Functional Interactions Between Ipsi- and Contralaterally Evoked Inhibition in the Dorsal Nucleus of the Lateral Lemniscus and Inferior Colliculus

Wednesday, March 10, 1999 - 10:30am - 11:15am
Keller 3-180
George Pollak (The University of Texas at Austin)
The dorsal nucleus of the lateral lemniscus (DNLL) and inferior colliculus (IC) are of interest because both contain large populations of E-I neurons and because the DNLL provides a strong inhibitory innervation to many EI cells in the IC. But while the neuronal populations in both nuclei are superficially similar, in that they both express the same binaural EI property and receive a similar complement of projections, a deeper analysis reveals that their properties are considerably different in a number of ways. Here I focus on the roles of inhibition generated by stimulation of the contra- and ipsilateral ears, and their functional consequences for generating or modifying E-I properties of neurons in the DNLL and IC.

There are five principal findings. First, in most IC cells, contralateral signals evoke an inhibition that persists for many ms beyond the duration of the acoustic signal. In contrast, contralateral stimulation evokes little or no persistent inhibition in DNLL cells. Second, ipsilateral stimulation evokes a long persistent inhibition in many DNLL and many IC neurons. Third, the ipsilateral inhibitions in the DNLL and IC have very different effects on contralaterally evoked discharges. Ipsilateral inhibition in DNLL does not suppress contralaterally evoked discharges which are suppressed in a lower nucleus. Rather the inhibition is only evoked by ipsilateral intensities that have already completely suppressed discharges. In contrast, ipsilateral inhibition in the IC suppresses contralaterally evoked discharges in many neurons and thus forms or shapes their IID functions. Fourth, ipsilateral inhibition in DNLL plays a major role in suppressing responses to trailing signals that evoke vigorous discharges when presented alone. Fifth, we tested an hypothesis we previously advanced concerning the influence that the DNLL has on IC cells when a first sound is followed by a trailing sound. We proposed that due to the persistent inhibition in the DNLL, the IC cell must be deprived of its inhibition, and thus should discharge to a trailing sound that would not elicit discharges if presented by itself. This hypothesis was clearly confirmed in a some IC cells. In the majority of IC cells, however, the persistent inhibition at the IC that was evoked by the first signal prevented the IC cells from responding to the trailing binaural signals. In these cases, we could not determine whether or not the DNLL had any influence on ipsilateral spike suppression.

These findings suggest that although the response properties of IC cells are partially formed by the excitatory and inhibitory innervation they receive from lower nuclei, there are additional features which emerge in the IC, that interact with and can obscure the responses evoked by the afferent innervation. One of these emergent features is contralaterally evoked persistent inhibition which acts to suppress trailing sounds. The contralateral persistent inhibition is a robust and ubiquitous feature of the IC and yet its functional significance is both perplexing and poorly understood.