Faculty Bibliography

Soft-pelleted, high-fat diets (HFD) are greasy and crumble easily leading to food wastage and hair coat grease accumulation when mice are fed using commercially available feeders. The ideal HFD feeder design should reduce food wastage, facilitate mouse weight gain, and minimize variables such as hair coat grease accumulation that have the potential to alter scratching behaviors. Our study compared the feeding efficiency of 2 commercially available feeders (feeders A and E) to 4 novel feeder designs (feeders B, C, D, and F). Novel feeders had alterations in feeding aperture size, feeding surface area, feeder configuration, and level of food presentation. Male C57BL/6NCrl mice (n = 120; 4/cage) were randomly assigned to cages containing one of the 6 feeder types and were fed HFD for 12 wk. Feeders and cage bottoms were weighed before use and then weekly at the time of cage change. Mice were weighed before starting the HFD and then biweekly. Scratching behavior was video recorded at 0, 4, 8, and 12 wk. Hair coat grease accumulation was visually scored biweekly. Feeder A use was associated with the highest feed cost due to HFD wastage ($36.98 ± 1.54/cage/wk). Mice fed using Feeder A had the highest average weight gain (23.75 ± 0.8 g, P < 0.005). However, mice also had significantly higher hair coat grease accumulation scores (P &lt; 0.05) and significantly increased scratching frequency at 4 wk (P < 0.05) when compared with mice fed using other feeder types. Novel feeder designs utilized 10 to 21 times less HFD dispensed when compared to feeder A. Mice fed using novel feeders also displayed improved welfare, as evidenced by low hair coat grease accumulation scores, and no significant differences in scratching frequency when compared with baseline behavior.

BACKGROUND/UNASSIGNED:neuroimaging and behavioral studies in a well-validated OA animal model. METHODS/UNASSIGNED:F]MeFWAY). Tracer bindings of 17 ROIs were evaluated based on averaged SUVR values over the last 10 min using CB as the reference region. We subsequently examined the neurochemical and behavioral alterations in OA animals (induction with monosodium iodoacetate (MIA) injection), as compared to control animals, via neuroimaging and behavioral assessment. Further, we examined the effects of repeated low-dose CBD treatment on mechanical allodynia (von Frey tests) and anxiety-like (light/dark box tests, L/D), depressive-like (forced swim tests, FST) behaviors in OA animals, as compared to after vehicle treatment. RESULTS/UNASSIGNED:receptor activation. There appeared to be a sex difference: females seem to be less responsive at the baseline towards pain stimuli, while being more sensitive to CBD treatment. CONCLUSION/UNASSIGNED:receptor. Behavioral studies with more pharmacological interventions to support the target involvement are needed to further confirm these critical findings.

Under neurodegenerative conditions, reactive astrocytes upregulate both aromatase (estrogen synthase) as well as estrogen and androgen receptors. This increased steroidogenic signal promotes neuroprotection and repair by promoting neurogenesis and decreasing cell death, but also by modulating the release of inflammatory molecules. Thus, endocrine - immune cross-talk is an essential component of estrogen mediated neuroprotection following brain injury. However, the exact mechanisms underlying this cross-talk remains unknown. cAMP response element-binding protein-binding protein (CBP) may be involved in the modulation of both the endocrine and inflammatory response following injury. CBP acts as both an estrogen receptor (ER) coactivator and as a promotor for NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) target genes and previous data suggests that ER and NF-κB compete for CBP. When CBP is displaced, target genes for NF-κB are repressed and inflammation is decreased. To test the role of CBP following injury, we examined CBP expression following penetrating injury in adult male and female zebra finches. Using immunohistochemistry, we were able to specifically examine glial CBP expression, as glial cells are important mediators of the neuroendocrine response to damage. Male but not female zebra finches upregulated glial CBP following damage to the brain. To determine if this upregulation was estrogen dependent, we decreased local estrogen levels with fadrozole (aromatase inhibitor) and reexamined glial CBP expression following injury. Aromatase inhibition resulted in no change in overall glial CBP expression suggesting that circulating estrogens do not mediate the upregulation of glial CBP following injury. Thus CBP may play a role in the both the estrogen and immune response to injury.