Recovery of structure and function of inner ear afferent synapses following kainic acid excitotoxicity
Reference (42)
- et al.
Immunocytochemical localization of glutamate immunoreactivity in the guinea pig cochlea
Hear. Res.
(1989) - et al.
Kainic acid: an evaluation of its action on cochlear potentials
Hear. Res.
(1981) - et al.
The totoxicity of 3,3′-iminodipropionitrile: functional and morphological evidence of cochlear damage
Hear. Res.
(1994) - et al.
Glutamate neurotoxicity in the developing rat cochlea: physiological and morphological approaches
Brain Res.
(1991) - et al.
The effects of kainic acid on the cochlear ganglion of the rat
Hear. Res.
(1989) - et al.
Intracochlear application of acetylcholine alters sound-induced mechanical events within the cochlear partition
Hear. Res.
(1992) - et al.
Kainate and NMDA toxicity for cultured developing and adult rat spiral ganglion neurons: further evidence for a glutamatergic excitatory neurotransmission at the inner hair cell synapse
Brain Res.
(1991) - et al.
Identification of a glutamate/aspartate transporter in the rat cochlea
Hear. Res.
(1994) - et al.
Electrophysiological evidence for the presence of NMDA receptors in the guinea pig cochlea
Hear. Res.
(1991) - et al.
Alphaamino-3-hydroxy-5-methyl-4-isoxazole propionic acid electrophysiological and neurotoxic effects in the guinea-pig cochlea
Neuroscience
(1991)
Kainic acid selectively alters auditory dendrites connected with cochlear inner hair cells
Hear. Res.
Functional significance of dendritic swelling after loud sounds in the guinea pig cochlea
Hear. Res.
Excitotoxicity and the NMDA receptor
Trends Neurosci.
Glutamate neurotoxicity in rat auditory system: cochlear nuclear complex
Neurotoxicol. Teratol.
Changes in distortion product otoacoustic emissions and outer hair cells following interrupted noise exposures
Hear. Res.
Effects of kainic acid on the cochlear potentials and distortion product otoacoustic emissions in chinchilla
Hear. Res.
Preliminary descriptions of transient-evoked and distortion-product otoacoustic emissions from graduates of an intensive care nursery
J. Am. Acad. Audiol.
Neurotoxic action of kainic acid
J. Neurochem.
Asynchronous neural activity recorded from the round window
J. Acoust. Soc. Am.
A microiontophoretic study of the role of excitatory amino acids at the afferent synapses of mammalian inner hair cells
Eur. Arch. Oto. Rhino-Laryngol.
Enzymes of acetylcholine metabolism in the rat cochlea
Ann. Otol. Rhinol. Laryngol.
Cited by (45)
The use of animal models to study cell transplantation in neuropathic hearing loss
2019, Hearing ResearchEffects of selective auditory-nerve damage on the behavioral audiogram and temporal integration in the budgerigar
2019, Hearing ResearchCitation Excerpt :These results agree with previous reports in birds and mammals that KA damages AN afferent neurons/synapses without impacting sensory hair cells (Bledsoe et al., 1981; Juiz et al., 1989; Sun et al., 2001). KA exposure in guinea pig, rat, chinchilla, and chicken causes immediate swelling and breakage of AN afferent synapses due to excitotoxicity (Pujol et al., 1985; Shero et al., 1998) followed by limited recovery over the first few days following exposure (Zheng et al., 1999, 1997). More extensive exposures cause permanent loss of AN synapses and subsequent degeneration of ganglion cell bodies over weeks or months (Juiz et al., 1989; Sun et al., 2001).
From development to disease: Diverse functions of NMDA-type glutamate receptors in the lower auditory pathway
2015, NeuroscienceCitation Excerpt :NMDA-Rs may therefore protect SGNs from acute insult during temporary noise exposure through the reduction of surface AMPA-R expression. Following acute insult, SGN dendrites reconnect to their IHC targets (Zheng et al., 1997; Wang and Green, 2011) and studies suggest that NMDA-Rs play a neurotrophic role in this restoration process (Pujol and Puel, 1999). In experiments by Puel et al. (1995), recovery of cochlear function was observed just days following acute insult.
Time course of cochlear injury discharge (excitotoxicity) determined by ABR monitoring of contralateral cochlear events
2014, Hearing ResearchCitation Excerpt :In other words, long-term tissue changes have been extensively studied but not the early minutes after insult. A number of studies have focussed on the long-term regenerative recovery of auditory neurons after using excitotoxic protocols such as the application of kainic acid (Zheng et al., 1997) or by noise trauma (Puel et al., 1998). These authors reported on the influence of AMPA perfusion on inner haircell synapse recovery, and found that there was a 30% recovery over 24 h with newly formed dendrites in contact with the inner hair cell base.
Hyperactivity in the auditory midbrain after acoustic trauma: dependence on cochlear activity
2009, NeuroscienceCitation Excerpt :CoCl2 has been shown to suppress spontaneous firing of single auditory nerve fibres (Robertson and Johnstone, 1979). Kainic acid is well known to evoke excitotoxic effects in the cochlea, resulting in a loss of firing in the auditory nerve fibres (Bledsoe et al., 1981; Pujol et al., 1985; Zheng et al., 1996, 1997). The rapid and parallel effects of these perfusions on CAP and spontaneous rate are consistent with an intracochlear action.