Effect of anesthesia on maximal cochlear microphonics.
During prolonged periods of pentobarbital anesthesia (6-8 h), cochlear microphonics (CM) in cats became reduced by approximately 6 dB, but only in the region of maximal responses ("truncation"). For the following reasons, this change is held to be neurally mediated, specifically by an impairment of the olivocochlear bundle (OCB): (1) Its onset coincided with the disappearance of efferent action potentials, normally superimposed on low-frequency CM. (2) OCB stimulation augments CM by approximately 6 dB, once more only in the region of maximal responses [4]. (3) Sectioning of the OCB reduces maximal CM responses [8]. (4) Truncation was produced by two neural blocking agents, azide and DFP [10], most likely also resulting from OCB impairments. (5) At the high input levels required to produce maximal responses, CM ought to become slightly elevated by acoustically-evoked OCB activity. This elevation should cease to occur on impairment of OCB under the effect of pro-longed anesthesia; thus there would be an apparent truncation.
D000777:Anesthetics / Q000494:pharmacology*; D000818:Animals; D002415:Cats; D003055:Cochlear Microphonic Potentials / Q000187:drug effects*; D003056:Cochlear Nerve / Q000187:drug effects; D005072:Evoked Potentials, Auditory / Q000187:drug effects*; D006198:Hair Cells, Auditory / Q000187:drug effects; D009847:Olivary Nucleus / Q000187:drug effects; D010424:Pentobarbital / Q000494:pharmacology
D000777:Anesthetics; D010424:Pentobarbital