Publications by authors named "Brandon Chelette"
Although cancer and its therapy are well known to be associated with fatigue, the exact nature of cancer-related fatigue remains ill-defined. We previously reported that fatigue-like behavior induced independently by tumor growth and by the chemotherapeutic agent cisplatin is characterized by reduced voluntary wheel running and an intact motivation to expand effort for food rewards. The present set of experiments was initiated to characterize the functional consequences of fatigue induced by chemoradiotherapy in tumor-bearing mice and relate them to changes in the expression of genes coding for inflammation, mitochondria dynamics and metabolism.
View Article and Find Full Text PDFCisplatin is a chemotherapeutic agent that is still commonly used to treat solid tumors. However, it has several toxic side effects due in large part to the mitochondrial damage that it induces. As this mitochondrial damage is likely to result in a decrease in the amount of metabolic energy that is available for behavioral activities, it is not surprising that fatigue develops in cancer patients treated with cisplatin.
View Article and Find Full Text PDFCancer-related fatigue is defined as a distressing persistent subjective sense of physical, emotional, and/or cognitive tiredness or exhaustion related to cancer or cancer treatment that is not proportional to recent activity and that interferes with usual functioning. This form of fatigue is highly prevalent during cancer treatment and in some patients, it can persist for years after treatment has ended. An understanding of the mechanisms that drive cancer-related fatigue is still lacking, which hampers the identification of effective treatment options.
View Article and Find Full Text PDFArticle Synopsis
- Excess nutrition leads to a reduction in olfactory sensory neurons (OSNs) and negatively impacts odor perception in mice, independent of overall fat storage or obesity.
- Through pair-feeding experiments with controlled isocaloric diets, researchers discovered that even mice with unchanged body weight and fat deposits experienced a loss of OSNs when fed a moderately high-fat diet.
- The study highlights that long-term imbalances in macronutrients can cause structural changes in the olfactory system, affecting its function, regardless of factors like energy expenditure or voluntary exercise.
Voluntary exercise is frequently employed as an intervention for obesity. The voltage-gated potassium channel K 1.3 is also receiving attention as a therapeutic target for obesity, in addition to potential therapeutic capabilities for neuroinflammatory diseases.
View Article and Find Full Text PDFArticle Synopsis
- The study investigates the relationship between olfaction and anxiety, particularly focusing on Kv1.3 knockout mice with heightened olfactory abilities.
- It finds that these mice exhibit increased anxiety levels compared to wild-type mice, indicating a potential inverse relationship between olfaction and anxiety.
- Additionally, treatment with methylphenidate (MPH) reduces anxiety in the Kv1.3-/- mice and helps with attention deficits, although the hyperactivity typically associated with these mice does not change significantly.
Article Synopsis
- Gene-targeted deletion of the Kv1.3 potassium channel leads to "Super-smeller" mice that exhibit enhanced olfactory abilities and alterations in their olfactory system, including more olfactory cilia and increased odorant receptor expression.
- Kv1.3(-∕-) mice also show a metabolic advantage, characterized by lower body weight, higher energy expenditure, and resistance to obesity when faced with high-fat diets.
- Research indicates that Kv1.3 and the GLUT4 glucose transporter are co-localized in the olfactory bulb, and changes in mitochondrial structure in Kv1.3(-∕-) mice may play a role in their metabolic resilience.