Ionic mechanism of the efferent olivo‐cochlear inhibition studied by cochlear perfusion in the cat.

1. A method for perfusing the scala tympani of the cat's cochlea from basal turn to apex is described. The perfusion with modified Krebs solution did not interfere with the recording of cochlear microphonic (CM) and neural responses to sound, nor with the efferent inhibition elicited by stereotaxic stimulation of the crossed olivo‐cochlear bundle (COCB) in the medulla. 2. Cochlear perfusion with solutions in which most of the chloride was replaced by large anions (sulphate or gluconate) decreased or eliminated auditory nerve or the ventral cochlear nucleus. These effects were reversible. They were only observed if the rate of perfusion (2–20 mul/min) was adequate to reduce the chloride concentration in perilymph below about 80 mM, this being estimated, in different perfusion of the same cochlea, by a chloride‐selective electrode. 3. The COCB‐induced negative shift of the endocochlear potential recorded with a glass micro‐electrode inserted into the scala media was abolished by I.V. strychnine o.2 mg/kg. It was decreased when the perilymph chloride was reduced to 50–70 mM and could be abolished when the perilymph chloride dropped to about 5 mM. 4. The COCB‐induced potentiation of the cochlear microphonic potential was also reduced by chloride substitution but the pattern of this effect differed from that of neural inhibition. 5. Similar cochlear perfusions with a solution in which the small diameter bromide anion was substituted for chloride did not affect the COCB‐efferent effects. 6. The data indicate that the inhibitory transmitter released by COCB terminals elicits an increased conductance to small anions (normally to chloride) in the membrane of the auditory dendrite and of the outer hair cell. The significance of the COCB‐induced negative shift of endocochlear potential and of the potentiation of CM is discussed, as well as the pre‐ and post‐synaptic mechanisms involved in the efferent gating exerted on the auditory input. The latter would seem to involve primarily a post‐synaptic mechanism at efferent axo‐dendritic synapses.