The effects of kainic acid on the cochlear ganglion of the rat

Juı́z, José M.; Rueda, Joaquı́n; Merchán, Jaime A.; Sala, Maria L.

doi:10.1016/0378-5955(89)90100-7

Cited by 72 publications

(42 citation statements)

References 38 publications

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“…These changes resemble those seen after application of glutamate or kainate, another glutamate agonist, into the scala tympani of mammals and birds [Bledsoe et al, 1981;Coyle, 1983;Kusakari et al, 1984;Pujol et al, 1985;Dolan et al, 1990;Janssen et al, 1991;Zheng et al, 1996Zheng et al, , 1997Sun et al, 2000Sun et al, , 2001. The anatomical results of the present experiments with AMPA show a similar massive swelling of auditory afferent dendrites under the inner hair cells as observed in mammals using glutamate analogues [Pujol et al, 1985;Juiz et al, 1989;Puel et al, 1994;Puel, 1995;Shero et al, 1998]. …”

Section: Less Recovery From Ampa Excitotoxicity In Birds Than In Mammalssupporting

confidence: 70%

“…Like glutamate, agonists such as kainic acid or ·-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) selectively destroy the type I afferent dendrites innervating mammalian inner hair cells [Bledsoe et al, 1981;Pujol et al, 1985;Juiz et al, 1989;Dolan et al, 1990;Puel et al, 1994;Puel, 1995;Zheng et al, 1997]. In the guinea pig, rat and chinchilla, the acute exposure of the inner ear to artificial perilymph containing AMPA or kainic acid results in complete elimination of the compound action potential (CAP), whereas the cochlear microphonic, distortion product otoacoustic emission and endolymphatic potential remain unaffected [Bledsoe et al, 1981;Juiz et al, 1989;Puel et al, 1991;Zheng et al, 1996]. However, repair of auditory afferent nerve synapses in these mammals after the excitotoxic insult occurs, at least with AMPA [Puel, 1995].…”

Section: Introductionmentioning

confidence: 99%

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Functional Recovery of Hearing following AMPA-Induced Reversible Disruption of Hair Cell Afferent Synapses in the Avian Inner Ear

Reng

Müller²,

Smolders³

2001

Audiol Neurotol

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Hair cells in the avian inner ear can regenerate after acoustic trauma or ototoxic insult, and significant functional recovery from hearing loss occurs. However, small residual deficits remain, possibly as a result of incomplete reestablishment of the hair cell neural synaptic contacts. The aim of the present study was to determine if intracochlear application of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), an excitotoxic glutamate agonist, causes reversible disruption of hair cell neural contacts in the bird, and to what extent functional recovery occurs if synaptic contacts are reestablished. Compound action potential (CAP) responses to tone bursts were recorded to determine hearing thresholds during a recovery period of up to 4 months. Subsequently, the response properties of single auditory nerve fibers were analyzed in the same animals. Instillation of AMPA into the perilymph of the scala tympani led to immediate abolition of CAP thresholds. Partial recovery occurred over a period of 2–3 weeks, without further improvement of thresholds thereafter. High-frequency thresholds did not reach control values even after 3–4 months of recovery. Single-ganglion cell response properties, obtained 3–4 months after AMPA treatment, showed elevated thresholds at the fiber’s characteristic frequency (CF) for units with CF above 0.3 kHz. Sharpness of tuning (Q_{10 dB}) was reduced in units with CF above 0.4 kHz. The spontaneous firing rate was higher in units with CF above 0.18 kHz. The maximum sound-evoked discharge rate was also increased. Transmission electron micrographs of the basilar papilla showed that, following AMPA treatment, the nerve endings went through a sequence of swelling, degeneration and recovery over a period of 3–7 days. The process of neosynaptogenesis was completed 14 days after exposure. The present findings are strong evidence for a role of glutamate or a related excitatory amino acid as the afferent transmitter in the avian inner ear. In addition they show that functional recovery after disruption and regeneration of hair cell neural synapses, without apparent damage to the hair cells, is incomplete.

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Section: Less Recovery From Ampa Excitotoxicity In Birds Than In Mammalssupporting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Functional Recovery of Hearing following AMPA-Induced Reversible Disruption of Hair Cell Afferent Synapses in the Avian Inner Ear

Reng

Müller²,

Smolders³

2001

Audiol Neurotol

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“…The dependency between hair cell excitability and the state of the nerve terminals was confirmed by the downregulation of I Na because the nerve fibers recontacted the hair cells 1 week after the kainate application. The lack of reafferentation after kainate treatment in 20% of the tested rats may result from the toxic effect of kainate previously reported on auditory ganglion neurons (Juiz et al, 1989). The persistence of I Na in a small population of adult hair cells under control conditions remains unexplained.…”

Section: Recovery Of Excitability In Adult Utricle Hair Cells After Nmentioning

confidence: 84%

Control of Hair Cell Excitability by Vestibular Primary Sensory Neurons

et al. 2007

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In the rat utricle, synaptic contacts between hair cells and the nerve fibers arising from the vestibular primary neurons form during the first week after birth. During that period, the sodium-based excitability that characterizes neonate utricle sensory cells is switched off. To investigate whether the establishment of synaptic contacts was responsible for the modulation of the hair cell excitability, we used an organotypic culture of rat utricle in which the setting of synapses was prevented. Under this condition, the voltage-gated sodium current and the underlying action potentials persisted in a large proportion of nonafferented hair cells. We then studied whether impairment of nerve terminals in the utricle of adult rats may also affect hair cell excitability. We induced selective and transient damages of afferent terminals using glutamate excitotoxicity in vivo. The efficiency of the excitotoxic injury was attested by selective swellings of the terminals and underlying altered vestibular behavior. Under this condition, the sodium-based excitability transiently recovered in hair cells. These results indicate that the modulation of hair cell excitability depends on the state of the afferent terminals. In adult utricle hair cells, this property may be essential to set the conditions required for restoration of the sensory network after damage. This is achieved via re-expression of a biological process that occurs during synaptogenesis.

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“…The afferent dendrites, originating from the type I spiral ganglion neurons, are sensitive to the excitotoxic actions of glutamate. Excessive osmotic imbalance from the influx of water causes dendritic swelling (11) and eventual loss of spiral ganglion neurons (12). Glutamate excitotoxicity leading to the degeneration of the afferent dendrites has been suggested as a mechanism underlying noise trauma.…”

Section: Discussionmentioning

confidence: 99%

Complementary roles of neurotrophin 3 and a N- methyl- d -aspartate antagonist in the protection of noise and aminoglycoside-induced ototoxicity

Duan

Agerman

Ernfors

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

174

122

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Recent progress has been made regarding the prevention of hearing loss. However, the complete protection of both hair cells and spiral ganglion neurons, with restored function, has not yet been achieved. It has been shown that spiral ganglion neuronal loss can be prevented by neurotrophin 3 (NT3) and hair cell damage by N-methyl-D-aspartate (NMDA) receptor antagonists. Here we demonstrate that the combined treatment with MK801, a NMDA antagonist, and NT3 protect both cochlear morphology and physiology from injury. Pretreatment with MK801 prevented hearing loss and the dendrites of the spiral ganglion neurons from swelling after noise-induced damage. The acute phase of insult with the aminoglycoside antibiotic amikacin resulted in swollen afferent dendrites beneath the inner hair cells. The chronic phase resulted in complete hair cell loss and near-complete loss of spiral ganglion neurons. This damage caused a near-complete loss of hearing sensitivity as displayed by elevated (>90-dB sound pressure levels) auditory brainstem response thresholds. The treatment of amikacin-exposed animals with MK801 gave only a partial protection of hearing. However, the combined treatment with NT3 and MK801 in the amikacin-comprised ear resulted in improved mean hearing within 20 dB of normal. Furthermore, hair cell loss was prevented in these animals and spiral ganglion neurons were completely protected. These results suggest that the NMDA antagonist MK801 protects against noise-induced excitotoxicity in the cochlea whereas the combined treatment of NT3 and MK801 has a potent effect on preserving both auditory physiology and morphology against aminoglycoside toxicity. O ne in 10 individuals is affected by hearing disorders. Hearing impairments can be caused by a variety of factors including noise, ototoxic substances such as aminoglycosides, and aging. These factors affect the hair cells in the mammalian organ of Corti that transduce auditory signals to the brain via the spiral ganglion neurons. Hearing deficiencies are caused by loss of hair cells or spiral ganglion neurons and these changes are often permanent. Sensory neurons and hair cells are not capable of postembryonic cellular mitosis to produce new hair cells and neurons. It is therefore necessary to develop pharmacological strategies aimed at preventing or repairing damaged hair cells or spiral ganglion neurons.The most important afferent neurotransmitter in the peripheral auditory system is the excitatory amino acid glutamate (1, 2). When glutamate is released from the inner hair cells it binds to N-methyl-D-aspartate (NMDA) receptors located on the terminals of the spiral ganglion neurons. NMDA receptors are expressed in the auditory neurons and little or no mRNA for the receptor subunits has been detected in other areas of the cochlea (3). It has been shown that NMDA receptors play a key role in excitotoxic cell death after ischemic, stroke, hypoglycemia, alcohol intoxication, and epilepsy (4). Cell death caused by excitotoxicity has been suggested to be caused by cy...

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The effects of kainic acid on the cochlear ganglion of the rat

Cited by 72 publications

References 38 publications

Functional Recovery of Hearing following AMPA-Induced Reversible Disruption of Hair Cell Afferent Synapses in the Avian Inner Ear

Functional Recovery of Hearing following AMPA-Induced Reversible Disruption of Hair Cell Afferent Synapses in the Avian Inner Ear

Control of Hair Cell Excitability by Vestibular Primary Sensory Neurons

Complementary roles of neurotrophin 3 and a N- methyl- d -aspartate antagonist in the protection of noise and aminoglycoside-induced ototoxicity

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