bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neurochemical Characterization of Body Weight-Regulating Leptin Receptor Neurons in the Nucleus of the Solitary Tract
Authors: Garfield Alastair S. , Patterson Christa , Skora Susanne , Gribble Fiona M. , Reimann Frank , Evans Mark L. , Myers Martin G. , Heisler Lora K. 
Published: September 2012

Abstract
The action of peripherally released leptin at long-form leptin receptors (LepRb) within the brain represents a fundamental axis in the regulation of energy homeostasis and body weight. Efforts to delineate the neuronal mediators of leptin action have recently focused on extrahypothalamic populations and have revealed that leptin action within the nucleus of the solitary tract (NTS) is critical for normal appetite and body weight regulation. To elucidate the neuronal circuits that mediate leptin action within the NTS, we employed multiple transgenic reporter lines to characterize the neurochemical identity of LepRb-expressing NTS neurons. LepRb expression was not detected in energy balance-associated NTS neurons that express cocaine- and amphetamine-regulated transcript, brain-derived neurotrophic factor, neuropeptide Y, nesfatin, catecholamines, γ-aminobutyric acid, prolactin-releasing peptide, or nitric oxide synthase. The population of LepRb-expressing NTS neurons was comprised of subpopulations marked by a proopiomelanocortin-enhanced green fluorescent protein (EGFP) transgene and distinct populations that express proglucagon and/or cholecystokinin. The significance of leptin action on these three populations of NTS neurons was assessed in leptin-deficient Ob/Ob mice, revealing increased NTS proglucagon and cholecystokinin, but not proopiomelanocortin, expression. These data provide new insight into the appetitive brainstem circuits engaged by leptin.
Filamin A Is a Regulator of Blood-Testis Barrier Assembly during Postnatal Development in the Rat Testis
Authors: Su Wenhui , Mruk Dolores D. , Lie Pearl P. Y. , Lui Wing-yee , Cheng C. Yan 
Published: September 2012

AbstractThe blood-testis barrier (BTB) is an important ultrastructure in the testis. A delay in its assembly during postnatal development leads to meiotic arrest. Also, a disruption of the BTB by toxicants in adult rats leads to a failure in spermatogonial differentiation. However, the regulation of BTB assembly remains unknown. Herein, filamin A, an actin filament cross-linker that is known to maintain and regulate cytoskeleton structure and function in other epithelia, was shown to be highly expressed during the assembly of Sertoli cell BTB in vitro and postnatal development of BTB in vivo, perhaps being used to maintain the actin filament network at the BTB. A knockdown of filamin A by RNA interference was found to partially perturb the Sertoli cell tight junction (TJ) permeability barrier both in vitro and in vivo. Interestingly, this down-regulating effect on the TJ barrier function after the knockdown of filamin A was associated with a mis-localization of both TJ and basal ectoplasmic specialization proteins. Filamin A knockdown also induced a disorganization of the actin filament network in Sertoli cells in vitro and in vivo. Collectively, these findings illustrate that filamin A regulates BTB assembly by recruiting these proteins to the microenvironment in the seminiferous epithelium to serve as the building blocks. In short, filamin A participates in BTB assembly by regulating protein recruitment during postnatal development in the rat testis.
GPRC6A Mediates the Effects of l-Arginine on Insulin Secretion in Mouse Pancreatic Islets
Authors: Pi Min , Wu Yunpeng , Lenchik Nataliya I , Gerling Ivan , Quarles L. Darryl 
Published: September 2012

Abstractl-Arginine (l-Arg) is an insulin secretagogue, but the molecular mechanism whereby it stimulates insulin secretion from β-cells is not known. The possibility that l-Arg regulates insulin secretion through a G protein-coupled receptor (GPCR)-mediated mechanism is suggested by the high expression of the nutrient receptor GPCR family C group 6 member A (GPRC6A) in the pancreas and TC-6 β-cells and the finding that Gprc6a−/]minus] mice have abnormalities in glucose homeostasis. To test the direct role of GPRC6A in regulating insulin secretion, we evaluated the response of pancreatic islets derived from Gprc6a−/]minus] mice to l-Arg. We found that the islet size and insulin content were decreased in pancreatic islets from Gprac6a−/]minus] mice. These alterations were selective for β-cells, because there were no abnormalities in serum glucagon levels or glucagon content of islets derived from Gprac6a−/]minus] mice. Significant reduction was observed in both the pancreatic ERK response to l-Arg administration to Gprc6a−/]minus] mice in vivo and l-Arg-induced insulin secretion and production ex vivo in islets isolated from Gprc6a−/]minus] mice. l-Arg stimulation of cAMP accumulation in isolated islets isolated from Gprc6a−/]minus] mice was also diminished. These findings suggest that l-Arg stimulation of insulin secretion in β-cells is mediated, at least in part, through GPRC6A activation of cAMP pathways.
Hepatic Insulin Signaling Changes: Possible Mechanism in Prenatal Hypoxia-Increased Susceptibility of Fatty Liver in Adulthood
Authors: Cao Li , Mao Caiping , Li Shigang , Zhang Yujuan , Lv Juanxiu , Jiang Shan , Xu Zhice 
Published: September 2012

Abstract
Nonalcoholic fatty liver disease (NAFLD) is strongly linked to insulin resistance. Prenatal hypoxia (PH) is a risk factor in programming of insulin resistance, glucose intolerance, and metabolic dysfunctions in later life, although the mechanisms are unclear. In this study, the role of metabolic and histological changes as well as the hepatic insulin signaling mechanisms were determined in increasing susceptibility of NAFLD in the fetus and offspring exposed to PH. Pregnant rats exposed to hypoxia (O2 10%) during pregnancy demonstrated decreased fetal body and liver weight as well as liver to body weight ratio, whereas these changes were not observed in the offspring. However, male liver to body weight ratio increased after PH stress. Microscopic analysis demonstrated that exposure to PH resulted in distorted architecture of the hepatic parenchyma cells with reduced cellularity in the fetus and offspring. Blood glucose and insulin levels were lower with enhanced insulin sensitivity and increased expression of hepatic insulin-signaling elements in the fetus. Furthermore, insulin resistance, impaired glucose homeostasis, and altered expression of insulin-signaling elements occurred in the offspring. Postnatal hypoxia increased hepatic lipid droplets and triglyceride in liver, whereas expressions of insulin-signaling elements were less in the offspring exposed to PH except glucose transporters 2. The results indicated that PH contributed to hepatocyte heteroplasia and metabolic changes that enhanced vulnerability for NAFLD in the offspring, probably via affecting insulin signaling pathway, including glucose transporters 2.
Gonadotrope Plasticity at Cellular and Population Levels
Authors: Alim Zahara , Hartshorn Cheryl , Mai Oliver , Stitt Iain , Clay Colin , Tobet Stuart , Boehm Ulrich 
Published: September 2012

Abstract
Hormone-secreting cells within the anterior pituitary gland may form organized and interdigitated networks that adapt to changing endocrine conditions in different physiological contexts. For gonadotropes, this might reflect a strategy to cope with acute changes throughout different female reproductive stages. The current study examined gonadotropes in female mice at characteristically different hormonal stages: prepubertal, postpubertal, and lactating. Gonadotrope plasticity was examined at the level of the whole population and single cells at different stages by imaging both fixed and live pituitary slices. The use of a model animal providing for the identification of selectively fluorescent gonadotropes allowed the particular advantage of defining cellular plasticity specifically for gonadotropes. In vivo analyses of gonadotropes relative to vasculature showed significantly different gonadotrope distributions across physiological states. Video microscopy studies using live slices ex vivo demonstrated pituitary cell plasticity in the form of movements and protrusions in response to GnRH. As positive feedback from rising estradiol levels is important for priming the anterior pituitary gland for the LH surge, experiments provide evidence of estradiol effects on GnRH signaling in gonadotropes. The experiments presented herein provide new insight into potential plasticity of gonadotropes within the anterior pituitary glands of female mice.
The Effects of Long-Term Treatment with Estradiol and Medroxyprogesterone Acetate on Tyrosine Hydroxylase Fibers and Neuron Number in the Medial Prefrontal Cortex of Aged Female Rats
Authors: Chisholm Nioka C. , Packard Alexandria R. , Koss Wendy A. , Juraska Janice M. 
Published: September 2012

AbstractMenopausal women often initiate hormone treatment to alleviate the symptoms of menopause. Research suggests that these treatments also affect cognition, and studies in young animals indicate that hormone treatment can alter several neuroanatomical measures. However, very little is known about the effects of long-term hormone treatment on the aging female brain. This study investigated the effects of hormone treatment on neuron number and tyrosine hydroxylase (TH) in the rat medial prefrontal cortex (mPFC). Female Long Evans rats were ovariectomized at middle age (12–13 months) and placed in one of four groups: no replacement (NR) (n = 12), 17β-estradiol (E2) (n = 12), E2 and progesterone (n = 7), or E2 and medroxyprogesterone acetate (MPA) (n = 10). Animals were euthanized at 20 months, and the brains were Nissl stained; a subset was immunostained for TH [NR (n = 5); E2 (n = 6); E2 + MPA (n = 4); E2 + progesterone (n = 6)]. E2 was administered through the drinking water, and progestagens were administered via pellets inserted at the nape of the neck. Neuron number and TH fiber density were quantified in the mPFC. Hormone treatment did not alter neuron number. Treatment with E2 and MPA resulted in greater TH densities than NR in layer 1 (P &lt; 0.05). In layers 2/3, animals receiving E2 had greater TH densities than NR animals (P &lt; 0.01). These results indicate that long-term hormone treatments alter dopaminergic fibers and potentially the functioning of the aging mPFC.
Hypoxia Induces Autophagy in Primary Human Trophoblasts
Authors: Chen Baosheng , Longtine Mark S. , Nelson D. Michael 
Published: September 2012

Abstract
Autophagy is a highly regulated and dynamic process that maintains cellular homeostasis and plays a prosurvival role in most cells. Although hypoxia has been shown to induce apoptosis in placental trophoblasts, the hypoxic effect on autophagy has not been studied. We hypothesized that autophagy plays a prosurvival role in the placental trophoblasts by antagonizing hypoxia-induced apoptosis. Our data show that the expression of Light chain 3-II (LC3-II), an autophagic marker and cleaved poly(ADP-ribose) polymerase, an apoptosis marker, are inversely related in cultured trophoblasts. Exposure to rapamycin or hypoxia inactivated mammalian target of rapamycin, as reflected by reduced phosphorylation of ribosomal protein S6, indicating that mammalian target of rapamycin regulates autophagy in cultured cytotrophoblasts. Bafilomycin prevented the degradation of cargo and increased LC3-II and p62 in cytotrophoblasts exposed to hypoxia, revealing enhanced autophagic flux. Importantly, bafilomycin enhanced expression of autophagy-related protein 7 (Atg7), parallel to the increased apoptosis measured by cleaved poly(ADP-ribose) polymerase. LY294002, a phosphatidylinositol 3-kinase inhibitor, increased apoptosis in the trophoblasts under hypoxia or standard conditions. Silencing of Atg7 decreased both apoptosis and LC3-II in the trophoblasts, suggesting a dual role of Atg7 in both autophagy and apoptosis. We conclude that there is a cross talk between autophagy and apoptosis in the placental trophoblasts; autophagy plays a prosurvival role and Atg7 has roles in both autophagy and apoptosis under hypoxia.
Task3 Potassium Channel Gene Invalidation Causes Low Renin and Salt-Sensitive Arterial Hypertension
Authors: Penton David , Bandulik Sascha , Schweda Frank , Haubs Sophia , Tauber Philipp , Reichold Markus , Cong Lu Dang , El Wakil Abeer , Budde Thomas , Lesage Florian , Lalli Enzo , Zennaro Maria-Christina , Warth Richard , Barhanin Jacques 
Published: September 2012

AbstractTask1 and Task3 potassium channels (Task: tandem of P domains in a weak inward rectifying K+ channel-related acid-sensitive K+ channel) are believed to control the membrane voltage of aldosterone-producing adrenal glomerulosa cells. This study aimed at understanding the role of Task3 for the control of aldosterone secretion. The adrenal phenotype of Task3−/− mice was investigated using electrophysiology, adrenal slices, and blood pressure measurements. Primary adrenocortical cells of Task3−/− mice were strongly depolarized compared with wild-type (−52 vs. −79 mV), and in fresh adrenal slices Ca2+ signaling of Task3−/− glomerulosa cells was abnormal. In living Task3−/− mice, the regulation of aldosterone secretion showed specific deficits: Under low Na+ and high K+ diets, protocols known to increase aldosterone, and under standard diet, Task3 inactivation was compensated and aldosterone was normal. However, high Na+ and low K+ diets, two protocols known to lower aldosterone, failed to lower aldosterone in Task3−/− mice. The physiological regulation of aldosterone was disturbed: aldosterone-renin ratio, an indicator of autonomous aldosterone secretion, was 3-fold elevated at standard and high Na+ diets. Isolated adrenal glands of Task3−/− produced 2-fold more aldosterone. As a consequence, Task3−/− mice showed salt-sensitive arterial hypertension (plus 10 mm Hg). In conclusion, Task3 plays an important role in the adaptation of aldosterone secretion to dietary salt intake.
Increased Neurokinin B (Tac2) Expression in the Mouse Arcuate Nucleus Is an Early Marker of Pubertal Onset with Differential Sensitivity to Sex Steroid-Negative Feedback than Kiss1
Authors: Gill John C. , Navarro Víctor M. , Kwong Cecilia , Noel Sekoni D. , Martin Cecilia , Xu Shuyun , Clifton Donald K. , Carroll Rona S. , Steiner Robert A. , Kaiser Ursula B. 
Published: September 2012

Abstract
At puberty, neurokinin B (NKB) and kisspeptin (Kiss1) may help to amplify GnRH secretion, but their precise roles remain ambiguous. We tested the hypothesis that NKB and Kiss1 are induced as a function of pubertal development, independently of the prevailing sex steroid milieu. We found that levels of Kiss1 mRNA in the arcuate nucleus (ARC) are increased prior to the age of puberty in GnRH/sex steroid-deficient hpg mice, yet levels of Kiss1 mRNA in wild-type mice remained constant, suggesting that sex steroids exert a negative feedback effect on Kiss1 expression early in development and across puberty. In contrast, levels of Tac2 mRNA, encoding NKB, and its receptor (NK3R; encoded by Tacr3) increased as a function of puberty in both wild-type and hpg mice, suggesting that during development Tac2 is less sensitive to sex steroid-dependent negative feedback than Kiss1. To compare the relative responsiveness of Tac2 and Kiss1 to the negative feedback effects of gonadal steroids, we examined the effect of estradiol (E2) on Tac2 and Kiss1 mRNA and found that Kiss1 gene expression was more sensitive than Tac2 to E2-induced inhibition at both juvenile and adult ages. This differential estrogen sensitivity was tested in vivo by the administration of E2. Low levels of E2 significantly suppressed Kiss1 expression in the ARC, whereas Tac2 suppression required higher E2 levels, supporting differential sensitivity to E2. Finally, to determine whether inhibition of NKB/NK3R signaling would block the onset of puberty, we administered an NK3R antagonist to prepubertal (before postnatal d 30) females and found no effect on markers of pubertal onset in either WT or hpg mice. These results indicate that the expression of Tac2 and Tacr3 in the ARC are markers of pubertal activation but that increased NKB/NK3R signaling alone is insufficient to trigger the onset of puberty in the mouse.
Suppression of the GnRH Pulse Generator by Neurokinin B Involves a κ-Opioid Receptor-Dependent Mechanism
Authors: Grachev P. , Li X. F. , Kinsey-Jones J. S. , di Domenico A. L. , Millar R. P. , Lightman S. L. , O'Byrne K. T. 
Published: September 2012

Abstract
Neurokinin B (NKB) and its receptor (NK3R) are coexpressed with kisspeptin, Dynorphin A (Dyn), and their receptors [G-protein-coupled receptor-54 (GPR54)] and κ-opioid receptor (KOR), respectively] within kisspeptin/NKB/Dyn (KNDy) neurons in the hypothalamic arcuate nucleus (ARC), the proposed site of the GnRH pulse generator. Much previous research has employed intracerebroventricular (icv) administration of KNDy agonists and antagonists to address the functions of KNDy neurons. We performed a series of in vivo neuropharmacological experiments aiming to determine the role of NKB/NK3R signaling in modulating the GnRH pulse generator and elucidate the interaction between KNDy neuropeptide signaling systems, targeting our interventions to ARC KNDy neurons. First, we investigated the effect of intra-ARC administration of the selective NK3R agonist, senktide, on pulsatile LH secretion using a frequent automated serial sampling method to obtain blood samples from freely moving ovariectomized 17β-estradiol-replaced rats. Our results show that senktide suppresses LH pulses in a dose-dependent manner. Intra-ARC administration of U50488, a selective KOR agonist, also caused a dose-dependent, albeit more modest, decrease in LH pulse frequency. Thus we tested the hypothesis that Dyn/KOR signaling localized to the ARC mediates the senktide-induced suppression of the LH pulse by profiling pulsatile LH secretion in response to senktide in rats pretreated with nor-binaltorphimine, a selective KOR antagonist. We show that nor-binaltorphimine blocks the senktide-induced suppression of pulsatile LH secretion but does not affect LH pulse frequency per se. In order to address the effects of acute activation of ARC NK3R, we quantified (using quantitative RT-PCR) changes in mRNA levels of KNDy-associated genes in hypothalamic micropunches following intra-ARC administration of senktide. Senktide down-regulated expression of genes encoding GnRH and GPR54 (GNRH1 and Kiss1r, respectively), but did not affect the expression of Kiss1 (which encodes kisspeptin). We conclude that NKB suppresses the GnRH pulse generator in a KOR-dependent fashion and regulates gene expression in GnRH neurons.
Feature-positive and feature-negative learning in honey bees
Authors: Abramson Charles I. , Cakmak Ibrahim , Duell Meghan E. , Bates-Albers Leah M. , Zuniga Enoc M. , Pendegraft Loma , Barnett Amanda , Cowo Carmen L. , Warren Joshua J. , Albritton-Ford Aaron C. , Barthell John F. , Hranitz John M. , Wells Harrington 
Published: September 2012

SummaryHoney bees (Apis mellifera) were presented sequential trials where bees were given the choice between a feeding plate with one blue and two white circles, and one with three white circles. Each bee was tested under two different reward scenarios (treatments). During the feature-positive treatment bees received 4 μl of 2 M sucrose when choosing the feeding plate with one blue and two white circles, but received 4 μl of saturated NaCl solution when choosing the feeding plate with three white circles. During the feature-negative treatment bees were rewarded when visiting the feeding plate with three white circles, while visitation to the feeding plate with one blue and two white circles only offered bees the NaCl solution. As an experimental control a set of bees was offered sequential trials where both the feeding plate with one blue and two white circles, and the one with three white circles offered the sucrose reward. Bee feeding plate choice differed between the feature-positive and feature-negative treatment. Bees favored the feeding plate type with the sucrose reward in each treatment, and never consumed the NaCl solution when encountered in either treatment. Further, behavior of bees during both the feature positive and the feature negative treatments differed from that of control bees. However, neither feature positive nor feature negative learning reached high levels of success. When we tested bees using simply the choice of blue versus white targets, where one color held the sucrose reward and the other the salt water, a bee's fidelity to the color offering the sugar reward quickly reached very high levels.
Walking on smooth and rough ground: activity and timing of the claw retractor muscle in the beetlePachnoda marginata peregrina(Coleoptera, Scarabaeidae)
Authors: Bußhardt Philipp , Gorb Stanislav N. 
Published: September 2012

SummaryThe activity pattern of the claw retractor muscle of Pachnoda marginata peregrina beetles was examined in this study. We found this muscle to be located in the tibia, without a femoral part, as is the case in other insects. Electromyograms (EMGs) of the muscle revealed a rather similar activity pattern during beetle locomotion on rough and smooth substrates. We recorded units with small and large amplitude, with the smaller one being active during almost the entire stance phase, the larger one roughly in the first half of stance. Small but significant differences were found in the precise onset and end of activity. Both small and large units began their activity earlier on the rough surface. While there was no difference at the end of activity in the small unit between both surfaces, the large unit ended its activity significantly earlier on the rough substrate. The spike frequencies on both surfaces were also significantly different for both small and large units. The small unit showed a higher spike frequency on the smooth surface, while the large unit had a higher spike frequency on the rough surface. From our experiments, we conclude that the muscle is controlled by the same basic activity pattern on different surfaces, with some adjustments due to sensory feedback. The adjustments cause differences in onset and end of activity, as well as in spike frequency of the involved muscle units.
Protein-induced weight increase of the gastrointestinal tract of locusts improves net nutrient uptake via larger meals rather than more efficient nutrient absorption
Authors: Clissold Fiona J , Brown Zuben P , Simpson Stephen J 
Published: September 2012

Summary
Increasing the tissue biomass and/or volume of the gastrointestinal tract (GIT) is commonly seen when animals feed on poor quality diets. This increase can simply permit larger meal sizes, but may also rebalance nutritionally imbalanced ingesta by allowing selective absorption of limiting nutrients. In an insect herbivore, the migratory locust, a synthetic diet with a high ratio of protein to carbohydrate was found to induce weight enhancement of the GIT. When normalized for sex and overall body size, increases to the mass of the foregut and midgut caeca resulted in higher absorption (20-30%) of both protein and carbohydrate when subsequently feeding on three chemically and structurally different grasses. Greater net absorption of macronutrients occurred because these locusts ate larger meals that transited at the same time and with the same digestive efficiency as locusts in which the GIT was not enlarged. Thus, plasticity of the GIT did not improve nutritional homeostasis, but increased the rate of nutrient uptake.