Elsevier

Hearing Research

Volume 4, Issue 1, March 1981, Pages 109-120
Hearing Research

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

https://doi.org/10.1016/0378-5955(81)90040-XGet rights and content

Abstract

Artificial perilymph containing kainic acid (KA) at various concentrations was perfused through the scala tympani in guinea pigs, and its effects on the whole nerve action potential (AP), cochlear microphonics (CM), summating potential (SP), endocochlear potential (EP), crossed olivocochlear potential (COCP), and cochlear ganglion-cell spontaneous activity studied. The administration of a 10 nmol dose of KA abolished AP but had little, if any, effect on CM, SP, EP or the COCP. The elimination of AP at this dose of KA appeared to be irreversible. Results obtained at lower doses (0.1, 0.25, 0.5, 1.0, and 2.5 nmol) suggested a very steep dose-response relationship in the action of KA. As expected, auditory nerve ganglion-cell recordings revealed the elimination of AP is most probably consequent to the suppression of afferent neural activity following an excitatory process. All these findings provide evidence that KA may exert a selective action on afferent auditory nerve fibers and are consistent with the hypothesis that KA interacts with excitatory receptors located on postsynaptic membranes.

References (60)

  • E.G. McGeer et al.

    Kainate-induced degeneration of neostriatal neurons: dependence upon corticostriatal tract

    Brain Res.

    (1978)
  • W.J. Nicklas et al.

    Amino acids in rat neostriatum: alteration by kainic acid lesion

    Brain Res.

    (1979)
  • J.W. Olney et al.

    The fate of synaptic receptors in the kainate-lesioned striatum

    Brain Res.

    (1978)
  • J.W. Olney et al.

    Acute dendrotoxic changes in the hippocampus of kainate treated rats

    Brain Res.

    (1979)
  • R. Schwarcz et al.

    Striatal lesions with kainic acid: neurochemical characteristics

    Brain Res.

    (1977)
  • R. Schwarcz et al.

    Structure-activity relations for the neurotoxicity of kainic acid derivatives and glutamate analogues

    Neuropharmacology

    (1978)
  • H. Shinozaki et al.

    Actions of several anthelmintics and insecticides on rat cortical neurones

    Brain Res.

    (1970)
  • P. Streit et al.

    Kainate-induced lesion in the optic tectum: dependency upon optic nerve afferents or glutamate

    Brain Res.

    (1980)
  • S.R. Vincent et al.

    Kainic acid binding to membranes of striatal neurones

    Life Sci.

    (1979)
  • S. Yazulla et al.

    The effects of intraocular injection of kainic acid on the synaptic organization of the goldfish retina

    Brain Res.

    (1980)
  • S.J. Bird et al.

    Kainic acid injections result in degeneration of cochlear nucleus cells innervated by the auditory nerve

    Science

    (1978)
  • T.J. Biscoe et al.

    Structure-activity relations of excitatory amino acids on frog and rat spinal neurons

    Br. J. Pharmacol.

    (1976)
  • S.C. Bledsoe et al.

    Effect of intracochlear kainic acid on cochlear potentials in guinea pigs

    Neurosci. Abstr.

    (1979)
  • S.C. Bledsoe et al.

    Stimulus-induced release of endogenous amino acids from skins containing the lateral-line organ in Xenopus laevis

    Exp. Brain Res.

    (1980)
  • R.P. Bobbin

    Glutamate and aspartate mimic the afferent transmitter in the cochlea

    Exp. Brain Res.

    (1979)
  • R.P. Bobbin et al.

    Action of cholinergic and anticholinergic drugs at the crossed olivocochlear bundle-hair cell junction

    Acta Otolaryngol.

    (1974)
  • R.P. Bobbin et al.

    Effects of putative transmitters on afferent cochlear transmission

    Ann. Otol. Rhinol. Laryngol.

    (1978)
  • P. Campochiaro et al.

    Ontogenetic development of kainate neurotoxicity: correlates with glutamatergic innervation

  • S.D. Comis et al.

    Action of putative neurotransmitters in the guinea pig cochlea

    Exp. Brain Res.

    (1979)
  • J.T. Coyle et al.

    In situ injection of kainic acid: a new method for selectively lesioning neuronal cell bodies while sparing axons of passage

    J. Comp. Neurol.

    (1978)
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