Differential Response Properties to Amplitude Modulated Signals in the
Dorsal Nucleus of the Lateral Lemniscus of the Mustache Bat and the Roles of
Yang, Lichuan and George D. Pollak.
Department of Zoology, The University of Texas at Austin, Austin, Texas
APStracts 3:0220N, 1996.
We studied the phase-locking of 89 neurons in the dorsal nucleus of the
lateral lemniscus (DNLL) of the mustache bat to sinusoidally amplitude
modulated (SAM) signals and the influence that GABAergic inhibition had on
their response properties. Response properties were determined with tone
bursts at each neuron's best frequency and then with a series of SAM signals
that had modulation frequencies ranging from 50-100 Hz to 800 Hz in steps of
100 Hz. DNLL neurons were divided into two principal types: 1) Sustained
neurons (55%) responded throughout the duration of the tone burst. 2) Onset
neurons (45%) responded only at the beginning of the tone burst. Sustained and
onset neurons responded differently to SAM signals. Sustained neurons
responded with phase-locked discharges to modulation frequencies up to 400-800
Hz. In contrast, 70% of the onset neurons phase-locked only to low modulation
frequencies of 100-300 Hz, while 30% of the onset neurons did not phase-lock
to any modulation frequency. Signal intensity differentially affected the
phase-locking of sustained and onset neurons. Sustained neurons exhibited
tight phase-locking only at low intensities, 10-30 dB above threshold. Onset
neurons, in contrast, maintained strong phase-locking even at relatively high
intensities. Blocking GABAergic inhibition with bicuculline had different
effects on the phase-locking of sustained and onset neurons. In sustained
neurons, there was an overall decline in phase-locking at all modulation
frequencies. In contrast, 70% of the onset neurons phase-locked to much higher
modulation frequencies than they did when inhibition was intact. The other 30%
of onset neurons phase-locked to SAM signals although they fired only with an
onset response to the same signals before inhibition was blocked. In both
cases, blocking GABAergic inhibition transformed their responses to SAM
signals into patterns that were more like those of sustained neurons. We also
propose mechanisms that could explain the differential effects of GABAergic
inhibition on onset neurons that locked to low modulation frequencies and on
onset neurons that did not lock to any SAM signals before inhibition was
blocked. The key features of the proposed mechanisms are the absolute
latencies and temporal synchrony of the excitatory and inhibitory inputs.
Received 17 September 1996; accepted in final form 11 June 1996.
APS Manuscript Number J467-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996