Principal neurons in the medial nucleus of the trapezoid body (MNTB) receive strong, and temporally precise excitatory input from glutamatergic globular bushy cells (GBC) in the cochlear nucleus through the highly specialized calyx of Held terminal. The extremely large synaptic currents produced by the calyx have sometimes led to the view of the MNTB as a simple relay synapse which converts incoming excitation to outgoing inhibition without performing any spike train transformation. However, in-vitro studies have shown the additional presence of inhibitory glycinergic currents, which are large enough to suppress firing of MNTB neurons.
The source of inhibition to the MNTB is not yet fully understood. Our tracing experiments, which are consistent with the findings of Kuwabara et al., 1991, suggest that one source of glycinergic inhibitory inputs to MNTB originates from the ventral nucleus of the trapezoid body (VNTB). However, there seem to be additional source/s of glycinergic terminals present on MNTB cell bodies. Kuwabara and Zook, 1991, found that some portion of MNTB cells projecting outside the MNTB also had recurrent axonal collaterals that re-entered MNTB.
We hypothesized that these principal cells' collaterals that terminate inside the MNTB nucleus provide an additional glycinergic inhibition to other principal cells, thus creating inhibitory microcircuit inside the nucleus. Such a microcircuit could produce side band inhibition and enhance frequency tuning of MNTB neurons. Here we provide first morphological characterization of inhibitory microcircuits in the MNTB.