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The ventral nucleus of the lateral lemniscus (VNLL) is an important nucleus in the central auditory pathway which connects the lower brainstem and the midbrain inferior colliculus (IC). Previous studies have demonstrated that neurons in the VNLL could respond to sound signal parameters. Frequency tuning curves (FTCs) of VNLL neurons are generally wider than FTCs of IC neurons, suggesting that the VNLL does not enhance abilities of frequency discrimination and coding. Two types of rate-intensity functions (RIFs) are found in the VNLL: monotonic and non-monotonic RIFs. Intensity-tuning of VNLL neurons are affected by the temporal firing patterns during processing and encoding intensity. There are multiple temporal firing patterns in VNLL neurons. Onset pattern has a precise timing characteristic which is well suited to encode temporal features of stimuli, and also very important to animal behavior including bat's echolocation. The VNLL accepts inputs from lower nuclei, uploads glycine inhibitory outputs to IC, and modulates response characteristics generating and acoustic signal processing of IC neurons. Recent research suggests that fast inhibitory projection from the VNLL may delay the first spike latency of IC neurons, and the delayed inhibitory projection from the VNLL may mediate the temporal firing patterns of IC neurons. But how inhibitory inputs from the VNLL integrate in IC, and how inhibitory inputs from the VNLL enhance the ability of detecting sound signal of IC neurons are not very clear and need more direct evidence at the level of neurons. These questions will help further understand the role of upload during IC processes acoustic signal, which are our research target in the future. This article reviews the current literature regarding the roles of the VNLL in sound signal processing and the auditory ascending transmission, including advances in the relevant research in our laboratory.

Objective: It has been known that glial line-cell derived neurotrophic factor (GDNF) has the nutritional and protective effect in motor neurons. In this experiment, we investigated the character of GDNF mRNA expression in a facial nerve-striking model; combined with other scholars' experimental results; and analyzed what role GDNF plays in the regeneration process of injured motor nerves., Methods: We established a striking model in rabbit facial nerves with a striking gun with the striking velocity of 10 m/s and the total striking energy of 7.5 J. Then we detected the GDNF mRNA expression in facial neurons and axons with in situ hybridization on days 3, 7, 14 and 21 after striking. We counted the expression numbers of facial neurons and, compared with normal facial neurons and peripheral facial nerves., Results: We detected GDNF mRNA expression in the facial neurons from day 3 to day 21 after the facial nerve injured by striking. The peak of GDNF mRNA expression appeared on the 7th day, and then the expression number of facial neurons decreased gradually. A high level expression was also detected on day 21. GDNF mRNA expression was not detected neither in Schwann cells nor in normal facial neurons from the 3rd day to the 21st day., Conclusion: GDNF is a kind of neurotrophic growing factor (NGF) that could be activated by injury. The character of GDNF mRNA expression was accordant to the process of nerve regeneration. These results showed that GDNF plays a very important role in the regeneration of injured motor nerves.