Biology subjects

Herrera, Y. N.

Publications and source records attributed to Herrera, Y. N..

4 recordsLinked to original sources

bioRxiv2026

Optogenetic circuit mapping reveals connectivity and synaptic physiology of T-stellate projections from the cochlear nucleus to the auditory midbrain

T-stellate neurons in the ventral cochlear nucleus (VCN) receive synaptic input from the cochlear nerve and encode information about sound frequency and intensity, including rapid fluctuations in sound intensity that are important for speech processing. T-stellate neurons are the only neuron class in the VCN that projects directly to the inferior colliculus (IC), the midbrain hub of auditory processing. However, which IC neuron populations receive T-stellate input and how T-stellate input influences IC neuron excitability remain unknown. Using channelrhodopsin-assisted circuit mapping and whole-cell patch clamp recordings in brain slices, we compared the synaptic strength, prevalence, and short-term synaptic plasticity of T-stellate input to two molecularly defined classes of IC neurons: GABAergic neuropeptide Y (NPY) neurons and glutamatergic vasoactive intestinal peptide (VIP) neurons. Our results revealed that T-stellate neurons provide excitatory input to both NPY and VIP neurons, with T-stellate input to NPY neurons having a higher incident rate, larger magnitude, and faster kinetics than T-stellate input to VIP neurons. In many instances, T-stellate input also recruited feedforward inhibition and feedforward excitation onto NPY and VIP neurons. In addition, T-stellate input to NPY and VIP neurons exhibited short-term synaptic depression that became larger in amplitude at higher stimulation frequencies. These data provide insights on how T-stellate neurons influence individual neuron types and local circuits in the IC, laying a mechanistic foundation for investigating how T-stellate input contributes to frequency tuning, amplitude modulation selectivity, and speech processing in the IC.

neuroscience↗

bioRxiv2025

The Ventral Tectal Longitudinal Column: A Midbrain Nucleus for Modulation of Auditory Processing in the Cochlear Nucleus, Superior Olivary Complex and Inferior Colliculus

A ventral tectal longitudinal column (TLCv) has been described in rats and is hypothesized to provide multisensory modulation of acoustic processing in the superior olivary complex (Saldana et al., 2007, J Neurosci 27, 13108-16). The TLCv is a column of cells in the dorsomedial tectum extending rostro-caudally through the inferior and superior colliculi. It receives ascending auditory input and projects to the superior olivary complex. Further insight into TLCv function has been hampered by limited information on its connections. Here, we provide evidence that a TLCv is recognizable in mice and that it has more extensive connections than previously believed. Deposit of retrograde tracer into the superior olivary complex labels cells bilaterally in the TLCv, comparable to results seen in rats. Viral labeling of neuronal projections demonstrate input to the TLCv from the superior olivary complex and from the inferior colliculus. Thus, the TLCv in mice has inputs and outputs similar to those described in rats. Additional experiments with retrograde tracers revealed more extensive outputs from the TLCv. Neurons in the TLCv are labeled after deposit of retrograde tracers into the cochlear nucleus or into the inferior colliculus. The projections from the TLCv to these targets, like those to the superior olivary complex, are bilateral. These projections are much broader than those described previously. The results suggest that the TLCv could exert modulation over a wide expanse of the auditory brainstem, from the cochlear nucleus through the inferior colliculus.

neuroscience↗

bioRxiv2024

Lineage-tracing reveals an expanded population of NPY neurons in the inferior colliculus

Growing evidence suggests that neuropeptide signaling shapes auditory computations. We previously showed that neuropeptide Y (NPY) is expressed in the inferior colliculus (IC) by a population of GABAergic stellate neurons and that NPY regulates the strength of local excitatory circuits in the IC. NPY neurons were initially characterized using the NPY-hrGFP reporter mouse, in which hrGFP expression indicates NPY expression at the time of assay, i.e., an expression-tracking approach. However, studies in other brain regions have shown that NPY expression can vary based on a range of factors, suggesting that the NPY-hrGFP mouse might miss NPY neurons not expressing NPY proximal to the experiment date. Here, we hypothesized that neurons with the ability to express NPY represent a larger population of IC GABAergic neurons than previously reported. To test this hypothesis, we used a lineage-tracing approach to irreversibly tag neurons that expressed NPY at any point prior to the experiment date. We then compared the physiological and anatomical features of neurons labeled with this lineage-tracing approach to our prior data set, revealing a larger population of NPY neurons than previously found. In addition, we used optogenetics to test the local connectivity of NPY neurons and found that NPY neurons routinely provide inhibitory synaptic input to other neurons in the ipsilateral IC. Together, our data expand the definition of NPY neurons in the IC, suggest that NPY expression might be dynamically regulated in the IC, and provide functional evidence that NPY neurons form local inhibitory circuits in the IC.

neuroscience↗

bioRxiv2023

GluN2D-containing NMDA receptors enhance temporal integration in VIP neurons in the inferior colliculus

Along the ascending auditory pathway, there is a broad shift from temporal coding, which is common in the lower auditory brainstem, to rate coding, which predominates in auditory cortex. This temporal-to-rate transition is particularly prominent in the inferior colliculus (IC), the midbrain hub of the auditory system, but the mechanisms that govern how individual IC neurons integrate information across time remain largely unknown. Here, we report the widespread expression of Glun2c and Glun2d mRNA in IC neurons. GluN2C/D-containing NMDA receptors are relatively insensitive to voltage-dependent Mg2+ block, and thus can conduct current at resting membrane potential. Using in situ hybridization and pharmacology, we show that VIP neurons in the IC express GluN2D-containing NMDA receptors that are activatable by commissural inputs from the contralateral IC. In addition, GluN2C/D-containing receptors have much slower kinetics than other NMDA receptors, and we found that GluN2D-containing receptors facilitate temporal summation of synaptic inputs in VIP neurons. In a model neuron, we show that a GluN2C/D-like conductance interacts with the passive membrane properties of the neuron to alter temporal and rate coding of stimulus trains. Consistent with this, we show in vivo that blocking GluN2C/D-containing receptors decreases both the spontaneous firing rate and the overall firing rate elicited by amplitude-modulated (AM) sounds in many IC neurons. These results suggest that GluN2C/D-containing NMDA receptors influence rate coding for auditory stimuli in the IC by facilitating the temporal integration of synaptic inputs. Significance statementNMDA receptors are critical components of most glutamatergic circuits in the brain, and the diversity of NMDA receptor subtypes yields receptors with a variety of functions. We found that many neurons in the auditory midbrain express GluN2C and/or GluN2D NMDA receptor subunits, which are less sensitive to Mg2+ block than the more commonly expressed GluN2A/B subunits. We showed that GluN2C/D-containing receptors conducted current at resting membrane potential and enhanced temporal summation of synaptic inputs. In a model, we show that GluN2C/D-containing receptors provide additive gain for input-output functions driven by trains of synaptic inputs. In line with this, we found that blocking GluN2C/D-containing NMDA receptors in vivo decreased both spontaneous firing rates and firing evoked by amplitude-modulated sounds.

neuroscience↗