Kainic acid: An evaluation of its action on cockle ar potentials

Bledsoe, Sanford C.; Bobbin, Richard P.; Chihal, D. M.

doi:10.1016/0378-5955(81)90040-x

Cited by 86 publications

(51 citation statements)

References 48 publications

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“…After AMPA treatment, the CAP was either totally abolished or the CAP amplitudes were significantly reduced. 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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“…Accumulating evidence suggests that fast excitatory synaptic transmission in the cochlea is mediated by an excitatory amino acid. The strongest evidence supporting this hypothesis is the expression of f unctional glutamate receptors by SGNs and their localization postsynaptic of the hair cell synapse (Bledsoe et al, 1981;Puel et al, 1991a,b;Ryan et al, 1991;Safieddine and Eybalin, 1992b;Kuriyama et al, 1994;Niedzielski and Wenthold, 1995). Although glutamate is present in hair cells, and its release from hair cells is stimulated by K ϩ in a Ca 2ϩ -dependent manner (Jenisson et al, 1985;Bobbin et al, 1990Bobbin et al, , 1991Kataoka and Ohmori, 1994; for review, see Eybalin, 1993), some studies suggest that a novel excitatory amino acid may be f unctioning at this synapse (Sewell and Morz, 1987).…”

Section: Abstract: Cochlea; Vestibular End Organ; Hair Cells; Spiralmentioning

confidence: 93%

“…First, they may f unction as autoreceptors. Several lines of evidence indicate that the neurotransmitter of the inner ear hair cells is an excitatory amino acid (Bledsoe et al, 1981(Bledsoe et al, , 1989Annoni et al, 1984;Soto and Vega, 1988;Puel et al, 1991aPuel et al, ,b, 1994Kataoka and Ohmori, 1994), and ␦1 may regulate its release from the hair cell. Restriction of ␦1 expression to IHCs in the organ of Corti is consistent with the fact that most (90 -95%) afferent transmission is from IHCs (Spoendlin, 1972;Berglund and Ryugo, 1987); OHCs may not need to regulate their excitatory amino acid release, which may occur only at modest levels, because OHCs form synapses on the remaining 5% of type II SGNs.…”

Section: Discussionmentioning

confidence: 99%

The Glutamate Receptor Subunit δ1 Is Highly Expressed in Hair Cells of the Auditory and Vestibular Systems

Safieddine

Wenthold

1997

J. Neurosci.

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In the inner ear, fast excitatory synaptic transmission is mediated by ionotropic glutamate receptors, including AMPA, kainate, and NMDA receptors. The recently identified ␦1 and ␦2 glutamate receptors share low homology with the other three types, and no clear response or ligand binding has been obtained from cells transfected with ␦ alone or in combination with other ionotropic receptors. Studies of mice lacking expression of ␦2 show that this subunit plays a crucial role in plasticity of cerebellar glutamatergic synapses. In addition, these mice show a deficit in vestibular compensation. These findings and the nature of glutamatergic synapses between vestibulocochlear hair cells and primary afferent dendrites suggest that ␦ receptors may be functionally important in the inner ear and prompted us to investigate the expression of ␦ receptors in the cochlea and peripheral vestibular system. Reverse transcription and DNA amplification by PCR combined with immunocytochemistry and in situ hybridization were used. Our results show that the expression of ␦1 in the organ of Corti is intense and restricted to the inner hair cells, whereas ␦1 is expressed in all spiral ganglion neurons as well as in their satellite glial cells. In the vestibular end organ, ␦1 was highly expressed in both hair cell types and also was expressed in the vestibular ganglion neurons. The prominent expression of ␦1 in inner hair cells and in type I and type II vestibular hair cells suggests a functional role in hair cell neurotransmission. Key words: cochlea; vestibular end organ; hair cells; spiral ganglion neurons; PCR; in situ hybridization; Western blot; immunocytochemistryAuditory and vestibular stimuli are detected by hair cells in the inner ear and are transmitted to the brain by way of the auditory and vestibular nerves. Of the two types of hair cells found in the organ of Corti, inner hair cells (IHC s) and outer hair cells (OHC s), IHC s are the primary transducers of sensory information. IHC s form chemical synapses with dendrites of type I spiral ganglion neurons (SGNs) that constitute 90 -95% of the SGNs. OHC s synapse on the remaining type II SGNs (Spoendlin, 1972;Berglund and Ryugo, 1987). The vestibular epithelium contains two types of sensory hair cells. T ype I cells (V HCI) are flaskshaped and surrounded by an afferent nerve caly x, whereas type

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“…Kainic acid has an excitotoxic effect on the cochlea, where it specifically affects the radial dendrites in nervating the inner hair cells. When it is applied to the cochlea, the radial afferent den drites contacting the inner hair cells show swelling, whereas the dendrites under the out er hair cells are not affected [5], It has been demonstrated that kainic acid selectively de creases the auditory nerve action potential, while there is little effect on cochlear micro phonics, summating potential, or endocochlear potential [6],…”

mentioning

confidence: 99%

Forward Masking Is Dependent on Inner Hair Cell Activity

Duan¹,

Canlon²

1996

Audiol Neurotol

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The goal of this study was to test the hypothesis that the inner hair cell complex (inner hair cell and dendritic contacts) is solely responsible for generating the slope of the forward masking curve. To test this hypothesis two experiments were performed. The first was to measure forward masking from the Bronx waltzing mouse, a mutant possessing an inner hair cell defect. The Bronx waltzing mouse demonstrated an approximately 60-dB auditory brainstem response (ABR) threshold shift compared to CBA/CBA mice at 8 and 12 kHz. The slope of the forward masking curve was significantly reduced compared to the control group, particularly at the early delay times between 0 and 4 ms. The second model employed kainic acid to affect the dendrites beneath the inner hair cell. After the intracochlear infusion of kainic acid, there was an approximately 47-dB ABR threshold shift at 4 and 8 kHz compared to pre-infusion thresholds. The slope of the forward masking curve from the kainic-acid group was significantly reduced compared to the artificial-perilymph group. Primarily the early delay times were affected by kainic acid (0-4 ms). Morphological analysis showed that there was extensive swelling of the afferent nerve radial dendrites under the inner hair cells. The results from the present study, as well as the preceding article, suggest that the analysis of the slope of the forward masking curve may be used for the detection of inner hair cell or radial dendrite damage, independent of outer hair cell damage. The present finding could provide a useful means of employing a clinical test for determining the function of the inner hair cell complex using a non-invasive measure of auditory function.

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Kainic acid: An evaluation of its action on cockle ar potentials

Cited by 86 publications

References 48 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

The Glutamate Receptor Subunit δ1 Is Highly Expressed in Hair Cells of the Auditory and Vestibular Systems

Forward Masking Is Dependent on Inner Hair Cell Activity

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