Abstract
The authors have previously demonstrated in rats that acute alcohol adminstration has the depressive effect of progressively prolonging the latencies of successive peaks of the brainstem auditory evoked potential. In this study the analogous experiment was also conducted in the awake, paralyzed cat in order to rule out any possibility of non-neural influences on the brainstem potentials under alcohol. Several conclusions can be made on the basis of these studies. First, alcohol has a depressive effect on neural transmission within the primary auditory pathway in both humans and cats. Second, alcohol had no effect on the latency of the earliest brainstem potential peaks. Since it is likely that peak I in the human brainstem potential waveform represents neural activity in the auditory nerve, it is reasonable to conclude that alcohol exerts its primary effect on more central structures. Third, there was a progressive increase in the latencies of peaks II through VII for the human subjects and analagous results were found for the cats, suggesting that the effects of alcohol are widespread and relatively uniform throughout the brainstem structures contributing to the far-field auditory brainstem potential waveform. Finally, alcohol had no significant effect on the amplitudes of any of the potentials. The consistency with which the primary auditory pathway is affected by alcohol suggests that functional dissection of brainstem connections in an intact subject may be possible through systematic correlations of the effects of drugs with known effects on different central pathways.
| Original language | English |
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| Pages | 227-231 |
| Number of pages | 5 |
| State | Published - 1978 |
| Event | San Diego Biomedical Symposium - San Diego, CA, USA Duration: 01 02 1978 → 03 02 1978 |
Conference
| Conference | San Diego Biomedical Symposium |
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| City | San Diego, CA, USA |
| Period | 01/02/78 → 03/02/78 |