Inflammation of the retinal pigment epithelium drives early-onset photoreceptor degeneration in -associated retinitis pigmentosa.

Severe, early-onset photoreceptor (PR) degeneration associated with mutations is thought to result from failed phagocytosis by retinal pigment epithelium (RPE). Notwithstanding, the severity and onset of PR degeneration in mouse models of ablation are determined by the hypomorphic expression or the loss of the paralog . Here, we find that loss of and reduced expression/loss of led to RPE inflammation even before eye-opening.

Tissue-specific modifier alleles determine loss-of-function traits.

Knockout (KO) mouse models play critical roles in elucidating biological processes behind disease-associated or disease-resistant traits. As a presumed consequence of gene KO, mice display certain phenotypes. Based on insight into the molecular role of said gene in a biological process, it is inferred that the particular biological process causally underlies the trait.

Daily changes in light influence mood via inhibitory networks within the thalamic perihabenular nucleus.

Exposure to irregular lighting schedules leads to deficits in affective behaviors. The retino-recipient perihabenular nucleus (PHb) of the dorsal thalamus has been shown to mediate these effects in mice. However, the mechanisms of how light information is processed within the PHb remains unknown.

Cell death in development, maintenance, and diseases of the nervous system.

Cell death, be it of neurons or glial cells, marks the development of the nervous system. Albeit relatively less so than in tissues such as the gut, cell death is also a feature of nervous system homeostasis-especially in context of adult neurogenesis. Finally, cell death is commonplace in acute brain injuries, chronic neurodegenerative diseases, and in some central nervous system tumors such as glioblastoma.

Melatonin prevents early pituitary dysfunction induced by sucrose-rich diets.

While physiological levels of glucocorticoids are required to ensure proper functions of the body, consistently high levels may engender several deleterious consequences. We have previously shown an increase in the activity of the hypothalamic-pituitary-adrenal (HPA) axis in rats fed sucrose-rich diets (SRD). The main goal of this study was to analyze the processes involved in the modulation of the pituitary production of ACTH by SRD, and to test melatonin as a possible therapeutic agent for the prevention of the HPA axis dysfunction.