In mammals, thermoregulation is a key feature in the maintenance of homeostasis. Thermoregulatory capacities are strongly related to energy balance and animals are constantly seeking to limit the energy costs of normothermia. In case of thermal changes, physiological mechanisms are enhanced, increasing rates of energy expenditure. However, behavioral adjustments are available for species to lower the autonomic work, and thus reduce the energy costs of thermoregulatory responses. Hence, thermogenesis-induced metabolic costs can be reduced during cold exposure, and hyperthermia associated to dehydration can be avoided during heat exposure. Hypothermia avoidance consists in a concomitant decrease in heat dissipation and increase in heat production. Inversely, heat exchange is enhanced and body heat production is reduced when avoiding hyperthermia. The different behavioral strategies available for mammal species to cope with both decreased and increased levels of ambient temperature are reviewed. Moreover, thermoregulation function is under the control of central, metabolic, energetic and endocrine systems, which induces that parameters such as hour of the day, season, gender or aging may affect thermoregulatory adjustments. Some examples will be given.

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In primates, age determination using lines of arrested growth (LAGs) from bones has rarely been attempted, and the reliability of these structures has never been experimentally validated. In order to test skeletochronology in primates, LAGs were studied mainly in the long bones of known age Microcebus murinus, a small primate, whose potential longevity may reach 12 years. LAGs were extensively studied in 43 males and 23 females ranging from juveniles to 11-year-old adults. All individuals were born and reared in captivity. Some young individuals were injected with fluorescent dyes to quantify bone growth rates. LAGs in the diaphysis of the tibia are well correlated with age and this skeletal element appears to be the best for assessing skeletochronology in Microcebus murinus. There is strong evidence that the seasonal cycle of photoperiodicity is more important than age alone in producing LAGs.

The Ca 2؉ -binding proteins (CBPs) parvalbumin, calbindin, and calretinin are phenotypic markers of terminally differentiated neurons in the adult brain. Although subtle phylogenetic variations in the neuronal distribution of these CBPs may occur, morphologically and functionally diverse subclasses of interneurons harbor these proteins in olfactory and corticolimbic areas. Secretagogin (scgn) is a recently cloned CBP from pancreatic ␤ and neuroendocrine cells. We hypothesized that scgn is expressed in the mammalian brain. We find that scgn is a marker of neuroblasts commuting in the rostral migratory stream. Terminally differentiated neurons in the olfactory bulb retain scgn expression, with scgn being present in periglomerular cells and granular layer interneurons. In the corticolimbic system, scgn identifies granule cells distributed along the dentate gyrus, indusium griseum, and anterior hippocampal continuation emphasizing the shared developmental origins, and cytoarchitectural and functional similarities of these neurons. We also uncover unexpected phylogenetic differences in scgn expression, since this CBP is restricted to primate cholinergic basal forebrain neurons. Overall, we characterize scgn as a neuronspecific CBP whose distribution identifies neuronal subtypes and hierarchical organizing principles in the mammalian brain.cortex ͉ development ͉ interneuron ͉ neurogenesis ͉ stem cell T he ability to release neurotransmitters at chemical synapses, to integrate the activity of diverse synaptic inputs and trigger molecular mechanisms underlying neuronal adaptation, as well as to maintain excitability in neurons rely on the refined spatial and temporal control of momentary changes in cytosolic [Ca 2ϩ ] (1, 2). Ca 2ϩ -binding proteins (CBPs) represent a means to effectively regulate intracellular Ca 2ϩ dynamics (3). Members of the EF-hand family of CBPs invariably contain a 3-D motif to bind Ca 2ϩ at its physiological cytosolic concentrations (4). Some ancestral representatives of this protein family, such as calmodulin, are ubiquitously expressed with a high degree of evolutionary conservation and are involved in the control of fundamental cellular functions ranging from the cell cycle, cell motility and axon polarization to synaptic signaling (3). In contrast, the parvalbumin (PV) and calbindin subfamilies of CBPs, the latter including the vitamin D-dependent 28 kDa isoform of calbindin (CB) and calretinin (CR), exhibit restricted tissue-specific expression patterns in vertebrates (5, 6). During the past decades, PV, CB, and CR received significant attention because of their exquisite developmentally regulated cell type-specific expression in the mammalian nervous system (6-8).CBPs show a unique association with newly generated neurons in the adult brain (9, 10). Neural progenitors that are born in the subependymal zone and migrate in the rostral migratory stream (RMS) to differentiate into interneurons in the olfactory bulb (OB) commonly express CR at their neuroblast stage with select subpopulations ...

Classic theories of ageing consider extrinsic mortality (EM) a major factor in shaping longevity and ageing, yet most studies of functional ageing focus on species with low EM. This bias may cause overestimation of the influence of senescent declines in performance over condition-dependent mortality on demographic processes across taxa. To simultaneously investigate the roles of functional senescence (FS) and intrinsic, extrinsic and condition-dependent mortality in a species with a high predation risk in nature, we compared age trajectories of body mass (BM) in wild and captive grey mouse lemurs (Microcebus murinus) using longitudinal data (853 individuals followed through adulthood). We found evidence of non-random mortality in both settings. In captivity, the oldest animals showed senescence in their ability to regain lost BM, whereas no evidence of FS was found in the wild. Overall, captive animals lived longer, but a reversed sex bias in lifespan was observed between wild and captive populations. We suggest that even moderately condition-dependent EM may lead to negligible FS in the wild. While high EM may act to reduce the average lifespan, this evolutionary process may be counteracted by the increased fitness of the long-lived, high-quality individuals.