DIFFERENTIAL RESPONSE PROPERTIES TO AMPLITUDE-MODULATED SIGNALS IN THE DORSAL NUCLEUS OF THE LATERAL LEMNISCUS OF THE MOUSTACHE BAT AND THEROLES OF GABAERGIC INHIBITION

We studied the phase-locking of 89 neurons in the dorsal nucleus of th e lateral lemniscus (DNLL) of the mustache bat to sinusoidally amplitu de 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 seri es of SAM signals that had modulation frequencies ranging from 50-100 to 800 Hz in 100-Hz steps. DNLL neurons were divided into two principa l types: sustained neurons (55%), which responded throughout the durat ion of the tone burst, and onset neurons (45%), which responded only a t the beginning of the tone burst. Sustained and onset neurons respond ed differently to SAM signals. Sustained neurons responded with phase- locked discharges to modulation frequencies less than or equal to 400- 800 Hz. In contrast, 70% of the onset neurons phase-locked only to low modulation frequencies of 100-300 Hz, whereas 30% of the onset neuron s did not phase-lock to any modulation frequency. Signal intensity dif ferentially affected the phase-locking of sustained and onset neurons. Sustained neurons exhibited tight phase-locking only at low intensiti es, 10-30 dB above threshold. Onset neurons, in contrast, maintained s trong phase-locking even at relatively high intensities. Blocking GABA ergic inhibition with bicuculline had different effects on the phase-l ocking 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 modula tion frequencies than they did when inhibition was intact. The other 3 0% of onset neurons phase-locked to SAM signals, although they fired o nly with an onset response to the same signals before inhibition was b locked. In both cases, blocking GABAergic inhibition transformed their responses to SAM signals into patterns that were more like those of s ustained neurons. We also propose mechanisms that could explain the di fferential effects of GABAergic inhibition on onset neurons that locke d 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 synch rony of the excitatory and inhibitory inputs.