Neuronal contributions to auditory brainstem potentials (ABR)

Abstract

ABRs were studied in cats for up to 45 days after kainic acid injections into the superior olivary complex (SOC) or cochlear nucleus (CN), which destroyed neurons while sparing fibers of passage and the terminals of axons of extrinsic origin. With destruction of the CN neurons, there was a loss of components P2 (III), and P3 (IV) and only a modest attenuation and prolongation of the latency of components P4 (V) and P5 (VI). Unexpectedly, to stimulation of the ear contralateral to the injection side, waves P2 (III), P3 (IV), and P4 (V) were also attenuated and delayed in latency. The sustained potential shift from which the components arose was not affected. Following bilateral SOC destruction, there was a moderate attenuation of wave P2 (III), and a marked attenuation of up to 80% of P3 (IV), P4 (V), P5 (VI), and the sustained potential shift. No component of the ABR was totally abolished. The results are compatible with multiple brain regions contributing to the generation of the components of the ABR beginning with P2 (III) and that components P3 (IV), P4 (V), and P5 (VI) and the sustained potential shift depend particularly on the integrity of the neurons of the SOC bilaterally.