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  • 1
    ISSN: 1573-6903
    Keywords: Neuropeptide-Y ; NPY ; feeding ; norepinephrine ; dopamine ; serotonin ; food intake ; HPLCCD ; satiety ; hypothalamus ; push-pull perfusion ; hunger ; paraventricular nucleus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the unrestrained rat, the hyperphagic-like ingestion of food evoked by the sustained elevation of neuropeptide-Y (NPY) in the hypothalamus was correlated with the release and turnover of monoaminergic transmitters in this structure. A single guide tube was implanted stereotaxically in the perifornical region of the hypothalamus for localized push-pull perfusion of an artificial CSF vehicle or NPY1–36 in a concentration of 10, 50, or 100 ng/1.0 μl. After the rat was fully satiated, a site reactive to NPY was perfused repeatedly at a rate of 20 μl/min for 6.0 min with an interval of 6.0–12 min elapsing between each perfusion. Samples of perfusate were analyzed by HPLC with coulometric detection for DA, HVA, DOPAC, NE, MHPG, 5-HT, and 5-HIAA. Although control perfusions were without effect on feeding or monoamine activity, NPY evoked mean cumulative intakes of food of 14±2.4, 25.6±3.0 and 26.5±3.2 g in response to 10, 50, or 100 ng/μl concentrations of NPY, respectively, over the 4.0–5.0 hr test interval. HPLC analyses showed that during feeding the release of both NE and DA was enhanced significantly. The turnover of both catecholamines likewise increased significantly as reflected by the elevated levels of MHPG, DOPAC and HVA. However, neither the basal efflux of 5-HT nor its turnover, as reflected by the output of 5-HIAA, was affected during feeding induced by NPY perfused in the hypothalamus. These results suggest that a sustained elevation of NPY in the hypothalamus causes a perturbation in the basal activity of NE and DA which are both implicated in the neuronal mechanism regulating normal eating behavior. Thus, these catecholamine neurotransmitters are envisaged to comprise an intermediary step in the functional role played by NPY in the hypothalamus in integrating the control of energy metabolism and caloric intake.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-6903
    Keywords: Fever ; macrophage inflammatory protein-1 (MIP-1) ; MIP-1α ; MIP-1β ; body temperature ; pyrogen ; endotoxin ; feeding ; hypothalamus micro-injection ; thermoregulation ; water intake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes in body temperature (Tb) and feeding were characterized in unrestrained rats following the micro-injection into the anterior hypothalamic preoptic area (AH/POA) of macrophage inflammatory protein-1 (MIP-1), MIP-1α or MIP-1β. After the rats recovered from the stereotaxic implantation of a single guide tube placed in the AH/POA, either one of the MIP-1 compounds or control CSF was micro-injected in a volume of 1.0 μl into this area. Changes in body temperature (Tb) and food and water intakes were monitored throughout each experiment. When micro-injected into the AH/POA in a dose of 28 or 280 pg, doublet MIP-1 and MIP-1β evoked a monophasic fever which increased above baseline to a mean maximum of 2.17±0.14°C and 2.1±0.24°C, respectively. MIP-1α micro-injected similarly evoked a biphasic fever, with the Tb declining transiently at the 30 min point ≥0.4°C lower than the congruent rises in Tb evoked by doublet MIP-1 or MIP-1β. The secondary rise in Tb induced by MIP-1α had a latency of 1.5–2.0 hrs and reached a maximum of 1.56±0.16°C. Although all three cytokines significantly attentuated the rats' mean intake of food during the 24 hr interval after their micro-injection into the AH/POA, doublet MIP-1 exerted the most potent anorexic effect in comparison to that of the saline control rats. However, neither body weight nor intake of water was altered significantly by the three cytokines. These results demonstrate a functional distinction between the febrile actions of MIP-1α and MIP-1β on cells of the AH/POA. It is envisaged that MIP-1β underlies the initial phase of a pyrogen-induced fever, whereas MIP-1α could mediate the secondary phase of a biphasic fever. Clearly, the localized elevation of either MIP-1α or MIP-1β in the AH/POA perturbs the neuronal mechanism underlying the “set-point” for body temperature. Thus, both MIP-1α and MIP-1β could play a functional role in the pathological events occurring in neurons of the AH/POA in response to an endotoxin or other pyrogen challenge.
    Type of Medium: Electronic Resource
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