The reliability and frequency specificity of the 80-Hz amplitude-modulation-following response (80-Hz AMFR) during sleep detected by phase coherence as a measure of the hearing threshold was evaluated in 169 affected ears of 125 children with hearing impairment. The 80-Hz AMFR at a carrier frequency of 1000 Hz was monitored in all 169 ears and the auditory brainstem response (ABR) elicited by 1000-Hz tone pips was evaluated in 93 ears. Both responses were examined during sleep, and the thresholds were compared with the behavioral hearing threshold, which was determined by standard pure-tone audiometry or play audiometry. In 24 ears of 22 children with various patterns of audiogram, the 80-Hz AMFR was examined at different carrier frequencies, and the threshold pattern was compared with the pure-tone audiogram to investigate the frequency specificity of 80-Hz AMFR. The mean and standard deviation of the difference between the 80-Hz AMFR at a carrier frequency of 1000 Hz and pure-tone thresholds of 1000 Hz was 3.8 and 12.9 dB, and that between the ABR and pure-tone thresholds was 6.8 and 14.1 dB, respectively. The threshold patterns of 80-Hz AMFR clearly followed the corresponding audiogram patterns in all types of hearing impairment. The measurement of 80-Hz AMFR thus appears to be accurate in hearing assessment and to have good frequency specificity in children during sleep.

No abstract

No abstract

The effects of the mono- and tetrasialogangliosides, GM1 and GQ1b, on ATP-induced long-term potentiation (LTP) were studied in CA1 neurons of guinea pig hippocampal slices. Application of 5 or 10 microM ATP for 10 min resulted in a transient depression followed by a slow augmentation of synaptic transmission, leading to LTP. LTP induced by treatment with 5 microM ATP was facilitated in hippocampal slices prepared from animals treated for 6 days with a ceramide analog, L-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propranol, which stimulates ganglioside biosynthesis. In addition, LTP induced by 5 microM ATP was significantly enhanced when naive slices were incubated with GQ1b but not with GM1. These results suggest that a cooperative effect between extracellular ATP and GQ1b enhances ATP-induced LTP in hippocampal CA1 neurons. In addition, the LTP induced by 10 microM ATP was blocked by coapplication of the NMDA antagonist AP5 (5 microM or 50 microM), and this effect was partially inhibited by GQ1b pretreatment of the slices, suggesting that in hippocampal CA1 neurons, the enhancing effect of GQ1b on ATP-induced LTP is mediated by modulation of NMDA receptors/Ca(2+) channels.

No abstract