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Kenneth D. Carr - One of the best experts on this subject based on the ideXlab platform.
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Effects of Food Restriction on expression of place conditioning and biochemical correlates in rat nucleus accumbens
Psychopharmacology, 2016Co-Authors: Caroline Jung, Soledad Cabeza De Vaca, Ariana Rabinowitsch, Wei Ting Lee, Danielle Zheng, Kenneth D. CarrAbstract:Rationale When ad libitum-fed rats undergo cocaine place preference conditioning (CPP) but are switched to Food Restriction for testing, CPP becomes resistant to extinction and correlates with phosphorylation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor GluA1 at Ser845 in nucleus accumbens (NAc) core. Objectives This study tested whether Food Restriction increases persistence of morphine CPP and conditioned place aversions (CPA) induced by LiCl and naloxone-precipitated morphine withdrawal. Materials and methods Ad libitum-fed rats were conditioned with morphine (6.0 mg/kg, i.p.), LiCl (50.0/75.0 mg/kg, i.p.), or naloxone (1.0 mg/kg, s.c.) 22 h post-morphine (20.0 mg/kg, s.c.). Half of the subjects were then switched to Food Restriction. Daily testing resumed 3 weeks later, and brains were harvested when one diet group met extinction criterion. Western analyses probed for pSer845-GluA1, pERK1, and pERK2 in NAc. Results Food Restriction increased persistence of morphine CPP and preference scores correlated with pSer845-GluA1 in NAc core and shell. LiCl CPA was curtailed by Food Restriction, yet pSer845-GluA1 and pERK2 were elevated in NAc core of Food-restricted rats. Food Restriction increased persistence of naloxone CPA and elevated pSer845-GluA1 in NAc core and shell, and aversion scores were negatively correlated with pERK1 and pERK2 in NAc core. Conclusions These results suggest that Food Restriction prolongs responsiveness to environmental contexts paired with subjective effects of both morphine and morphine withdrawal. A mechanistic scheme, attributing these effects to upregulation of pSer845-GluA1, but subject to override by CPA-specific, pERK2-mediated extinction learning, is explored to accommodate opposite effects of Food Restriction on LiCl and naloxone CPA.
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Chronic Food Restriction and dopamine transporter function in rat striatum.
Brain research, 2006Co-Authors: Juan Zhen, Maarten E. A. Reith, Kenneth D. CarrAbstract:Abstract The present communication reports on DA uptake in rat striatum in a model of chronic Food Restriction. The Km for DA uptake was unaltered, but the Vmax was reduced by 32%, not supporting the idea that the enhanced behavioral sensitivity to cocaine or d -amphetamine upon chronic Food Restriction is due to a greater density of DAT at the plasma membrane for drug interaction. Chronic Food Restriction did not alter the potency of cocaine or d -amphetamine in inhibiting DA uptake in the striatum, suggesting that the enhanced behavioral sensitivity to these drugs upon chronic Food Restriction is not due to their enhanced affinity for DAT. These results point to factors other than DAT density or affinity underlying the sensitized response to psychostimulants in Food Restriction.
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augmentation of drug reward by chronic Food Restriction behavioral evidence and underlying mechanisms
Physiology & Behavior, 2002Co-Authors: Kenneth D. CarrAbstract:Chronic Food Restriction and maintenance of low body weight have long been known to increase the self-administration and motor-activating effects of abused drugs. Using a lateral hypothalamic self-stimulation (LHSS) rate-frequency method, it is shown that chronic Food Restriction augments the rewarding (i.e., threshold lowering) effect of diverse drugs of abuse. Further, the effect is attributed to increased sensitivity of a neural substrate, rather than a change in drug bioavailability or pharmacokinetics, because it is preserved when drugs are injected directly into the lateral cerebral ventricle (intracerebroventricularly). The Food Restriction regimen that augments drug reward also increases the induction of c-fos, by intracerebroventricular amphetamine, in limbic forebrain dopamine (DA) terminal areas. The possibility of increased DA receptor function is suggested by findings that rewarding and motor-activating effects of direct DA receptor agonists are augmented by Food Restriction, and the augmented behavioral effects of amphetamine are reversed by an otherwise subthreshold dose of D-1 antagonist. Initial studies of DA receptor-mediated signal transduction, that are focused on the D-2 receptor, suggest increased functional coupling between receptor and G-protein (i.e., quinpirole-stimulated [(35)S]GTPgammaS binding) in dorsal striatum. Unlike behavioral sensitization induced by intermittent stress or psychostimulant treatment, which persist indefinitely following induction, the augmenting effect of Food Restriction abates within 1 week of restored ad libitum feeding and weight gain. The possible involvement of endocrine hormones and/or 'feeding-related' neuropeptides, whose levels change dynamically with depletion and repletion of adipose stores, is therefore under investigation. Initial tests have been limited to acute treatments aimed at attenuating the effects of hypoinsulinemia, hypoleptinemia and elevated corticosterone levels in Food-restricted rats. None of these treatments has attenuated the behavioral effect of Food Restriction. While a melanocortin receptor agonist has been found to enhance drug reward, melanocortin receptors do not seem to mediate the augmenting effect of Food Restriction. Continuing investigations of endocrine adiposity signals, 'feeding-related' neuropeptides and dopaminergic signal transduction may further elucidate the way in which drugs of abuse exploit mechanisms that mediate survival-related behavior, and help explain the high comorbidity of drug abuse and eating disorders.
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Food Restriction Enhances the Central Rewarding Effect of Abused Drugs
The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998Co-Authors: Soledad Cabeza De Vaca, Kenneth D. CarrAbstract:Chronic Food Restriction increases the systemic self-administration and locomotor-stimulating effect of abused drugs. However, it is not clear whether these behavioral changes reflect enhanced rewarding potency or a CNS-based modulatory process. The purpose of this study was to determine whether Food Restriction specifically increases the rewarding potency of drugs, as indexed by their threshold-lowering effect on lateral hypothalamic self-stimulation, and whether any such effect can be attributed to an enhanced central response rather than changes in drug disposition. When drugs were administered systemically, Food Restriction potentiated the threshold-lowering effect of amphetamine (0.125, 0.25, and 0.5 mg/kg, i.p.), phencyclidine (1.0, 2.0, and 3.0 mg/kg, i.p.), and dizocilpine (MK-801) (0.0125, 0.05, and 0.1 mg/kg, i.p.) but not nicotine (0.15, 0.3, 0.45 mg/kg, s.c.). When amphetamine (25.0, 50.0, and 100.0 μg) and MK-801 (5.0, 10.0, and 20.0 μg) were administered via the intracerebroventricular route, Food Restriction again potentiated the threshold-lowering effects and increased the locomotor-stimulating effects of both drugs. These results indicate that Food Restriction increases the sensitivity of neural substrates for rewarding and stimulant effects of drugs. In light of work that attributes rewarding effects of MK-801 to blockade of NMDA receptors on medium spiny neurons in nucleus accumbens, the elements affected by Food Restriction may lie downstream from the mesoaccumbens dopamine neurons whose terminals are the site of amphetamine-rewarding action. Possible metabolic–endocrine triggers of this effect are discussed, as is the likelihood that mechanisms mediating the modulatory effect of Food Restriction differ from those mediating sensitization by intermittent drug exposure.
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Effects of chronic Food Restriction on prodynorphin-derived peptides in rat brain regions
Brain Research, 1994Co-Authors: Yemiliya Berman, Lakshmi A. Devi, Kenneth D. CarrAbstract:Abstract Chronic Food Restriction produces a variety of physiological and behavioral adaptations including a potentiation of the reinforcing effect of Food, drugs and lateral hypothalamic electrical stimulation. Previous work in this laboratory has revealed that the lowering of self-stimulation threshold by Food Restriction is reduced by μ- and κ-selective opioid antagonists. In the present study, the effect of chronic Food Restriction on levels of three prodynorphin-derived peptides, namely dynorphin A1–17 (A1–17), dynorphin A1–8 (A1–8) and dynorphin B1–13 (B1–13) were measured in eleven brain regions known to be involved in appetite, taste and reward. Food Restriction increased levels of A1–17 in dorsal medial (+ 19.6%), ventral medial (+ 24.2%) and medial preoptic (+ 82.9%) hypothalamic areas. Levels of A1–17 decreased in the central nucleus of the amygdala (− 35.1%). Food Restriction increased levels of A1–8 in nucleus accumbens (+ 34.4%), bed nucleus of the stria terminalis (+ 24.5%) and lateral hypothalamus (+ 41.9%). Food Restriction had no effect on levels of B1–13. A1–17 is highly κ-preferring and the brain regions in which levels increased all have a high ratio of κ:μ and δ receptors. A1–8 is less discriminating among opioid receptor types and the brain regions in which levels increased have a low ratio of κ:μ and δ receptors. The present results suggest that Food Restriction alters posttranslational processing within the dynorphin A domain of the prodynorphin precursor, possibly leading to a change in the balance between κ and non-κ opioid receptor stimulation in specific brain regions.
Raphaelle Winsky-sommerer - One of the best experts on this subject based on the ideXlab platform.
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Food Restriction induces functional resilience to sleep Restriction in rats.
Sleep, 2020Co-Authors: Sally Loomis, Andrew Mccarthy, Derk-jan Dijk, Gary Gilmour, Raphaelle Winsky-sommererAbstract:STUDY OBJECTIVES Sleep Restriction (SR) leads to performance decrements across cognitive domains but underlying mechanisms remain largely unknown. The impact of SR on performance in rodents is often assessed using tasks in which Food is the reward. Investigating how the drives of hunger and sleep interact to modulate performance may provide insights into mechanisms underlying sleep loss-related performance decrements. METHODS Three experiments were conducted in male adult Wistar rats to assess: (1) effects of Food Restriction on performance in the simple response latency task (SRLT) across the diurnal cycle (n = 30); (2) interaction of Food Restriction and SR (11 h) on SRLT performance, sleep electroencephalogram, and event-related potentials (ERP) (n = 10-13); and (3) effects of Food Restriction and SR on progressive ratio (PR) task performance to probe the reward value of Food reinforcement (n = 19). RESULTS Food Restriction increased premature responding on the SRLT at the end of the light period of the diurnal cycle. SR led to marked impairments in SRLT performance in the ad libitum-fed group, which were absent in the Food-restricted group. After SR, Food-restricted rats displayed a higher amplitude of cue-evoked ERP components during the SRLT compared with the ad libitum group. SR did not affect PR performance, while Food Restriction improved performance. CONCLUSIONS Hunger may induce a functional resilience to negative effects of sleep loss during subsequent task performance, possibly by maintaining attention to Food-related cues.
Sally Loomis - One of the best experts on this subject based on the ideXlab platform.
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Food Restriction induces functional resilience to sleep Restriction in rats.
Sleep, 2020Co-Authors: Sally Loomis, Andrew Mccarthy, Derk-jan Dijk, Gary Gilmour, Raphaelle Winsky-sommererAbstract:STUDY OBJECTIVES Sleep Restriction (SR) leads to performance decrements across cognitive domains but underlying mechanisms remain largely unknown. The impact of SR on performance in rodents is often assessed using tasks in which Food is the reward. Investigating how the drives of hunger and sleep interact to modulate performance may provide insights into mechanisms underlying sleep loss-related performance decrements. METHODS Three experiments were conducted in male adult Wistar rats to assess: (1) effects of Food Restriction on performance in the simple response latency task (SRLT) across the diurnal cycle (n = 30); (2) interaction of Food Restriction and SR (11 h) on SRLT performance, sleep electroencephalogram, and event-related potentials (ERP) (n = 10-13); and (3) effects of Food Restriction and SR on progressive ratio (PR) task performance to probe the reward value of Food reinforcement (n = 19). RESULTS Food Restriction increased premature responding on the SRLT at the end of the light period of the diurnal cycle. SR led to marked impairments in SRLT performance in the ad libitum-fed group, which were absent in the Food-restricted group. After SR, Food-restricted rats displayed a higher amplitude of cue-evoked ERP components during the SRLT compared with the ad libitum group. SR did not affect PR performance, while Food Restriction improved performance. CONCLUSIONS Hunger may induce a functional resilience to negative effects of sleep loss during subsequent task performance, possibly by maintaining attention to Food-related cues.
Cyrilla H. Wideman - One of the best experts on this subject based on the ideXlab platform.
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Interactions between vasopressin and Food Restriction on stress-induced analgesia
Peptides, 1996Co-Authors: Cyrilla H. Wideman, Helen M. Murphy, Sally B. MccartneyAbstract:To investigate the role of the hormone vasopressin (VP) in mediating the response of an organism to Food Restriction stress-induced analgesia, tail flick latencies and scored qualitative behavioral responses were recorded in VP-containing (LE) rats and VP-deficient (DI) rats. These variables were measured under nonstressed (ad lib) and stressed (Food Restriction) conditions. In the ad lib condition, DI and LE rats had a similar tail flick latency and scored qualitative behavioral response to the stimulus eliciting the tail flick. During the Food Restriction condition, however, LE animals developed significant Food Restriction stress-induced analgesia, as measured by tail flick latency. On the other hand, DI animals did not develop significant analgesia. In addition, DI animals exhibited a significantly greater scored qualitative behavioral response to the stimulus eliciting the tail flick than LE animals. These results demonstrate that VP plays an important role in the regulation of Food Restriction stress-induced analgesia, as well as the scored qualitative behavioral response elicited by the tail flick stimulus.
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Modulatory effects of vasopressin on glucose and protein metabolism during Food-Restriction stress
Peptides, 1993Co-Authors: Cyrilla H. Wideman, Helen M. MurphyAbstract:Plasma levels of glucose and urea nitrogen were compared in vasopressin-containing (LE) and vasopressin-deficient (DI) rats under ad lib and Food-restricted conditions. In the ad lib situation, DI and LE rats had similar levels of glucose and urea nitrogen. Variations in this pattern were observed under Food-restricted conditions. The DI animals exhibited lower levels of glucose and higher levels of urea nitrogen than their LE counterparts. During Food Restriction, the glucose levels of LE animals were not different from that observed under ad lib conditions. A significant decrease, however, was observed in the glucose levels in DI animals during Food Restriction. Urea nitrogen levels in LE animals decreased during Food Restriction as compared to the ad lib situation, whereas urea nitrogen levels of DI animals increased during Food Restriction. These observations indicate that vasopressin has a modulatory role on glucose and protein metabolism during the stress of Food Restriction.
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Vasopressin, corticosterone levels, and gastric ulcers during Food-Restriction stress.
Peptides, 1992Co-Authors: Helen M. Murphy, Cyrilla H. WidemanAbstract:Corticosterone levels and ulcers were compared in vasopressin-containing (LE) and vasopressin-deficient (DI) rats under ad lib and Food-restricted conditions. In the ad lib situation, DI and LE rats had similar corticosterone levels and no ulcers. After 1 day of Food Restriction, the corticosterone levels were elevated in DI and LE rats, with a significantly higher level in LE rats. No ulcers were present in either strain. After 2 days of Food Restriction, the corticosterone levels were similar in DI and LE rats. The level in DI rats was comparable to that of the preceding day, but the level in LE animals dropped significantly from the previous day. Significant ulceration was evident in DI rats, but absent in LE rats. Following 3 days of Food Restriction, the corticosterone level in LE rats had returned to the ad lib level, whereas, for DI rats, an elevated level was maintained. There were no ulcers in LE rats, but they were present in DI rats. Thus LE and DI rats responded differently to the stress of Food Restriction. The mechanism underlying the response is most likely related to changes in the hypothalamic-pituitary-adrenocortical axis and its reaction to stress.
Julian Swierczynski - One of the best experts on this subject based on the ideXlab platform.
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Chemerin gene expression is regulated by Food Restriction and Food Restriction–refeeding in rat adipose tissue but not in liver
Regulatory peptides, 2013Co-Authors: Ewa Stelmanska, Tomasz Sledzinski, Jacek Turyn, Malgorzata Presler, Justyna Korczynska, Julian SwierczynskiAbstract:Abstract Chemerin is an adipokine that regulates adipocyte development and metabolism as well as inflammatory and immune function of some cells. Although chemerin may be linked to obesity and related diseases, little is known about the nutritional regulation of chemerin gene expression. We investigated the effect of prolonged Food Restriction, a common approach in treating obesity and related diseases, and prolonged Food Restriction–refeeding on chemerin gene expression in rat white adipose tissue and liver. The prolonged Food Restriction was accompanied by an approximately 2-fold decrease in chemerin mRNA level in rat white adipose tissue. Upon refeeding, an increase (approximately 8-fold as compared to rats maintained on restricted diet and 4-fold as compared to control) in chemerin mRNA level in white adipose tissue was found. Surprisingly, no effect of Food Restriction and Food Restriction–refeeding on chemerin mRNA level in the liver was found. Chemerin mRNA level in adipose tissue was positively correlated with serum insulin concentration. Moreover insulin increased significantly chemerin gene expression in primary rat adipocytes. The changes in chemerin mRNA level in adipose tissue and serum chemerin concentrations were associated with changes in serum leptin and free fatty acid concentrations. Collectively, the data presented here indicate that chemerin gene expression is regulated by nutritional status in rat adipose tissue but not in liver. It seems that insulin plays important role in stimulation of chemerin gene expression in adipose tissue. However, changes in serum leptin and free fatty acids concentrations after Food Restriction–refeeding suggest that the role of these factors in the regulation of chemerin gene expression in adipose tissue cannot be excluded. Lack of the effect of Food Restriction and Food Restriction–refeeding on liver chemerin gene expression suggests that adipose tissue is the dietary modifiable source of serum chemerin concentration.
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Chronic Food Restriction up-regulates 11-β-hydroxysteroid dehydrogenase
Central European Journal of Biology, 2011Co-Authors: Tomasz Sledzinski, Ewa Stelmanska, Jacek Turyn, Malgorzata Presler, Jerzy Klimek, Julian SwierczynskiAbstract:Corticosterone — product of 11-β-hydroxysteroid dehydrogenase type I (11βHSD1) stimulates adipocytes differentiation and activates lipogenic enzymes gene expression in white adipose tissue (WAT) of rats. The aim of the study was to examine the effect of chronic Food Restriction, often practised by obese individuals trying to lose body mass, on: a) 11βHSD1 gene expression, b) expression of genes associated with adipocyte differentiation (PPARg, SREBP-1, adiponectin), and c) expression of genes associated with lipogenesis in WAT of rats. Two-month old rats were divided into a control and a Food restricted group obtaining 50% of Food consumed by controls for 30 days. mRNA levels of studied genes in perirenal WAT were analysed by real-time PCR. 11βHSD1 and lipogenic enzymes activities were measured by radiometric conversion assay and by spectrophotometric assay respectively. Food Restriction caused significant increase of 11βHSD1, PPARg, SREBP1, adiponectin and lipogenic enzymes mRNA levels in perirenal WAT. 11βHSD1 and some lipogenic enzymes activities were also increased by Food Restriction. The coordinated up-regulation of 11βHSD1, and genes associated with adipocyte differentiation and lipogenesis by Food Restriction suggests that such nutritional condition shifts WAT metabolism, that would permit this tissue to synthesize and accumulate triacylglycerols immediately after refeeding.
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Up-regulation of stearoyl-CoA desaturase 1 and elongase 6 genes expression in rat lipogenic tissues by chronic Food Restriction and chronic Food Restriction/refeeding.
Molecular and Cellular Biochemistry, 2010Co-Authors: Jacek Turyn, Magdalena Stojek, Julian SwierczynskiAbstract:Successful treatment of obesity and related diseases by chronic Food Restriction requires the understanding of the effect of such nutritional therapy on the expression of genes which have been implicated to be involved in some diseases associated with obesity. The purpose of this study was to examine the effect of chronic Food Restriction and chronic Food Restriction/refeeding on lipogenic enzymes, especially the expression of genes encoding the stearoyl-CoA desaturase 1 (Scd1) and elongase6 (Elovl6) in rat liver and adipose tissue. We found that both chronic Food Restriction and chronic Food Restriction/refeeding caused increased expression of the Scd1 and Elovl6 genes in both the liver and adipose tissue. The increase was more pronounced in case of chronic Food Restriction/refeeding (several-fold increase) than that in chronic Food Restriction alone (two to threefold increase). Essentially, similar results were obtained when the expression of fatty acid synthase, acetyl-CoA carboxylase, ATP-citrate lyase, and malic enzyme genes was studied. Moreover, we found that chronic Food Restriction and short-term fasting exert opposite effects on the expression of lipogenic enzymes genes. The increased expression of the genes encoding Scd1, Elovl6, and other key lipogenic enzymes may favor fat storage after chronic Food Restriction/refeeding and may be part of the molecular mechanism by which Food Restriction/refeeding increases body weight and enhances susceptibility to insulin resistance.