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  1. Article ; Online: Benzannulation and Hydrocarboxylation Methods for the Synthesis of a Neopentylene-Fused Analogue of Ibuprofen.

    Martin, A C / Rogers, Jessica A / Batsomboon, Paratchata / Morrison, Alec E / Ramsubhag, Ron R / Popp, Brian V / Dudley, Gregory B

    ACS omega

    2021  Volume 6, Issue 44, Page(s) 30108–30114

    Abstract: Neopentylene ring fusions (ring-fused 4,4-dimethylcyclopentane polycycles) are found in many natural products, but they are largely absent from synthetic compound libraries and focused medicinal chemistry research. Here is reported a synthetic approach ... ...

    Abstract Neopentylene ring fusions (ring-fused 4,4-dimethylcyclopentane polycycles) are found in many natural products, but they are largely absent from synthetic compound libraries and focused medicinal chemistry research. Here is reported a synthetic approach to one of the few non-natural product-based target compounds from medicinal chemistry that includes a neopentylene ring fusion: an analogue of ibuprofen referred to herein as "neoprofen". The approach features ring-opening fragmentation reactions of dimedone derivatives coupled with transition metal-catalyzed benzannulation and hydrocarboxylation methods.
    Language English
    Publishing date 2021-10-26
    Publishing country United States
    Document type Journal Article
    ISSN 2470-1343
    ISSN (online) 2470-1343
    DOI 10.1021/acsomega.1c04943
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Effects of insulin and leptin in the ventral tegmental area and arcuate hypothalamic nucleus on food intake and brain reward function in female rats.

    Bruijnzeel, Adrie W / Corrie, Lu W / Rogers, Jessica A / Yamada, Hidetaka

    Behavioural brain research

    2011  Volume 219, Issue 2, Page(s) 254–264

    Abstract: There is evidence for a role of insulin and leptin in food intake, but the effects of these adiposity signals on the brain reward system are not well understood. Furthermore, the effects of insulin and leptin on food intake in females are ... ...

    Abstract There is evidence for a role of insulin and leptin in food intake, but the effects of these adiposity signals on the brain reward system are not well understood. Furthermore, the effects of insulin and leptin on food intake in females are underinvestigated. These studies investigated the role of insulin and leptin in the ventral tegmental area (VTA) and the arcuate hypothalamic nucleus (Arc) on food intake and brain reward function in female rats. The intracranial self-stimulation procedure was used to assess the effects of insulin and leptin on the reward system. Elevations in brain reward thresholds are indicative of a decrease in brain reward function. The bilateral administration of leptin into the VTA (15-500 ng/side) or Arc (15-150 ng/side) decreased food intake for 72 h. The infusion of leptin into the VTA or Arc resulted in weight loss during the first 48 (VTA) or 24 h (Arc) after the infusions. The administration of insulin (0.005-5 mU/side) into the VTA or Arc decreased food intake for 24 h but did not affect body weights. The bilateral administration of low, but not high, doses of leptin (15 ng/side) or insulin (0.005 mU/side) into the VTA elevated brain reward thresholds. Neither insulin nor leptin in the Arc affected brain reward thresholds. These studies suggest that a small increase in leptin or insulin levels in the VTA leads to a decrease in brain reward function. A relatively large increase in insulin or leptin levels in the VTA or Arc decreases food intake.
    MeSH term(s) Animals ; Arcuate Nucleus of Hypothalamus/physiology ; Brain/physiology ; Conditioning, Operant/drug effects ; Eating/drug effects ; Electrodes, Implanted ; Female ; Hypoglycemic Agents/administration & dosage ; Hypoglycemic Agents/pharmacology ; Insulin/administration & dosage ; Insulin/pharmacology ; Leptin/administration & dosage ; Leptin/pharmacology ; Microinjections ; Rats ; Rats, Sprague-Dawley ; Reward ; Self Stimulation ; Ventral Tegmental Area/physiology
    Chemical Substances Hypoglycemic Agents ; Insulin ; Leptin
    Language English
    Publishing date 2011-01-19
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 449927-x
    ISSN 1872-7549 ; 0166-4328
    ISSN (online) 1872-7549
    ISSN 0166-4328
    DOI 10.1016/j.bbr.2011.01.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Blockade of CRF1 receptors in the central nucleus of the amygdala attenuates the dysphoria associated with nicotine withdrawal in rats.

    Bruijnzeel, Adrie W / Ford, Jenna / Rogers, Jessica A / Scheick, Stacey / Ji, Yue / Bishnoi, Mahendra / Alexander, Jon C

    Pharmacology, biochemistry, and behavior

    2011  Volume 101, Issue 1, Page(s) 62–68

    Abstract: The majority of smokers relapse during the acute withdrawal phase when withdrawal symptoms are most severe. The goal of the present studies was to investigate the role of corticotropin-releasing factor (CRF) and noradrenergic transmission in the central ... ...

    Abstract The majority of smokers relapse during the acute withdrawal phase when withdrawal symptoms are most severe. The goal of the present studies was to investigate the role of corticotropin-releasing factor (CRF) and noradrenergic transmission in the central nucleus of the amygdala (CeA) in the dysphoria associated with smoking cessation. It was investigated if blockade of CRF1 receptors, blockade of α1-adrenergic receptors, or stimulation of α2-adrenergic receptors in the CeA diminishes the deficit in brain reward function associated with nicotine withdrawal in rats. Nicotine dependence was induced by implanting minipumps that delivered a nicotine solution. Withdrawal was precipitated with the nicotinic acetylcholine receptor antagonist mecamylamine. A discrete-trial intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Elevations in brain reward thresholds are indicative of a deficit in brain reward function. In all the experiments, mecamylamine elevated the brain reward thresholds of the rats chronically treated with nicotine and did not affect the brain reward thresholds of the saline-treated control rats. Intra-CeA administration of the CRF1 receptor antagonist R278995/CRA0450 completely prevented the mecamylamine-induced elevations in brain reward thresholds in the nicotine-treated rats and did not affect the brain reward thresholds of the saline-treated control rats. R278995/CRA0450 has also been shown to block sigma-1 receptors but there is no evidence that this could affect negative mood states. Intra-CeA administration of the α1-adrenergic receptor antagonist prazosin or the α2-adrenergic receptor agonist clonidine did not affect the brain reward thresholds of the nicotine or saline-treated rats. These studies suggest that CRF1 receptor antagonists may diminish the dysphoria associated with smoking cessation by blocking CRF1 receptors in the CeA.
    MeSH term(s) Adrenergic alpha-1 Receptor Antagonists/pharmacology ; Adrenergic alpha-2 Receptor Antagonists/pharmacology ; Amygdala/drug effects ; Animals ; Benzenesulfonates/pharmacology ; Clonidine/pharmacology ; Electrodes, Implanted ; Male ; Mecamylamine/pharmacology ; Nicotine/pharmacology ; Nicotinic Agonists/pharmacology ; Nicotinic Antagonists/pharmacology ; Prazosin/pharmacology ; Quinolines/pharmacology ; Rats ; Rats, Wistar ; Receptors, Corticotropin-Releasing Hormone/antagonists & inhibitors ; Reward ; Smoking Cessation/psychology ; Substance Withdrawal Syndrome/drug therapy ; Substance Withdrawal Syndrome/psychology ; Tobacco Use Disorder/psychology
    Chemical Substances 1-(8-(2,4-dichlorophenyl)-2-methylquinolin-4-yl)-1,2,3,6-tetrahydropyridine-4-carboxamide benzenesulfonate ; Adrenergic alpha-1 Receptor Antagonists ; Adrenergic alpha-2 Receptor Antagonists ; Benzenesulfonates ; Nicotinic Agonists ; Nicotinic Antagonists ; Quinolines ; Receptors, Corticotropin-Releasing Hormone ; CRF receptor type 1 (5CLY6W2H1M) ; Mecamylamine (6EE945D3OK) ; Nicotine (6M3C89ZY6R) ; Clonidine (MN3L5RMN02) ; Prazosin (XM03YJ541D)
    Language English
    Publishing date 2011-12-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 191042-5
    ISSN 1873-5177 ; 0091-3057
    ISSN (online) 1873-5177
    ISSN 0091-3057
    DOI 10.1016/j.pbb.2011.12.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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