Excitotoxicity, Synaptic Repair, and Functional Recovery in the Mammalian Cochlea: A Review of Recent Findings

  title={Excitotoxicity, Synaptic Repair, and Functional Recovery in the Mammalian Cochlea: A Review of Recent Findings},
  author={Re´my Pujol and Jean-Luc Puel},
  journal={Annals of the New York Academy of Sciences},
  • R. Pujol, J. Puel
  • Published 1 November 1999
  • Biology
  • Annals of the New York Academy of Sciences
ABSTRACT: Besides its fast excitatory properties, glutamate is known to have neurotoxic properties when released in large amounts or when incompletely recycled. This so‐called excitotoxicity is involved in a number of acute and/or degenerative forms of neuropathology such as epilepsy, Alzheimer's, Parkinson's, stroke, and retinal ischemia. In the cochlea, excitotoxicity may occur in two pathological conditions: anoxia and noise trauma. It is characterized by a two‐step mechanism: (1) An acute… 
Morphological and functional correlates of vestibular synaptic deafferentation and repair in a mouse model of acute-onset vertigo
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Inhibition of the Adenosine A2A Receptor Mitigates Excitotoxic Injury in Organotypic Tissue Cultures of the Rat Cochlea
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Perinatal hipoxic ischemic injury in the auditory pathway and the effect of several neuroprotective agents
The effects of Nicotine, Melatonin, Resveratrol and DHA on the neonatal auditory system via measurement of auditory evoked potentials and characterization of the morphological, molecular and cellular integrity of the IC are studied.


Pathophysiology of the glutamatergic synapses in the cochlea.
Results indicate that the two classes of glutamate receptors (AMPA/kainate and NMDA), both found to be electrophysiologically active at the IHC-auditory nerve synapse, are also involved in the excitotoxic processes.
Synaptic regeneration and functional recovery after excitotoxic injury in the guinea pig cochlea.
An up-regulation of NMDA and metabotropic glutamate receptors in the primary auditory neurons occurred during this process of recovery and probably accounts for restoring hearing after temporary losses due to excitotoxic-related pathologies.
Implication of non‐NMDA and NMDA receptors in cochlear ischemia
The results suggest that, in the cochlea, the acute ischemic swelling of dendrite swelling primarily occurs via non-NMDA receptors, however, in radial dendrites contacting the IHCs on their modiolar side, NMDA receptors may contribute to excitotoxicity.
Chemical synaptic transmission in the cochlea
  • J. Puel
  • Biology
    Progress in Neurobiology
  • 1995
Excitotoxicity and repair of cochlear synapses after noise‐trauma induced hearing loss
The high degree of protection observed with kynurenate attests that dendritic damage is an important component in noise-induced hearing loss and demonstrates that a synaptic repair mechanism occurring within the first few days post-exposure is partly responsible for the recovery of temporary threshold shifts after an acoustic trauma.
The role of glutamate neurotoxicity in hypoxic-ischemic neuronal death.
Dennis W. ChoiDepartment of Neurology, Stanford University, Stanford,California 94305Steven M. RothmanDepartments of Pediatrics, Neurology, and Anatomy and Neurobiology,Washington University, St.
Excitatory amino acid antagonists protect cochlear auditory neurons from excitotoxicity
Results suggest that the acute swelling of radial dendrites primarily occurs via AMPA/kainate receptors, however, in radial d endrites contacting the inner hair cells on their modiolar side, NMDA receptors may be also involved.