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  • American Physiological Society  (6)
  • Kotz, Catherine M.  (6)
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  • American Physiological Society  (6)
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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 283, No. 1 ( 2002-07-01), p. R161-R167
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 283, No. 1 ( 2002-07-01), p. R161-R167
    Abstract: It has been suggested that an opioidergic feeding pathway exists between the nucleus of the solitary tract (NTS) and the central nucleus of the amygdala. We studied the following three groups of rats: 1) artificial cerebrospinal fluid (CSF) infused in the NTS, 2) naltrexone (100 μg/day) infused for 13 days in the NTS, and 3) artificial CSF infused in the NTS of rats pair fed to the naltrexone-infused group. Naltrexone administration resulted in a decrease in body weight and food intake. Also, naltrexone infusion increased dynorphin, but not enkephalin, gene expression in the amygdala, independent of the naltrexone-induced reduction in food intake. Gene expression of neuropeptide Y in the arcuate nucleus and neuropeptide Y peptide levels in the paraventricular nucleus did not change because of naltrexone infusion. However, naltrexone induced an increase in serum leptin compared with pair-fed controls. Thus chronic administration of naltrexone in the NTS increased dynorphin gene expression in the amygdala, further supporting an opioidergic feeding pathway between these two brain sites.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 280, No. 2 ( 2001-02-01), p. R473-R480
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 280, No. 2 ( 2001-02-01), p. R473-R480
    Abstract: Ventricular administration of urocortin (UCN) inhibits feeding, but specific site(s) of UCN action are unknown. In the current studies we examined the effect of UCN in the hypothalamic paraventricular nucleus (PVN) on feeding. We tested UCN administered into the PVN in several paradigms: deprivation-induced, nocturnal, and neuropeptide Y (NPY)-induced feeding. We compared the effect of equimolar doses of UCN and corticotrophin releasing hormone (CRH) on NPY-induced and nocturnal feeding, determined whether UCN in the PVN produced a conditioned taste aversion (CTA) and induced changes in c-Fos immunoreactivity (c-Fos-ir) after UCN and NPY administration in the PVN. UCN in the PVN significantly decreased NPY and nocturnal and deprivation-induced feeding at doses of 1, 10, and 100 pmol, respectively. UCN anorectic effects lasted longer than those attributed to CRH. Ten and thirty picomoles UCN did not induce a CTA, whereas 100 pmol UCN produced a CTA. UCN (100 pmol) in the PVN neither increased c-Fos-ir in any brain region assayed nor altered c-Fos-ir patterns resulting from PVN NPY administration. These data suggest the hypothalamic PVN as a site of UCN action.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 275, No. 2 ( 1998-08-01), p. R478-R484
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 275, No. 2 ( 1998-08-01), p. R478-R484
    Abstract: Inhibition of a signal that produces positive energy balance involving neuropeptide Y (NPY) projection from arcuate nucleus (Arc; site of NPY synthesis) to paraventricular nucleus (PVN; site of NPY release) is one potential mechanism of leptin action. NPY in the PVN increases feeding and decreases uncoupling protein (UCP) activity in brown fat, whereas leptin decreases NPY biosynthesis in the Arc, which presumably decreases PVN NPY. It is hypothesized that decreased NPY activity is necessary for the satiety and thermogenic effects of leptin. To test this, we first determined the effect of leptin on feeding in two paradigms: satiated rats and food-deprived rats. Leptin was effective in decreasing feeding in the satiated rats but ineffective in the food-deprived rats. Next, we determined that leptin decreases NPY and increases UCP gene expression. Finally, we injected leptin intracerebroventricularly before specific PVN NPY microinjection. We found that repletion of NPY in PVN by specific NPY microinjection reverses the feeding-inhibitory and thermogenic effects of centrally administered leptin, the first functional evidence indicating that leptin acts on the Arc-PVN feeding-regulatory pathway.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 282, No. 2 ( 2002-02-01), p. R546-R551
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 282, No. 2 ( 2002-02-01), p. R546-R551
    Abstract: The hypothalamic paraventricular nucleus (PVN) plays a primary role in energy homeostasis, and urocortin (UCN) decreases feeding after injection into the PVN. Peripheral uncoupling proteins (UCPs) may influence energy metabolism. The effect of UCN administered into the PVN on UCPs is unknown. We injected PVN-cannulated rats with either UCN (200 pmol) or artificial cerebrospinal fluid (aCSF) at 0800, 2000, and again at 0800. An aCSF-injected group with food intake restricted to the level of UCN-treated animals was included to control for decreased feeding in the UCN-treated rats. Two hours after the final set of injections, rats were killed, and white adipose tissue, brown adipose tissue, and biceps femoris and acromiotrapezius muscle tissues were taken for analysis of UCP-1, -2, and -3. Trunk blood was collected for measurement of plasma leptin. Relative to food-restricted control animals, UCN in the PVN significantly increased plasma leptin and UCP-1 mRNA in brown adipose tissue and decreased UCP-3 mRNA in acromiotrapezius muscle, suggesting a role for PVN UCN in the regulation of energy balance.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 278, No. 3 ( 2000-03-01), p. R712-R719
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 278, No. 3 ( 2000-03-01), p. R712-R719
    Abstract: —Opioids have long been known to have an important role in feeding behavior, particularly related to the rewarding aspects of food. Considerable behavioral evidence suggests that sucrose consumption induces endogenous opioid release, affecting feeding behavior as well as other opioid-mediated behaviors, such as analgesia, dependence, and withdrawal. In the present study, rats were given access to a 10% sucrose solution or water for 3 wk, then they were injected with 10 mg/kg naloxone or saline. Brains were subsequently analyzed for c-Fos immunoreactivity (c-Fos-IR) in limbic and autonomic regions in the forebrain and hindbrain. Main effects of sucrose consumption or naloxone injection were seen in several areas, but a significant interaction was seen only in the central nucleus of the amygdala and in the lateral division of the periaqueductal gray. In the central nucleus of the amygdala, naloxone administration to those rats drinking water significantly increased c-Fos-IR, an effect that was significantly enhanced by sucrose consumption, suggesting an upregulation of endogenous opioid tone in this area. The data from this study indicate that the central nucleus of the amygdala has a key role in the integration of gustatory, hedonic, and autonomic signals as they relate to sucrose consumption, if not to food intake regulation in general. Furthermore, the data from this study lend further support to the hypothesis that sucrose consumption induces the release of endogenous opioids.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 275, No. 2 ( 1998-08-01), p. R471-R477
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 275, No. 2 ( 1998-08-01), p. R471-R477
    Abstract: Neuropeptide Y (NPY) injected into the paraventricular nucleus (PVN) increases feeding and decreases brown adipose tissue (BAT) uncoupling protein (UCP) and lipoprotein lipase (LPL) mRNA. Previously we reported that the feeding and BAT effects induced by NPY in the PVN are blocked by 50 μg naltrexone (NTX) in the rostral nucleus of the solitary tract (rNTS). We sought to determine whether the effect of rNTS NTX on PVN NPY-induced alterations in energy metabolism occurred at lower doses of NTX. Male Sprague-Dawley rats were fitted with cannulas into two sites: PVN and rNTS. Feeding response, BAT UCP, and LPL mRNA were measured after injection of 0, 5, 10, and 25 μg NTX in the rNTS ± 1 μg NPY in the PVN. One-hour feeding response to PVN NPY was significantly and dose dependently decreased by 10 and 25 μg rNTS NTX (−23 and −31%, respectively). However, rNTS NTX did not block the PVN NPY-induced decrease in BAT UCP or LPL mRNA. BAT β-actin mRNA (as a measure of overall changes in gene expression) was unchanged among treatment groups. These results indicate a possible divergence in the PVN NPY feeding-stimulatory/BAT-inhibitory pathway, such that PVN NPY feeding effects may be routed through the rNTS whereas BAT effects may be due to alterations at another neural site.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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