The functional role of the dorsal nucleus of the lateral lemniscus in acoustic processing
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The mammalian auditory system is composed of a number of parallel and serial pathways devoted to processing different aspects of acoustic signals. The focus of this dissertation is to examine the interactions among nuclei in the pathway devoted to processing interaural intensity disparities (IIDs), the cue animals use to localize high frequency sounds. IIDs are processed by neurons that are excited by sound in one ear and inhibited by sound in the other and thus are referred to as EI neurons. EI response properties are the dominant response feature expressed in three interconnected nuclei that process IIDs; the lateral superior olive (LSO), the dorsal nucleus of the lateral lemniscus (DNLL), and the inferior colliculus (IC). While EI properties are first formed in the LSO, recent studies have shown that EI properties are either modified or created de novo in the ICc through a convergence of inputs from lower nuclei. A prominent GABAergic input from the DNLL provides roughly 30% of the inhibitory innervation to the IC and has been shown to influence IID processing. While this degree of convergence indicates a significant amount of processing, the EI properties expressed in the ICc are strikingly similar to those observed in the LSO. Thus, the central question of these studies is: What is the functional significance of the convergence at the IC if response properties are so similar to those observed below? A possible answer to this question was proposed by Yang and Pollak, following the discovery of a response feature of the DNLL referred to as persistent inhibition. Persistent inhibition is a long lasting inhibition evoked by signals that favor the inhibitory ear. Their hypothesis predicts that ICc neurons that derive their EI properties from DNLL input will differentially process IIDs for multiple signals emanating from different regions of space. Here I confirm this hypotheses with recordings from the auditory system of Mexican-free tailed bats, where I blocked GABAergic inhibition at the IC as well as reversibly inactivated the DNLL while recording from IC neurons. I show that reception of an initial signal reconfigures the IID circuitry by functionally inactivating the DNLL, thereby depriving a population of IC cells of their inhibitory input, and temporarily transforming their EI properties. This property of the DNLL may provide one of the neural mechanisms that underlie the precedence effect.