Features of ipsilaterally evoked inhibition in the dorsal nucleus of the lateral lemniscus.
The dorsal nucleus of the lateral lemniscus (DNLL) is a binaural nucleus whose neurons are excited by stimulation of the contralateral ear and inhibited by stimulation of the ipsilateral ear. Here we report on several features of the ipsilaterally evoked inhibition in 95 DNLL neurons of the mustache bat. These features include its dependence on intensity, its tuning and the types of stimuli that are capable of evoking it. Inhibition was studied by evoking discharges with the iontophoretic application of glutamate, and then evaluating the strength and duration of the inhibition of the glutamate evoked background activity produced by stimulation of the ipsilateral ear. Excitatory responses were evoked by stimulation of the contralateral ear with best frequency (BF) tone bursts. Glutamate evoked discharges could be inhibited in all DNLL neurons and the inhibition often persisted for periods ranging from 10 to 50 ms beyond the duration of the tone burst that evoked it. The duration of the persistent inhibition increased with stimulus intensity. Stimulus duration had little influence on the duration of the persistent inhibition. Signals as short as 2 ms suppressed discharges for as long as 30 ms after the signal had ended. The frequency tuning of the total period of inhibition and the period of persistent inhibition were both closely matched to the tuning evoked by stimulation of the contralateral ear. Moreover, the effectiveness of complex signals for evoking persistent inhibition, such as brief FM sweeps and sinusoidally amplitude and frequency modulated signals, was comparable to that of tone bursts at the neuron's excitatory BF, so long as the complex signal contained frequencies at or around the neuron's excitatory BF. We also challenged DNLL cells with binaural paradigms. In one experiment, we presented a relatively long (40 ms) BF tone burst of fixed intensity to the contralateral ear, which evoked a sustained discharge, and a shorter, 10 ms signal of variable intensity to the ipsilateral ear. As the intensity of the 10 ms ipsilateral signal increased, it generated progressively longer periods of persistent inhibition and thus the discharges were suppressed for periods far longer than the 10 ms duration of the ipsilateral signal. With interaural time disparities, ipsilateral signals that led contralateral signals evoked a persistent inhibition that suppressed the responses to the trailing contralateral signals for periods of a least 15 ms. This suggests that an initial binaural sound that favors the ipsilateral ear should suppress the responses to trailing sounds that normally would be excitatory if they were presented alone. We hypothesize a circuit that generates the persistent inhibition and discuss how the results with binaural signals support that hypothesis.
Department of Zoology, University of Texas at Austin, 78712, USA.
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Pollak
D000161:Acoustic Stimulation; D000818:Animals; D002685:Chiroptera; D017626:Cochlear Nucleus / Q000502:physiology*; D004567:Electrodes, Implanted; D016057:Evoked Potentials, Auditory, Brain Stem / Q000502:physiology*; D007839:Functional Laterality; D005829:Geniculate Bodies / Q000502:physiology; D009474:Neurons / Q000502:physiology; D011149:Pons / Q000502:physiology; D013997:Time Factors; D017557:Ventral Tegmental Area / Q000502:physiology*