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Nucleus accumbens neuronal maturation differences in young rats bred for low versus high voluntary running behaviour.
Roberts MD, Toedebusch RG, Wells KD, Company JM, Brown JD, Cruthirds CL, Heese AJ, Zhu C, Rottinghaus GE, Childs TE, Booth FW
(2014) J Physiol 592: 2119-35
MeSH Terms: Animals, Behavior, Animal, Female, Gene Expression Regulation, Developmental, Humans, Motor Activity, Nerve Tissue Proteins, Neuronal Plasticity, Neurons, Nucleus Accumbens, Rats, Rats, Inbred Strains, Running, Volition
Show Abstract · Added October 23, 2017
We compared the nucleus accumbens (NAc) transcriptomes of generation 8 (G8), 34-day-old rats selectively bred for low (LVR) versus high voluntary running (HVR) behaviours in rats that never ran (LVR(non-run) and HVR(non-run)), as well as in rats after 6 days of voluntary wheel running (LVR(run) and HVR(run)). In addition, the NAc transcriptome of wild-type Wistar rats was compared. The purpose of this transcriptomics approach was to generate testable hypotheses as to possible NAc features that may be contributing to running motivation differences between lines. Ingenuity Pathway Analysis and Gene Ontology analyses suggested that 'cell cycle'-related transcripts and the running-induced plasticity of dopamine-related transcripts were lower in LVR versus HVR rats. From these data, a hypothesis was generated that LVR rats might have less NAc neuron maturation than HVR rats. Follow-up immunohistochemistry in G9-10 LVR(non-run) rats suggested that the LVR line inherently possessed fewer mature medium spiny (Darpp-32-positive) neurons (P < 0.001) and fewer immature (Dcx-positive) neurons (P < 0.001) than their G9-10 HVR counterparts. However, voluntary running wheel access in our G9-10 LVRs uniquely increased their Darpp-32-positive and Dcx-positive neuron densities. In summary, NAc cellularity differences and/or the lack of running-induced plasticity in dopamine signalling-related transcripts may contribute to low voluntary running motivation in LVR rats.
© 2014 The Authors. The Journal of Physiology © 2014 The Physiological Society.
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14 MeSH Terms
Enhanced cardiac protein glycosylation (O-GlcNAc) of selected mitochondrial proteins in rats artificially selected for low running capacity.
Johnsen VL, Belke DD, Hughey CC, Hittel DS, Hepple RT, Koch LG, Britton SL, Shearer J
(2013) Physiol Genomics 45: 17-25
MeSH Terms: Absorptiometry, Photon, Analysis of Variance, Animals, Carbon Radioisotopes, Citrate (si)-Synthase, Fatty Acids, Nonesterified, Glucose, Glucose Clamp Technique, Glycosylation, Immunoblotting, Insulin Resistance, Kinetics, Mitochondrial Proteins, Models, Animal, Myocardium, N-Acetylglucosaminyltransferases, Oxidative Phosphorylation, Rats, Rats, Inbred Strains, Running
Show Abstract · Added April 24, 2014
O-linked β-N-acetyl glucosamine (O-GlcNAc) is a posttranslational modification consisting of a single N-acetylglucosamine moiety attached by an O-β-glycosidic linkage to serine and threonine residues of both nuclear and cytosolic proteins. Analogous to phosphorylation, the modification is reversible and dynamic, changing in response to stress, nutrients, hormones, and exercise. Aims of this study were to examine differences in O-GlcNAc protein modification in the cardiac tissue of rats artificially selected for low (LCR) or high (HCR) running capacity. Hyperinsulinemic-euglycemic clamps in conscious animals assessed insulin sensitivity while 2-[(14)C] deoxyglucose tracked both whole body and tissue-specific glucose disposal. Immunoblots of cardiac muscle examined global O-GlcNAc modification, enzymes that control its regulation (OGT, OGA), and specific proteins involved in mitochondrial oxidative phosphorylation. LCR rats were insulin resistant disposing of 65% less glucose than HCR. Global tissue O-GlcNAc, OGT, OGA, and citrate synthase were similar between groups. Analysis of cardiac proteins revealed enhanced O-GlcNAcylation of mitochondrial Complex I, Complex IV, VDAC, and SERCA in LCR compared with HCR. These results are the first to establish an increase in specific protein O-GlcNAcylation in LCR animals that may contribute to progressive mitochondrial dysfunction and the pathogenesis of insulin resistance observed in the LCR phenotype.
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20 MeSH Terms
Potentiation of mGlu5 receptors with the novel enhancer, VU0360172, reduces spontaneous absence seizures in WAG/Rij rats.
D'Amore V, Santolini I, van Rijn CM, Biagioni F, Molinaro G, Prete A, Conn PJ, Lindsley CW, Zhou Y, Vinson PN, Rodriguez AL, Jones CK, Stauffer SR, Nicoletti F, van Luijtelaar G, Ngomba RT
(2013) Neuropharmacology 66: 330-8
MeSH Terms: Age Factors, Animals, Brain Waves, Cerebral Cortex, Disease Models, Animal, Electroencephalography, Epilepsy, Absence, Excitatory Amino Acid Agonists, Excitatory Amino Acid Antagonists, Hydrolysis, Male, Motor Activity, Niacinamide, Phosphatidylinositol Phosphates, Pyridines, Rats, Rats, Inbred Strains, Receptor, Metabotropic Glutamate 5, Receptors, Metabotropic Glutamate, Somatosensory Cortex, Thiazoles, Ventral Thalamic Nuclei
Show Abstract · Added February 19, 2015
Absence epilepsy is generated by the cortico-thalamo-cortical network, which undergoes a finely tuned regulation by metabotropic glutamate (mGlu) receptors. We have shown previously that potentiation of mGlu1 receptors reduces spontaneous occurring spike and wave discharges (SWDs) in the WAG/Rij rat model of absence epilepsy, whereas activation of mGlu2/3 and mGlu4 receptors produces the opposite effect. Here, we have extended the study to mGlu5 receptors, which are known to be highly expressed within the cortico-thalamo-cortical network. We used presymptomatic and symptomatic WAG/Rij rats and aged-matched ACI rats. WAG/Rij rats showed a reduction in the mGlu5 receptor protein levels and in the mGlu5-receptor mediated stimulation of polyphosphoinositide hydrolysis in the ventrobasal thalamus, whereas the expression of mGlu5 receptors was increased in the somatosensory cortex. Interestingly, these changes preceded the onset of the epileptic phenotype, being already visible in pre-symptomatic WAG/Rij rats. SWDs in symptomatic WAG/Rij rats were not influenced by pharmacological blockade of mGlu5 receptors with MTEP (10 or 30 mg/kg, i.p.), but were significantly decreased by mGlu5 receptor potentiation with the novel enhancer, VU0360172 (3 or 10 mg/kg, s.c.), without affecting motor behaviour. The effect of VU0360172 was prevented by co-treatment with MTEP. These findings suggest that changes in mGlu5 receptors might lie at the core of the absence-seizure prone phenotype of WAG/Rij rats, and that mGlu5 receptor enhancers are potential candidates to the treatment of absence epilepsy. This article is part of a Special Issue entitled 'Metabotropic Glutamate Receptors'.
Copyright © 2012 Elsevier Ltd. All rights reserved.
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22 MeSH Terms
CITED1 expression in Wilms' tumor and embryonic kidney.
Lovvorn HN, Westrup J, Opperman S, Boyle S, Shi G, Anderson J, Perlman EJ, Perantoni AO, Wills M, de Caestecker M
(2007) Neoplasia 9: 589-600
MeSH Terms: Animals, Biomarkers, Tumor, Humans, Kidney, Kidney Neoplasms, Neoplasm Staging, Nuclear Proteins, RNA, Messenger, Rats, Rats, Inbred Strains, Transcription Factors, Wilms Tumor
Show Abstract · Added December 26, 2013
Wilms' tumors, or nephroblastomas, are thought to arise from abnormal postnatal retention and dysregulated differentiation of nephrogenic progenitor cells that originate as a condensed metanephric mesenchyme within embryonic kidneys. We have previously shown that the transcriptional regulator CITED1 (CBP/p300-interacting transactivators with glutamic acid [E]/aspartic acid [D]-rich C-terminal domain) is expressed exclusively in these nephrogenic progenitor cells and is downregulated as they differentiate to form nephronic epithelia. In the current study, we show that CITED1 expression persists in blastemal cell populations of both experimental rat nephroblastomas and human Wilms' tumors, and that primary human Wilms' tumors presenting with disseminated disease show the highest level of CITED1 expression. Unlike the predominantly cytoplasmic subcellular localization of CITED1 in the normal developing kidney, CITED1 is clearly detectable in the nuclear compartment of Wilms' tumor blastema. These findings indicate that CITED1 is a marker of primitive blastema in Wilms' tumors and suggest that persistent expression and/or altered subcellular localization of CITED1 in the condensed metanephric mesenchyme could play a role in Wilms' tumor initiation and pathogenesis.
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12 MeSH Terms
Insulin replacement restores the behavioral effects of quinpirole and raclopride in streptozotocin-treated rats.
Sevak RJ, Koek W, Galli A, France CP
(2007) J Pharmacol Exp Ther 320: 1216-23
MeSH Terms: Amphetamine, Animals, Behavior, Animal, Blood Glucose, Body Weight, Diabetes Mellitus, Experimental, Dopamine Agonists, Dopamine Antagonists, Insulin, Male, Quinpirole, Raclopride, Rats, Rats, Inbred Strains, Receptors, Dopamine, Streptozocin
Show Abstract · Added February 19, 2015
Streptozotocin (STZ)-induced diabetes can modulate dopamine (DA) neurotransmission and thereby modify the behavioral effects of drugs acting on DA systems. Insulin replacement, and in some conditions repeated treatment with amphetamine, can partially restore sensitivity of STZ-treated rats to dopaminergic drugs. The present study sought to characterize the role of insulin and amphetamine in modulating the behavioral effects of drugs that selectively act on D2/D3 receptors. In control rats, quinpirole and quinelorane produced yawning, whereas raclopride and gamma-hydroxybutyric acid (GHB) produced catalepsy. Raclopride antagonized quinpirole- and quinelorane-induced yawning with similar potency. STZ treatment increased blood glucose concentration, decreased body weight, and markedly reduced sensitivity to quinpirole-induced yawning, quinelorane-induced yawning as well as to raclopride-induced catalepsy, while enhancing sensitivity to GHB-induced catalepsy. Repeated treatment with amphetamine partially restored sensitivity of STZ-treated rats to amphetamine-stimulated locomotion and also produced conditioned place preference, without affecting blood glucose and body weight changes. However, amphetamine treatment did not restore sensitivity to the behavioral effects of quinpirole, raclopride, or GHB, suggesting differential regulation of dopamine transporter activity and sensitivity of D2 receptors in hypoinsulinemic rats. Insulin replacement in STZ-treated rats normalized blood glucose and body weight changes and fully restored sensitivity to quinpirole-induced yawning, as well as to raclopride-induced catalepsy, while reducing sensitivity to GHB-induced catalepsy. Overall, these data indicate that changes in insulin status markedly affect sensitivity to the behavioral effects of dopaminergic drugs. The results underscore the importance of insulin in modulating DA neurotransmission; these effects might be especially relevant to understanding the co-morbidity of eating disorders and substance abuse.
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16 MeSH Terms
Leptin action in the forebrain regulates the hindbrain response to satiety signals.
Morton GJ, Blevins JE, Williams DL, Niswender KD, Gelling RW, Rhodes CJ, Baskin DG, Schwartz MW
(2005) J Clin Invest 115: 703-10
MeSH Terms: Animals, Cholecystokinin, Eating, Feeding Behavior, Genetic Therapy, Homeostasis, Humans, Leptin, Male, Neurons, Obesity, Prosencephalon, Proto-Oncogene Proteins c-fos, Rats, Rats, Inbred Strains, Receptors, Cell Surface, Receptors, Leptin, Recombinant Fusion Proteins, Rhombencephalon, Satiety Response, Signal Transduction
Show Abstract · Added February 15, 2016
The capacity to adjust energy intake in response to changing energy requirements is a defining feature of energy homeostasis. Despite the identification of leptin as a key mediator of this process, the mechanism whereby changes of body adiposity are coupled to adaptive, short-term adjustments of energy intake remains poorly understood. To investigate the physiological role of leptin in the control of meal size and the response to satiety signals, and to identify brain areas mediating this effect, we studied Koletsky (fa(k)/fa(k)) rats, which develop severe obesity due to the genetic absence of leptin receptors. Our finding of markedly increased meal size and reduced satiety in response to the gut peptide cholecystokinin (CCK) in these leptin receptor-deficient animals suggests a critical role for leptin signaling in the response to endogenous signals that promote meal termination. To determine if the hypothalamic arcuate nucleus (ARC) (a key forebrain site of leptin action) mediates this leptin effect, we used adenoviral gene therapy to express either functional leptin receptors or a reporter gene in the area of the ARC of fa(k)/fa(k) rats. Restoration of leptin signaling to this brain area normalized the effect of CCK on the activation of neurons in the nucleus of the solitary tract and area postrema, key hindbrain areas for processing satiety-related inputs. This intervention also reduced meal size and enhanced CCK-induced satiety in fa(k)/fa(k) rats. These findings demonstrate that forebrain signaling by leptin, a long-term regulator of body adiposity, limits food intake on a meal-to-meal basis by regulating the hindbrain response to short-acting satiety signals.
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21 MeSH Terms
Vascular endothelial growth factor is increased in devascularized rat islets of Langerhans in vitro.
Gorden DL, Mandriota SJ, Montesano R, Orci L, Pepper MS
(1997) Transplantation 63: 436-43
MeSH Terms: Animals, Cell Separation, Endothelial Growth Factors, Hypoxia, Insulinoma, Islets of Langerhans, Lymphokines, Neovascularization, Physiologic, Pancreatic Neoplasms, Rats, Rats, Inbred Strains, Tumor Cells, Cultured, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factors
Show Abstract · Added March 5, 2014
Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen with potent angiogenic and vascular permeability-inducing properties, both of which may be important for the function of islets of Langerhans. In this study, we have examined the expression of VEGF and its tyrosine kinase receptors (flt and flk-1) in isolated rat islets of Langerhans in vitro. When analyzed by in situ hybridization, islet tissue showed a significant 4.6-fold increase in VEGF mRNA expression over time in culture from 0 to 7 days. Islet tissue exposed to hypoxic/anoxic conditions for a period of 8 hr showed a 3.7-fold increase in VEGF mRNA when analyzed by Northern blot hybridization. Reverse transcriptase-polymerase chain reaction revealed the presence of both flt and flk-1 in freshly isolated islets, and two VEGF isoforms, namely VEGF120 and VEGF164. Three rodent beta-cell lines derived from insulinomas (RINm5F-2A, INS-1, and MIN6) were also found to express VEGF by Northern blot hybridization. However, neither hypoxia/anoxia nor low (0.3 g/L)- or high (3.0 g/L)-glucose culture conditions modulated their expression of VEGF. VEGF derived from RINm5F-2A cells was bioactive in a three-dimensional in vitro model of angiogenesis, which assays for endothelial cell invasion and capillary morphogenesis. These findings demonstrate, first, that devascularization increases VEGF expression in isolated islet tissue, and they point to VEGF as a potentially important endogenous angiogenic stimulus for subsequent revascularization in vivo. Second, our observations raise the possibility that survival of transplanted islets may be improved by increasing VEGF expression before transplantation.
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14 MeSH Terms
Mechanisms of tolerance to rat heart allografts using posttransplant TLI. Changes in cytokine expression.
Zeng D, Ready A, Huie P, Hayamizu K, Holm B, Yin D, Sibley RK, Strober S
(1996) Transplantation 62: 510-7
MeSH Terms: Animals, Antilymphocyte Serum, Base Sequence, Cytokines, DNA Primers, Gene Expression, Graft Survival, Heart Transplantation, Immunization, Passive, Immunosuppression, Lymphatic Irradiation, Lymphocyte Activation, Lymphocyte Culture Test, Mixed, Male, Molecular Sequence Data, RNA, Messenger, Rabbits, Rats, Rats, Inbred Lew, Rats, Inbred Strains, Spleen, Whole-Body Irradiation
Show Abstract · Added December 10, 2013
Lewis rats were rendered tolerant to ACI heart allografts using a regimen of posttransplant total lymphoid irradiation (TLI), rabbit antithymocyte or antilymphocyte globulin (RATG or RALG), and a single donor blood transfusion. All three treatment modalities were required to induce tolerance. The mechanism of the maintenance of tolerance was investigated by comparing the secretion of cytokines in the MLR, and the expression of cytokine mRNA in the allografts of tolerant and nontolerant Lewis rats. Although, the 3H-thymidine incorporation and secretion of IL-2 was frequently comparable in the MLR from tolerant and nontolerant rats, the secretion of IFN-gamma was markedly reduced in the tolerant rats. This was reflected in a markedly reduced frequency of cells expressing IFN-gamma mRNA in the allografts of tolerant as compared with nontolerant hosts. The frequency of cells expressing IL-2 and IL-10 mRNA was also reduced, but no significant difference was observed for cells with IL-4 mRNA. Spleen cells from nontolerant rats rapidly rejected ACI allografts in irradiated adoptive hosts, but spleen cells from tolerant rats did not. Evaluation of the cytokine mRNA expression at early and late time points in the allografts of adoptive hosts showed a pattern similar to that of the primary hosts. Thus, the tolerant state was associated with a maintenance or elevation of IL-4 expression and a marked reduction of IFN-gamma expression. Previous reports have shown that TLI alone induced this shift in the early recovery phase after irradiation.
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22 MeSH Terms
The origin of the autoimmune disease-resistant LER rat: an outcross between the buffalo and autoimmune disease-prone Lewis inbred rat strains.
Goldmuntz EA, Wilder RL, Goldfarb Y, Cash JM, Zha H, Crofford LJ, Mathern P, Hansen CT, Remmers EF
(1993) J Neuroimmunol 44: 215-9
MeSH Terms: Alleles, Animals, Autoimmune Diseases, Base Sequence, Crosses, Genetic, Immunity, Innate, Molecular Sequence Data, Oligodeoxyribonucleotides, Polymorphism, Genetic, Rats, Rats, Inbred ACI, Rats, Inbred BUF, Rats, Inbred F344, Rats, Inbred Lew, Rats, Inbred Strains, Repetitive Sequences, Nucleic Acid, Species Specificity
Show Abstract · Added September 18, 2013
The Lewis (LEW) rat strain is highly susceptible to a large number of experimentally induced inflammatory and autoimmune diseases. The Lewis resistant (LER) rat strain, which reportedly arose as a spontaneous mutation in a closed colony of LEW rats, is resistant to many of these disorders. The mechanism of resistance is not yet clear. We report the analysis of 19 simple dinucleotide repeat polymorphisms in 13 rat strains including the LEW/N and LER/N rat strains. The LEW/N and LER/N alleles were the same in only 42% of cases. For all of the other polymorphisms, the LER/N and Buffalo (BUF/N) rat strain alleles were identical. These data provide evidence that the LER strain did not arise as a spontaneous mutation in the LEW strain but is the result of an outcross between the LEW and BUF rat strains. The LER rat strain is now a recombinant inbred rat strain. This information should facilitate the genetic analysis of the loci responsible for resistance to experimental autoimmune disease in the LER rat.
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17 MeSH Terms
Angiotensin converting enzyme inhibitor modulates glomerular function and structure by distinct mechanisms.
Tanaka R, Kon V, Yoshioka T, Ichikawa I, Fogo A
(1994) Kidney Int 45: 537-43
MeSH Terms: Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Animals, Bradykinin, Glomerulosclerosis, Focal Segmental, Kidney, Kidney Glomerulus, Male, Proteinuria, Punctures, Puromycin Aminonucleoside, Rats, Rats, Inbred Strains
Show Abstract · Added January 20, 2012
Rats with puromycin aminonucleoside (PAN) nephrosis were given either angiotensin I converting enzyme inhibitor (ACEI), angiotensin II type 1 receptor antagonist (Ang IIRA), or no treatment for four weeks and were then monitored for an additional 12 weeks. In untreated PAN rats, proteinuria reached a maximum at two weeks (271 +/- 38 mg/day). Proteinuria in this early phase was markedly attenuated by ACEI (96 +/- 35 mg/day, P < 0.01), but unaffected by Ang IIRA (306 +/- 34 mg/day). Acute administration of a bradykinin antagonist substantially dampened the antiproteinuric effect of ACEI in PAN rats, resulting in an average increase in proteinuria of 41 +/- 14% in ACEI-treated rats (P < 0.05, ACEI vs. ACEI+bradykinin antagonist). Acute phase therapy for four weeks with ACEI or Ang IIRA did not attenuate subsequent glomerulosclerosis. Separate groups of PAN rats with similar degree of glomerulosclerosis, assessed at 16 weeks after PAN by renal biopsy, were then treated as follows: ACEI [50 mg/liter drinking water (DW), or 200 mg/liter DW], Ang IIRA (20 mg/liter DW, or 80 mg/liter DW) or no treatment, starting after renal biopsy. Whereas glomerulosclerosis increased from biopsy to autopsy at 28 weeks with emergence of low grade proteinuria in untreated PAN rats, proteinuria was absent and glomerulosclerosis was ameliorated or reversed in ACEI and Ang IIRA groups. The results indicate that the early phase proteinuria of PAN nephropathy is independent of Ang II, and that the antiproteinuric effect of ACEI is, at least in part, channeled through activation of bradykinin, whereas the subsequent progression of glomerulosclerosis is caused by a mechanism involving endogenous Ang II actions.(ABSTRACT TRUNCATED AT 250 WORDS)
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13 MeSH Terms