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Seicol, B. J.

Publications and source records attributed to Seicol, B. J..

3 recordsLinked to original sources

Machine-Learning-Guided Video Analysis Identifies Sound-Evoked Pain Behaviors from Facial Grimace and Body Cues in Mice

Humans can experience sound-evoked pain, either from extremely loud sounds or in cases of pain hyperacusis from typically tolerable sounds. However, the mechanisms underlying sound-evoked pain remain poorly understood. Developing behavioral methods to measure sound-evoked pain in animal models is critical for elucidating these mechanisms. Here, a machine learning-based approach was developed to measure sound-evoked pain in freely moving mice by analyzing facial grimace and body position from video recordings during sound exposure. Facial grimace, a commonly used method to detect pain in mice, and body position, which can be used to measure postural and movement changes that also indicate pain, were both quantified using a deep neural network model trained to extract established facial and body features from video recorded by a single camera. To validate the models capability to detect pain, a known painful state, migraine induced by the injection of the neuropeptide calcitonin gene-related peptide (CGRP), was used. Using this machine learning-based approach, the ability to quantify a pain response from CGRP-induced migraine, distinct from baseline behavior, was demonstrated, resulting in a defined pain threshold. Sound exposures at high intensities elicited significant changes in facial grimace and body position, in comparison, surpassing the pain threshold calculated from CGRP-induced migraine. These behavioral changes were absent in Tmie-knockout mice, which lack functional sound transduction in the cochlea. This automated, high-throughput framework enables objective and sensitive analysis of pain providing a foundation for future studies investigating the peripheral and central mechanisms of sound-evoked pain. SignificanceThis study introduces a quantitative framework for assessing pain using a single-camera setup and machine learning guided analysis to capture and analyze mouse behavior. By integrating two established pain metrics, facial grimace and attenuated movement, this method enables precise, non-invasive quantification of pain-related behaviors. The approach was validated with a well-characterized pain model, migraine, induced by injection of the neuropeptide CGRP, demonstrating the ability to quantify a pain response distinct from baseline behavior. By applying this framework to sound-evoked pain, the data revealed that exposure to intense sound triggers significant pain behavioral responses. These novel findings provide insights into the behavioral manifestations and neural underpinnings of sound-evoked pain, offering a robust tool for studying the mechanisms of pain perception.

animal behavior and cognition↗

Activation of complement protein C3 depicts the dynamic tissue damage of the cochlea after noise trauma.

Hearing loss is characterized by dysfunction and pathological changes of the cochlea, including the loss of sensory hair cells and connected synapses. Growing evidence has revealed that the immune system plays critical roles in shaping cochlear responses to tissue injury and the clearance of damaged cells under pathological conditions such as noise-induced hearing loss (NIHL). However, the underlying mechanisms that regulate this process remain unclear. As a crucial part of the innate immune system, the complement system is widely known to respond to tissue damage and help remove cellular debris. Such functions are yet to be fully explored in the auditory system, especially in the cochlea. Among various complement factors, the activation of complement protein C3 is an essential functional hub of the complement cascade, resulting in the phagocytosis of dead or dying cells. In this study, we sought to investigate whether C3 exists in the cochlea and what roles it might play upon noise injury. To test this, we studied C3 activation using immunohistochemistry in the cochleae of various mouse models that were noise exposed to an octave band noise (8-16 kHz) for two hours at 112 dB SPL. Mice were sacrificed at various post exposure times to examine cochlear pathology. We found damage dependent C3 activity in the organ of Corti in mice after noise exposure (NE), especially in damaged outer hair cell (OHC) area. Specifically, C3 opsonized damaged cellular structures include degenerating OHCs, OHC debris, ribbon synapses, and efferent synaptic boutons, and the temporal dynamics of the opsonization closely resemble the timing of cochlear tissue damages post exposure. Unexpectedly, C3-deficient mice exhibited similar ABR thresholds and OHC counts at baseline as wild type mice, as well as comparable ABR threshold shifts and OHC loss after NE. However, we observed significantly reduced MOC terminal bouton degeneration in C3-deficient mice upon 112 dB SPL noise injury, indicating that C3 does modulate tissue damage and clearance, at least at the MOC terminals. Our results suggest that complement C3 is dynamically activated in the cochlea upon noise injury, which may play significant roles in damage recognition and further immune recruitment during the development of NIHL.

neuroscience↗

Biased Auditory Nerve Central Synaptopathy Exacerbates Age-related Hearing Loss

Sound information is transmitted from the cochlea to the brain by different subtypes of spiral ganglion neurons (SGN), which show varying degrees of vulnerbility under pathological conditions. It remains unclear how information from these SGNs reassemble among target neurons in the cochlear nucleus (CN) at the auditory nerve (AN) central synapses, and how different synapses change during hearing loss. Combining immunohistochemistry with electrophysiology, we investigated the giant endbulb of Held synapses and their postsynaptic bushy neurons in mice under normal hearing and age-related hearing loss (ARHL). We found that calretinin-expressing and non-calretinin-expressing endbulbs converge at continuously different ratios onto bushy neurons with varying physiological properties. Endbulbs degenerate during ARHL, and the degeneration is more severe in non-calretinin-expressing synapses, which correlates with a gradual decrease in neuronal subpopulation predominantly innervated by these inputs. Our findings suggest that biased AN central synaptopathy and shifted CN neuronal composition underlie reduced auditory input and altered central auditory processing during ARHL.

neuroscience↗