Quitting while you're ahead: Patch foraging and temporal cognition.

Theoretical models of foraging are based on the maximization of food intake rate. Remarkably, foragers often hew close to the predictions of rate maximization, except for a frequently observed bias to remain in patches for too long. By sticking with depleting options beyond the optimal patch residence time-a phenomenon referred to as overharvesting or overstaying-foragers miss out on food they could have earned had they sought a new option elsewhere. Here, we review potential causes of overstaying and consider the role that temporal cognition might play in this phenomenon. We first consider how an explicit, internal sense of time might inform foraging behaviors, and next examine patch-leaving choices from the perspective of intertemporal decision-making. Finally, we identify promising areas for future research that will provide a better understanding of how foraging decisions are made, and what factors drive the tendency to overharvest patches. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Kynurenine suppresses osteoblastic cell energetics in vitro and osteoblast numbers in vivo.

Aging is a progressive process associated with declining tissue function over time. Kynurenine, an oxidized metabolite of the essential amino acid tryptophan that increases in abundance with age, drives cellular processes of aging and dysfunction in many tissues, and recent work has focused on understanding the pathways involved in the harmful effects of kynurenine on bone. In this study, we sought to investigate the effects of controlled kynurenine administration on osteoblast bioenergetics, in vivo osteoblast abundance, and marrow fat accumulation. Additionally, as an extension of earlier studies with dietary administration of kynurenine, we investigated the effects of kynurenine on Hdac3 and NCoR1 expression and enzymatic deacetylase activity as potential mechanistic contributors to the effects of kynurenine on osteoblasts. Kynurenine administration suppressed cellular metabolism in osteoblasts at least in part through impaired mitochondrial respiration, and suppressed osteoblastic numbers in vivo with no concurrent effects on marrow adiposity. Deleterious effects of kynurenine treatment on osteoblasts were more pronounced in female models as compared to males. However, kynurenine treatment did not inhibit Hdac3's enzymatic deacetylase activity nor its repression of downstream glucocorticoid signaling. As such, future work will be necessary to determine the mechanisms by which increased kynurenine contributes to aging bone bioenergetics. The current study provides novel further support for the idea that kynurenine contributes to impaired osteoblastic function, and suggests that impaired matrix production by kynurenine-affected osteoblasts is attributed in part to impaired osteoblastic bioenergetics. As circulating kynurenine levels in increase with age, and human bone density inversely correlates with the serum kynurenine to tryptophan ratio, these mechanisms may have important relevance in the etiology and pathogenesis of osteoporosis in humans.