Disease relevance of A

• In this study, we show that thyroid hormone enhances and accelerates remyelination in an experimental model of chronic demyelination, i.e., experimental allergic encephalomyelitis in congenic female Dark Agouti rats immunized with complete guinea pig spinal cord [1].
• Because reduced glutathione and glutathione-related enzymes are known to play important roles in cellular resistance to transition metal toxicity, we determined the levels of reduced glutathione and glutathione-related enzymes in seven different tissues of Long-Evans Cinnamon and control Long-Evans Agouti rats [2].
• Chronic central infusion of ghrelin increases hypothalamic neuropeptide Y and Agouti-related protein mRNA levels and body weight in rats [3].
• This study was performed to elucidate pathophysiological events before and during the course of collagen-induced arthritis in Dark Agouti rats, a model for rheumatoid arthritis [4].
• These data, together with the increased expression of neuropeptide Y and agouti-related protein in specific neurons in the ARC, might indicate the existence of regulated programming in this nucleus and may provide a new aetiopathogenic concept in susceptibility to obesity [5].

Psychiatry related information on A

• Central administration of ghrelin and agouti-related protein (83-132) increases food intake and decreases spontaneous locomotor activity in rats [6].
• Dextrorotatory opioids induce stereotyped behavior in Sprague-Dawley and Dark Agouti rats [7].
• Functional analysis of the Ala67Thr polymorphism in agouti related protein associated with anorexia nervosa and leanness [8].
• Differential regulation of agouti-related protein and neuropeptide Y in hypothalamic neurons following a stressful event [9].
• Glucose injection reduces neuropeptide Y and agouti-related protein expression in the arcuate nucleus: a possible physiological role in eating behavior [10].

High impact information on A

• However, in Dark Agouti rats, the pathogenicity of MOG-specific T cells resembles the one of MBP-specific T cells in the Lewis rat [11].
• Activities and mRNA levels of N-acetylglucosaminyltransferase III and V (GnT-III and GnT-V, respectively) were determined during hepatocarcinogenesis in this rat using a LEA (Long-Evans with an agouti color) rat as a control [12].
• When TIQ 4-hydroxylase activity was compared in Wistar (an animal model of extensive debrisoquine metabolizers) and Dark Agouti (an animal model of poor debrisoquine metabolizers) rats, significant strain (Wistar greater than Dark Agouti) and sex (male greater than female) differences were observed [13].
• After induction of CIA in Dark Agouti rats, test animals were treated with or without Fc-OPG (3 mg/kg/day) subcutaneously for 5 days, beginning at the onset of disease [14].
• Effects of chronic central nervous system administration of agouti-related protein in pair-fed animals [15].

Chemical compound and disease context of A

• Ribavirin reduces clinical signs and pathological changes of experimental autoimmune encephalomyelitis in Dark Agouti rats [16].
• We observed no intrinsic neurotoxicity with glutamate and no interference with the cytotoxic efficacy of vincristine against a transplantable rat mammary adenocarcinoma grown s.c. in Dark Agouti rats [17].
• Hypo- and hyperthyroidism were induced in adult male rats, and the mRNA content of cocaine- and amphetamine-regulated transcript and agouti-related peptide was determined using in situ hybridization [18].
• Function of neuropeptide Y and agouti-related protein at weaning: relation to corticosterone, dietary carbohydrate and body weight [19].
• MDMA increased locomotor activity in Sprague-Dawley but not in Dark Agouti rats [20].

Biological context of A

• Ghrelin (500 nM), agouti-related peptide (1 microM); cocaine and amphetamine-related transcript (500 nM) and leptin (500 nM and 1 microM) did not modulate the firing rate and membrane potential of VTA neurons [21].
• Since present evidence suggests that poor debrisoquine hydroxylators are at risk, we designed an experimental study comparing its neurotoxic effects in dark Agouti (DA) rats, with poor hydroxylation of debrisoquine with that in Sprague Dawley (SD) rats, which are vigorous hydroxylators [22].
• The O-desmethyl and 5-hydroxy metabolites are deficient in poor metabolizers of debrisoquine and sparteine and the Dark Agouti rat model of this human phenotype [23].
• Here, intraperitoneal infusion of a Lewis-derived rat MHC class I molecule, RT1.A(l)-Fc, in Dark Agouti (RT1.A(a)) recipient rats prolonged cardiac graft survival, which led to permanent engraftment [24].
• To identify additional hypothalamic systems that might be important in mediating the increase in food intake and alterations in energy homeostasis during lactation, the present studies examined the expression of agouti-related protein (AGRP), a recently described homologue of the skin agouti protein [25].

Anatomical context of A

• In the Dark Agouti rat, active immunization with native BTN triggers an inflammatory response in the CNS characterized by the formation of scattered meningeal and perivascular infiltrates of T cells and macrophages [26].
• Moreover, this obese model showed an increase in the mRNA expression of cocaine- and amphetamine-regulated transcript, neuropeptide Y and agouti-related protein in the hypothalamic arcuate nucleus (ARC) [5].
• Agouti-related protein (Agrp) is present in rat and human hypothalamus and is structurally related to agouti protein [27].
• Detailed double labeling studies in the paraventricular hypothalamic nucleus demonstrated that GALP-containing fibers converged in a more rostral direction than did agouti-related protein-containing fibers [28].
• In the donor-recipient strain combination Lewis (RT1l) to Dark Agouti (RT1a), indefinite renal allograft survival (MST greater than 100 days) was induced by pretreating recipient animals i.v. with 10(6) to 10(8) viable spleen lymphocytes, seven days before transplantation [29].

Associations of A with chemical compounds

• In the present study, depletion of peripheral (hepatic) glutathione by 43% with dl-buthionine-(S,R)-sulfoximine (an inhibitor of glutathione synthesis) did not attenuate MDMA-induced neurotoxicity as indicated by the 34% loss of [(3) H]paroxetine binding to the serotonin uptake sites in Dark Agouti rats treated with the inhibitor [30].
• These findings indicate that glutathione depletion does not offer specific protection against MDMA-induced serotonin neurotoxicity in Dark Agouti rats [30].
• In contrast, among females only the d-methamphetamine-treated Dark Agouti rats showed deficits in spatial navigation [31].
• Diurnal rhythm of agouti-related protein and its relation to corticosterone and food intake [32].
• Thus, the low bunitrolol 4-hydroxylation in Dark Agouti rats was caused by the low level of CYP2D2 expression in this rat strain [33].

Regulatory relationships of A

• Neuropeptide Y, ghrelin, and agouti-related protein-induced food intake was counteracted by coadministration of NMS [34].
• It remains to be determined if local sources of neuropeptide Y-expressing cells within the dorsomedial hypothalamic nucleus and paraventricular nucleus also contribute to the neuropeptide Y-immunoreactive fibers within these regions prior to the development of arcuate-neuropeptide Y/agouti-related protein projections [35].
• Three of the four HCCs had c-myc expression levels approximately 30-fold higher than that in the liver of control Long-Evans rats with an agouti coat color (LEA), a sibling line of LEC rats, while the remaining HCC had an expression level sevenfold higher than that of control [36].
• Agouti-related peptide prevents steroid-induced luteinizing hormone and prolactin surges in female rats [37].

Other interactions of A

• Melanocortin-4 receptor (MC4-R) density is thought to be regulated by synaptic availability of endogenous agonist, alpha-melanocyte-stimulating hormone (alpha-MSH), and also by agouti-related protein (AGRP), which acts as a competitive antagonist [38].
• In this study, we examined whether ghrelin could stimulate GH secretion and feeding in chronic GHRH, neuropeptide Y, and agouti-related protein deficient rats that were neonatally treated with monosodium glutamate (MSG), which destroys the neurons in the hypothalamic arcuate nucleus (ARC) [39].
• Agouti-related peptide, neuropeptide Y, and somatostatin-producing neurons are targets for ghrelin actions in the rat hypothalamus [40].
• Increased Hsp27-immunoreactivity exclusively in the examined cortical areas reveals that Hsp27 is a sensitive marker of astroglial response to the effects of MDMA in these regions of Dark Agouti rat brain and suggests differential responses in astroglial Hsp27-expression between distinct brain areas [41].
• Melanocortin restraint is exerted through alpha-melanocortin-stimulating hormone derived from proopiomelanocortin (POMC) and is antagonized by agouti-related peptide produced in neurons located in the arcuate nucleus (ARC) [42].

Analytical, diagnostic and therapeutic context of A

• OBJECTIVE: To investigate the role of nitric oxide (NO) production and NO synthase (NOS) induction during adjuvant-induced arthritis (AIA) and collagen-induced arthritis (CIA) in Dark Agouti rats [43].
• METHODS: Heterotopic heart transplantations were performed from Dark Agouti to Wistar Furth rats [44].
• In this study, we generated Lewis T cell lines specific for Dark Agouti rat alloantigens and tested the potential of allospecific T lymphocytes as carriers of genes encoding therapeutic proteins in transplantation gene therapy [45].
• PVG recipients of Dark Agouti kidney allografts were treated with the oligos [46].
• METHODS: Orthotopic liver transplantation was performed in the PVG donor to Dark Agouti recipient rat strain combination, which accepts the graft (tolerance; TOL), and in the PVG-to-Lewis combination, which rejects the graft in 9 to 16 days (rejection; REJ) [47].

References