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GLUTAMATE NEUROTOXICITY IN THE DEVELOPING RAT COCHLEA IS ANTAGONIZED BY KUNURENIC ACID AND MK-801
Citation:
Janssen, R. GLUTAMATE NEUROTOXICITY IN THE DEVELOPING RAT COCHLEA IS ANTAGONIZED BY KUNURENIC ACID AND MK-801. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-92/435.
Description:
Glutamate (GLU) is neurotoxic in the neonatal rat cochlea, producing hearing impairment which is largely due to the death of spiral ganglion cells, whereas the receptor hair cells are spared. endritic fibers of the spiral ganglion are post-synaptic to the primary afferent synapse of the auditory system. he experiments reported here were designed to test whether this apparent excitotoxicity can be blocked by Gw antagonists. he broad-spectrum antagonist kynurenic acid was co-administered with GLU initially to determine whether the high-frequency hearing deficit caused by GLU may be mediated by excitatory amino acid receptors. ubsequently, the NMDA-specific receptor blocker MK-8O1 was used to test whether NMDA receptors may be involved in the effect. oth antagonists partially blocked the high-frequency hearing impairment caused by GLU. In addition, both KYNA and MK-8O1 were found to be toxic in themselves. he results are consistent with hypothesis that GLU or a similar excitatory amino acid is an important afferent transmitter in the cochlea.