A social and ecological assessment of tropical land uses at multiple scales: the Sustainable Amazon Network

Science has a critical role to play in guiding more sustainable development trajectories. Here, we present the Sustainable Amazon Network (Rede Amazonia Sustentavel, RAS): a multidisciplinary research initiative involving more than 30 partner organizations working to assess both social and ecological dimensions of land-use sustainability in eastern Brazilian Amazonia. The research approach adopted by RAS offers three advantages for addressing land-use sustainability problems: (i) the collection of synchronized and co-located ecological and socioeconomic data across broad gradients of past and present human use; (ii) a nested sampling design to aid comparison of ecological and socioeconomic conditions associated with different land uses across local, landscape and regional scales; and (iii) a strong engagement with a wide variety of actors and non-research institutions. Here, we elaborate on these key features, and identify the ways in which RAS can help in highlighting those problems in most urgent need of attention, and in guiding improvements in land-use sustainability in Amazonia and elsewhere in the tropics. We also discuss some of the practical lessons, limitations and realities faced during the development of the RAS initiative so far.Keywords: Social–ecological systems, Tropical forests, Land use, Interdisciplinary research, Sustainability, Trade-off

A Short-Day Photoperiod Delays the Timing of Puberty in Female Mice via Changes in the Kisspeptin System

The reproduction of seasonal breeders is modulated by exposure to light in an interval of 24 h defined as photoperiod. The interruption of reproductive functions in seasonally breeding rodents is accompanied by the suppression of the Kiss1 gene expression, which is known to be essential for reproduction. In non-seasonal male rodents, such as rats and mice, short-day photoperiod (SP) conditions or exogenous melatonin treatment also have anti-gonadotropic effects; however, whether photoperiod is able to modulate the puberty onset or Kiss1 gene expression in mice is unknown. In the present study, we investigated whether photoperiodism influences the sexual maturation of female mice via changes in the kisspeptin system. We observed that SP condition delayed the timing of puberty in female mice, decreased the hypothalamic expression of genes related to the reproductive axis and reduced the number of Kiss1-expressing neurons in the rostral hypothalamus. However, SP also reduced the body weight gain during development and affected the expression of neuropeptides involved in the energy balance regulation. When body weight was recovered via a reduction in litter size, the timing of puberty in mice born and raised in SP was advanced and the effects in hypothalamic mRNA expression were reverted. These results suggest that the SP delays the timing of puberty in female mice via changes in the kisspeptin system, although the effects on hypothalamic–pituitary–gonadal axis are likely secondary to changes in body weight gain

Pattern of gonadotropin secretion along the estrous cycle of C57BL/6 female mice

Abstract The pattern of gonadotropin secretion along the estrous cycle was elegantly described in rats. Less information exists about the pattern of gonadotropin secretion in gonad‐intact mice, particularly regarding the follicle‐stimulating hormone (FSH). Using serial blood collections from the tail‐tip of gonad‐intact C57BL/6 mice on the first day of cornification (transition from diestrus to estrus; hereafter called proestrus), we observed that the luteinizing hormone (LH) and FSH surge cannot be consistently detected since only one out of eight females (12%) showed increased LH levels. In contrast, a high percentage of mice (15 out of 21 animals; 71%) exhibited LH and FSH surges on the proestrus when a single serum sample was collected. Mice that exhibited LH and FSH surges on the proestrus showed c‐Fos expression in gonadotropin‐releasing hormone‐ (GnRH; 83.4% of co‐localization) and kisspeptin‐expressing neurons (42.3% of co‐localization) of the anteroventral periventricular nucleus (AVPV). Noteworthy, mice perfused on proestrus, but that failed to exhibit LH surge, showed a smaller, but significant expression of c‐Fos in GnRH (32.7%) and AVPVKisspeptin (14.0%) neurons. Finally, 96 serial blood samples were collected hourly in eight regular cycling C57BL/6 females to describe the pattern of LH and FSH secretion along the estrous cycle. Small elevations in LH and FSH levels were detected at the time expected for the LH surge. In summary, the present study improves our understanding of the pattern of gonadotropin secretion and the activation of central components of the hypothalamic–pituitary‐gonadal axis along the estrous cycle of C57BL/6 female mice

SIRT1 deacetylase in SF1 neurons protects against metabolic imbalance

SummaryChronic feeding on high-calorie diets causes obesity and type 2 diabetes mellitus (T2DM), illnesses that affect hundreds of millions. Thus, understanding the pathways protecting against diet-induced metabolic imbalance is of paramount medical importance. Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure. Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle. Mechanistically, these aberrations arise, in part, from impaired metabolic actions of the neuropeptide orexin-A and the hormone leptin. Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity. Our results unveil important protective roles of SIRT1 in SF1 neurons against dietary metabolic imbalance

Kiss1 neurons are not responsive to leptin before completion of sexual maturation.

<p>A-B. Brightfield and fluorescence photomicrographs showing lack of colocalization of Kiss1-Cre GFP and LepR mRNA (A) or leptin-induced phosphorylation of STAT3 (B) in prepubertal mice. <b>C-H.</b> Validation of Kiss1 human renilla GFP (Kiss1-hrGFP) mouse model. To optimize the detection of Kiss1 mRNA, we performed colocalization studies (Kiss1 mRNA and hrGFP) in ovariectomized (OVX) and OVX estrogen primed (OVX+E2) mice. Virtually all Kiss1 neurons in the anteroventral periventricular nucleus, anterior periventricular nucleus (AVPV/PeN) and arcuate nucleus (Arc) of OVX+E2 and OVX mice respectively coexpressed hrGFP immunoreactivity. C-D, F-G. Brightfield photomicrographs showing distribution of hrGFP immunoreactivity in the AVPV and Arc of OVX (C, F) and OVX+E2 (D, G) mice. Note changes in hrGFP expression due to sex steroids manipulation. E, H. Higher magnification of D and F, respectively (arrows indicate same cells), showing coexpression of hrGFP-ir and Kiss1 mRNA in the AVPV of OVX+E2 mice (E) and in the Arc of OVX mice (H). Scale bar: A-B  =  200 µm; C-D, F-G  =  400 µm; E, H  =  80 µm. 3V, third ventricle.</p

Re-expression of LepR selectively in Kiss1 neurons causes no amelioration of the reproductive or metabolic phenotype of LepR null mice.

<p>A. Agarose gel showing Cre-induced DNA recombination (higher band) of LepR<i>^Lox</i>^TB in the hypothalamus and testis (but not in the white adipose tissue and tail) of Kiss1-Cre LepR null mice. B. Survival graphs showing the progression of vaginal opening and pregnancy in wild type, LepR null and Kiss1-Cre LepR null mice; C. Image comparing the size of the uterus of a wild type female on diestrus and adult Kiss1-Cre LepR null mice; D. Image showing sections of the ovary of a female on diestrus and of an adult Kiss1-Cre LepR null female. Note the presence of corpora lutea (CL) only in the ovary of the wild type female mice. E. Graph showing the progression of body weight of wild type, LepR null and Kiss1-Cre LepR null female mice. F. Bar graphs showing body composition (percentage of fat and lean mass) of LepR null (black) and Kiss1-Cre LepR null (red) mice at 3 different ages: 20 weeks, 35 weeks (males) and 28 weeks (females).</p

Lack of re-expression of functional LepR in Kiss1-Cre LepR null mice.

<p>A-C. Brightfield photomicrographs showing the distribution of leptin-induced phosphorylation of STAT3 immunoreactivity (pSTAT3-ir) in the arcuate nucleus (Arc) of wild type female mice on diestrus (A) and lack of pSTAT3-ir in the Arc of LepR null (B) and of Kiss1-Cre LepR null (C) adult female mice; <b>D-G.</b> Identification of Kiss1-Cre/GFP cells for whole-cell patch-clamp recordings. (D) Brightfield illumination showing a targeted neuron; (E) the same neuron under fluorescent (FITC) illumination; (F) complete dialysis of AlexaFluor 594 from the intracellular pipette at the end of the recording; (G) colocalization of AlexaFluor 594 and GFP. <b>H</b>. A current-clamp recording demonstrates that leptin (100 nM) depolarizes Kiss1-Cre/GFP neurons. The dashed line indicates the resting membrane potential. Scale bar: A–C  =  400 µm.</p