Yes, there is a medial nucleus of the trapezoid body in humans

Abstract

The medial nucleus of the trapezoid body (MNTB) is a collection of brainstem neurons that function within the ascending auditory pathway. MNTB neurons are associated with a number of anatomical and physiological specializations which make these cells especially well-equipped to provide extremely fast and precise glycinergic inhibition to its target neurons in the superior olivary complex and ventral nucleus of the lateral lemniscus. The inhibitory influence of MNTB neurons plays essentials roles in the localization of sound sources and encoding temporal features of complex sounds. The morphology, afferent and efferent connections and physiological response properties of MNTB neurons have been well-characterized in a number of laboratory rodents and some carnivores. Furthermore, the MNTB has been positively identified in all mammals examined, ranging from opossum and mice to chimpanzees. From the early 1970s through 2009, a number of studies denied the existence of the MNTB in humans and consequentially, the existence of this nucleus in the human brain has been debated for nearly 50 years. The absence of the MNTB from the human brain would negate current principles of sound localization and would require a number of novel adaptations, entirely unique to humans. However, a number of recent studies of human post-mortem tissue have provided evidence supporting the existence of the MNTB in humans. It therefore seems timely to review the structure and function of the MNTB, critically review the literature which led to the denial of the human MNTB and then review recent investigations supporting the existence of the MNTB in the human brain.

Mechanism of auditory hypersensitivity in human autism using autism model rats

“…The MNTB has an inhibitory effect on the processing of sound neurotransmission (Fig. ) . We therefore hypothesized that there might be an impairment in MNTB function in the pathogenesis of auditory hypersensitivity.…”

“…We therefore hypothesized that there might be an impairment in MNTB function in the pathogenesis of auditory hypersensitivity. Because auditory nuclei are known to express a calcium‐binding protein called calbindin d28k and the characteristics of its distribution in the SOC has been well‐characterized in the rat, calbindin d28k antibody was used to visualize MNTB . As already known, SOC consists of MSO, LSO, SPO, MNTB, LNTB and VNTB (Fig.…”

“…After washing with TBST, sections were blocked with 2% normal goat serum in TBST, followed by primary antibody. For visualizing SOC, we used the anti‐calbindin d28k antibody (clone CB‐995, Sigma‐Aldrich, St Louis, MO, USA) . Sections were immunostained using the polymeric method and visualized with the chromogen 3,3′‐diaminobenzidine tetrahydrochloride (Vector, Burlingame, CA, USA).…”

“…In contrast, nerve fibers from the MNTB to the LSO have an inhibitory function, using glycine as a transmitter (Fig. ) . Therefore, auditory hypersensitivity might occur by abnormalities in or loss of function of the inhibitory neurons of the auditory nervous system.…”

Input timing for spatial processing is precisely tuned via constant synaptic delays and myelination patterns in the auditory brainstem

“…Intriguingly, we also discovered pronounced differences in axonal and myelin morphology within subpopulations of GBC axons tuned to low frequencies: although thicker in axon caliber, these GBC neurons exhibit shorter internode length, resulting in significantly faster conductance velocity and enhanced action potential precision (28). However, the MNTB targets not only MSO but many different auditory nuclei (29), including the LSO. It is therefore unclear whether differential myelination patterning and conduction velocity are specific adaptations for ITD processing or simply represent a general variation related to tonotopic organization per se.…”