Shofner W P, Young E D
Dept. of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore.
Hear Res. 1987;29(1):45-53. doi: 10.1016/0378-5955(87)90204-8.
Principal cells of the dorsal cochlear nucleus (DCN) receive a variety of inhibitory influences, including some that are associated with the anteroventral cochlear nucleus (AVCN). Electrical stimulation in the caudal part of the AVCN produces long-lasting inhibition of DCN units [(1973) Exp. Brain Res. 17, 428-442], including unit type IV, which is associated with principal cells. This inhibition may be mediated either by orthodromic activation of AVCN axons that terminate in DCN or by antidromic stimulation of DCN inhibitory interneurons whose axons send collaterals to the AVCN. These two possibilities cannot be distinguished with electrical stimulation alone. In this study, microinjections of lidocaine were made in the AVCN. These injections should block AVCN to DCN axons without directly affecting the activity, within the DCN, of DCN interneurons. Two effects of lidocaine injections were observed. In some cases, all activity of DCN cells was abolished by lidocaine. These cases involved either spread of lidocaine to the recording site or into the auditory nerve. In other cases, the inhibitory responses of DCN type IV units were weakened by lidocaine without changing the units' thresholds or spontaneous activity. The latter result demonstrates that there are inhibitory pathways originating in AVCN or passing through AVCN and terminating in the DCN.
