Biology subjects

Coden, K. M.

Publications and source records attributed to Coden, K. M..

3 recordsLinked to original sources

bioRxiv2026

Corncob Bedding Negatively Impacts Breeding Performance and Sexual Development in Mice

Corncob bedding is commonly used for housing rodents in research, but previous work has linked corncob to altered reproductive behavior, disrupted estrous cycling, aggression, and welfare impacts across non-murine rodents. Furthermore, corncob is used as a licensed commercial rodenticide. Corncob contains endocrine-disrupting compounds (EDCs) that interfere with aromatase activity and estrogen signaling, processes critical for normal sexual behavior and development, yet effects on reproductive outcomes in mice remain unexplored. We conducted two experiments to test whether corncob bedding influences breeding performance and male sexual development. In Experiment 1, we analyzed breeding records to compare breeding performance of NSG mice housed on corncob versus cellulose bedding across two 3-month phases (N = 488 litters). Pairs housed on corncob produced significantly fewer pups than pairs housed on cellulose. To understand this effect, in Experiment 2, hormonal and morphological effects of corncob were assessed in male mice from four genetic backgrounds (C57BL/6, BALB/c, FVB, and CD1; N = 32 cages). Mice were bred and born on aspen or corncob, with half switched at weaning and half unchanged. Corncob produced timing-dependent effects in male reproductive physiology and development. Early-life corncob exposure altered baculum morphology and reduced testosterone, estradiol, and anogenital distance. In contrast, post-weaning corncob exposure resulted in hyper-masculinization, indicated by increased anogenital distance. Alongside prior evidence that corncob contains EDCs, our results raise serious concerns about its suitability as bedding in animal research. Continued use of corncob introduces uncontrolled variation that compromises animal welfare, reproduction, experimental validity, and reproducibility.

physiology↗

bioRxiv2025

Risk reshapes amygdala representation of choice

Modifying behavior in response to changing environmental conditions is a crucial adaptive function. This capacity is exemplified when animals curtail pursuit of a valued outcome that risks being punished by aversive consequences, but the mediating brain mechanisms remain poorly understood. Here, using in vivo cellular-resolution calcium (Ca2+) imaging, optogenetics and chemogenetics, we show that risk of punishment dramatically alters animals choice between a large/risky and small- /safe reward and produces novel, causally necessary, patterns of activity in basolateral amygdala (BLA) neurons. We find that experience of a punished outcome generates a BLA representation that is selectively replayed when animals subsequently abort choice of the large/risky reward option. Additionally, we show that risk leads to the incorporation of newly encoding BLA neurons into the pre-choice representation, which predicts shifting away from the large/risky option. These findings reveal how dynamic reshaping of BLA representations underpins behavioral flexibility in the face of risk.

neuroscience↗

bioRxiv2025

Stereotypy is strongly linked to multiple biomarkers of oxidative stress--a potential common etiology for Abnormal Repetitive Behaviors

Spontaneous stereotypies (abnormal, repetitive, and seemingly goal-less behaviors) in captive animals resemble stereotypies documented in patients with neurodevelopmental disorders, including evidence of homologous cortico-striatal dysfunction and shared behavioral deficits. While environmental risk factors for stereotypies are well documented, their developmental pathophysiology remains unclear. However, as previously found for compulsive behavior, there is growing evidence that REDOX imbalance may be linked to stereotypy. To examine the nature of this relationship, we first tested whether plasma glutathione level, the gold-standard biomarker of REDOX imbalance, is predictive of stereotypy severity in N=19 C57BL/6 mice. After confirming the presence of this relationship, we used a proteomics approach (Olink) to identify a broader biomarker profile of dysfunction. We found expression of 9 proteins to correlate with plasma glutathione level, and expression of 15 proteins to correlate with stereotypy severity. A subset of these proteins additionally correlated with stereotypy severity in a validation cohort of CD1 mice (N=28). Further supporting a role for REDOX imbalance in the developmental pathophysiology of stereotypies, the identified proteins were associated with REDOX physiology, dopamine physiology, and stereotypy-presenting human neurodevelopmental disorders. These data suggest REDOX imbalance may contribute to the developmental pathophysiology of abnormal repetitive behaviors and highlight promising novel targets for intervention.

animal behavior and cognition↗