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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 126 (1996), S. 110-114 
    ISSN: 1432-2072
    Keywords: Motivation ; Naloxone ; Opioids ; Sucrose ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The opioid system plays an important role in feeding. In general, opioid agonists typically increase feeding and opioid antagonists decrease feeding in nonfood restricted animals. In food restricted animals the effects of these drugs are substantially reduced. Opioid antagonists have shown a marked effectiveness at reducing consumption of sweet foods. Explanations for this robust effect have typically focused on drug induced changes in taste, taste perception, or palatability. The current study relates the effects of the opioid antagonist naloxone on motivation to obtain different sucrose concentrations to the drug's effects on unrestricted sucrose solution consumption. Changes in motivation to respond were assessed under a progressive ratio reinforcement schedule (PR) which required increased response cost for each successive unit of sucrose solution. Motivation, as measured by the PR, increased as sucrose concentration increased and naloxone produced a dose-dependent decrease in motivation to respond for a given sucrose concentration. Thus, the effectiveness of naloxone was indirectly related to strength of the sucrose concentration. Under unrestricted access to sucrose solutions, naloxone reduced consumption greatest under the higher concentrations. The data suggest at least part of naloxone's effects on sweet tasting food may be mediated through endogenous opioid reward systems that are reflected in measures of motivation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Neuropeptide Y ; Insulin ; 2-Deoxyglucose ; Food deprivation ; Motivation ; Reinforcer efficacy ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The current study demonstrates the ability of neuropeptide Y (NPY) to increase break points under a progressive ratio 1 (PR1) reinforcement schedule. An initial response resulted in delivery of a food reinforcer (45 mg pellet) under the PR1, and an additional response was required foreach successive reinforcer. The break point, the number of responses emitted to obtain the last reinforcer, is considered a measure of reinforcing efficacy or motivational strength of the food reinforcer. NPY (0.3–10 µg) significantly increased break point to levels comparable to those produced by 36–48 h of food deprivation. Although insulin (3–8 U/kg) and 2-deoxyglucose (150–250 mg/kg) also increased food intake, neither increased break points to levels produced by NPY or food deprivation. These data suggest that NPY may change the value of food in ways that cannot be accounted for by changes in insulin, glucose levels or intracellular glucoprivation. These results emphasize that simply measuring the amount of freely available food eaten is not a fully adequate measure of the strength of the feeding behavior.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1211
    Keywords: Key words Transplantation ; Histocompatibility ; Embryonal carcinoma ; Teratocarcinoma ; Mouse Chromosome 8
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  Cytotoxic T lymphocytes play a predominant role in allograft rejection. They mediate this process through recognition of foreign major histocompatibility complex (MHC) class I surface molecules encoded at the H2 locus. Embryonal carcinoma cells, the undifferentiated, neoplastic derivatives of primordial germ cells, typically lack detectable MHC class I gene expression. Despite this, embryonal carcinoma cells are subject to allograft rejection in several different mouse strains. In many instances, the H2 locus appears to be genetically linked to resistance. However, rejection of allografts of the F9 embryonal carcinoma cell line, a nullipotent cell line derived from the 129 mouse strain, does not appear to be H2-linked. Resistance to F9 tumor formation in the C57BL/6 mouse strain has been attributed to a single, unidentified locus termed Gt(B6). To genetically map the Gt(B6) locus, a total of 463 (C57BL/6×129)F2 mice were challenged with F9 cells, and 78 tumor-resistant mice were identified. Markers encompassing two candidate regions, the H2 locus on Chromosome (Chr) 17 and a second candidate locus on Chr 2, showed no indication of linkage to the resistance phenotype. Instead, results of a genome wide scan implicated mouse Chr 8, and evidence is presented demonstrating that the Gt(B6) locus maps to a region of less than 10 cM on the medial portion of Chr 8.
    Type of Medium: Electronic Resource
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