCHLEA
Autore:
PUEL JL;
Indirizzi:
INSERM,U254,LAB NEUROBIOL AUDIT PLAST SYNAPT F-34295 MONTPELLIER 5 FRANCE UNIV MONTPELLIER 1,CHR HOSP ST CHARLES F-34295 MONTPELLIER 5 FRANCE
Titolo Testata:
Progress in neurobiology
fascicolo: 6, volume: 47, anno: 1995,
pagine: 449 -
SICI:
0301-0082(1995)47:6<449:CSTITC>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; EXCITATORY AMINO-ACIDS; METHYL-D-ASPARTATE; ACOUSTIC DISTORTION PRODUCTS; AUDITORY-NERVE RESPONSES; SPIRAL GANGLION NEURONS; ACTIVE MICROMECHANICAL PROPERTIES; CROSSED OLIVOCOCHLEAR BUNDLE; INOSITOL PHOSPHATE FORMATION;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
252
Recensione:
Indirizzi per estratti:
Citazione:
J.L. Puel, "CHEMICAL SYNAPTIC TRANSMISSION IN THE COCHLEA", Progress in neurobiology, 47(6), 1995, pp. 449

Abstract

The last two decades have witnessed major progress in the understanding of cochlear mechanical functioning, and in the emergence of cochlear neurochemistry and neuropharmacology. Recent models describe active processes within the cochlea that amplify and sharpen the mechanical response to sound. Although it is widely accepted that outer hair cells(OHCs) contribute to these processes, the nature of the medial efferent influence on cochlear mechanics needs further clarification. Acetylcholine (ACh) is the major transmitter released onto OHCs during the stimulation oi these efferents. The inhibitory influence of this systemis mediated by post and presynaptic nicontinic and muscarinic receptors and the role of other neuroactive substances [gamma-aminobutyric acid (GABA), calcitonin gene-related peptide (CGRP), adenosine 5'-triphosphate (ATP) or nitric oxide (NO)] remains to be determined. The innerhair cells (IHCs) that transduce the mechanical displacements into neural activity, release glutamate on receptor-activated channels of AMPA, kainate. and NMDA types. This synapse is in turn controlled and/or regulated by the lateral efferents containing a cocktail of neuroactive substances (ACh, GABA. dopamine, enkephalins, dynorphin, CGRP). Thisglutamatergic nature of the IHCs is responsible for the acute destruction of the nerve endings and subsequently For neuronal death, damage usually described in various cochlear diseases (noise-induced hearing losses, neural presbycusis and certain forms of sudden deafness or peripheral tinnitus). These pathologies also include a regrowth of new dendritic processes by surviving neurons up to IHCs. Understanding the subtle molecular mechanisms which underly the control of neuronal excitability. synaptic plasticity and neuronal death in cochlear function and disease is a very important issue for the development of future therapies.

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Documento generato il 04/12/20 alle ore 19:41:07