Short communicationKainic acid: An evaluation of its action on cockle ar potentials
References (60)
- et al.
Huntington's disease and its animal model: alterations in kainic acid binding
Life Sci.
(1979) - et al.
Evidence against a presynaptic mechanism for kainate neurotoxicity in the cochlear nucleus
Neurosci. Letters
(1979) - et al.
Influence of cortico-striatal afferents on striatal kainic acid neurotoxicity
Neurosci. Letters
(1978) - et al.
Selective resistance of sensory cells of the mesencephalic trigeminal nucleus to kainic acid-induced lesions
Brain Res.
(1979) - et al.
Behavioral and anatomical consequences of small intrastriatal injections of kainic acid in the rat
Brain Res.
(1978) - et al.
Release of radiolabeled dopamine, serotonin, acetylcholine and GABA from slices of rat striatum after intrastriatal kainic acid injections
Brain Res.
(1977) - et al.
Perforant path transections protect hippocampal granule cells from kainate lesion
Neurosci. Letters
(1978) - et al.
Kainate neurotoxicity and glutamate inactivation
Neurosci. Letters
(1979) - et al.
Phylogenetic distribution of [3H]kainic acid receptor binding sites in neuronal tissue
Brain Res.
(1980) - et al.
Selective destruction by kainic acid of neurons innervated by putative glutamergic afferents in septum and nucleus of the diagonal band
Brain Res.
(1980)
Kainate-induced degeneration of neostriatal neurons: dependence upon corticostriatal tract
Brain Res.
Amino acids in rat neostriatum: alteration by kainic acid lesion
Brain Res.
The fate of synaptic receptors in the kainate-lesioned striatum
Brain Res.
Acute dendrotoxic changes in the hippocampus of kainate treated rats
Brain Res.
Striatal lesions with kainic acid: neurochemical characteristics
Brain Res.
Structure-activity relations for the neurotoxicity of kainic acid derivatives and glutamate analogues
Neuropharmacology
Actions of several anthelmintics and insecticides on rat cortical neurones
Brain Res.
Kainate-induced lesion in the optic tectum: dependency upon optic nerve afferents or glutamate
Brain Res.
Kainic acid binding to membranes of striatal neurones
Life Sci.
The effects of intraocular injection of kainic acid on the synaptic organization of the goldfish retina
Brain Res.
Kainic acid injections result in degeneration of cochlear nucleus cells innervated by the auditory nerve
Science
Structure-activity relations of excitatory amino acids on frog and rat spinal neurons
Br. J. Pharmacol.
Effect of intracochlear kainic acid on cochlear potentials in guinea pigs
Neurosci. Abstr.
Stimulus-induced release of endogenous amino acids from skins containing the lateral-line organ in Xenopus laevis
Exp. Brain Res.
Glutamate and aspartate mimic the afferent transmitter in the cochlea
Exp. Brain Res.
Action of cholinergic and anticholinergic drugs at the crossed olivocochlear bundle-hair cell junction
Acta Otolaryngol.
Effects of putative transmitters on afferent cochlear transmission
Ann. Otol. Rhinol. Laryngol.
Ontogenetic development of kainate neurotoxicity: correlates with glutamatergic innervation
Action of putative neurotransmitters in the guinea pig cochlea
Exp. Brain Res.
In situ injection of kainic acid: a new method for selectively lesioning neuronal cell bodies while sparing axons of passage
J. Comp. Neurol.
Cited by (82)
Animals models of hidden hearing loss: Does auditory-nerve-fiber loss cause real-world listening difficulties?
2022, Molecular and Cellular NeuroscienceCitation Excerpt :Furthermore, while budgerigars and other avians differ from mammals in that they can regenerate hair cells within several weeks after noise trauma or exposure to ototoxic drugs (Corwin and Cotanche, 1988; Ryals et al., 2013), birds nonetheless lack the ability to regenerate auditory-nerve soma following neuropathy as in mammals (Henry and Abrams, 2018; Ryals et al., 1989; Sun et al., 2001) and even show age-related irreversible decline of cochlear auditory-nerve innervation (Ryals and Westbrook, 1988). Auditory-nerve damage in budgerigars was induced bilaterally through intracochlear infusion of kainic acid (Wong et al., 2019), the glutamate analog that damages auditory-nerve afferent synapses in mammals and birds due to excitotoxicity followed, after several weeks or months, by irreversible degeneration of neuron cell bodies in the auditory-nerve ganglion (Bledsoe et al., 1981; Juiz et al., 1989; Sun et al., 2001). Bilateral infusions of 1-mM kainic acid solution in budgerigars caused permanent, 40–70% reduction of ABR wave-I amplitude across animals (Fig. 5A) with no accompanying change in hair-cell generated otoacoustic emissions, consistent with moderate-to-severe auditory-nerve-fiber loss (Wong et al., 2019).
Effects of selective auditory-nerve damage on the behavioral audiogram and temporal integration in the budgerigar
2019, Hearing ResearchCitation Excerpt :In contrast, DPOAEs were unaffected by KA. 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).
Intracochlear drug delivery: Fluorescent tracer evaluation for quantification of distribution in the cochlear partition
2019, European Journal of Pharmaceutical SciencesPre- and postsynaptic ionotropic glutamate receptors in the auditory system of mammals
2018, Hearing ResearchHyperactivity in the auditory midbrain after acoustic trauma: dependence on cochlear activity
2009, NeuroscienceCitation Excerpt :The parallel nature of decrease and recovery in CAP amplitudes and spontaneous firing in CNIC is further illustrated in Fig. 10D. Cochlear perfusion with CoCl2 (a blocker of pre-synaptic transmitter release) (Robertson and Johnstone, 1979) or kainic acid (a post-synaptic excitotoxin acting on glutamate receptors) (Bledsoe et al., 1981) always showed the same effect on all neurons recorded (CoCl2 five neurons; kainic acid two neurons). Similar to cochlear cooling these perfusions resulted in a decrease of CAP amplitude until it could no longer be detected against baseline (indicated in figure as 0) (Fig. 11A, D).