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  • Wiley  (2)
  • Natural Sciences  (2)
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  • Wiley  (2)
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  • Natural Sciences  (2)
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  • 1
    Online Resource
    Online Resource
    Wiley ; 2003
    In:  Annals of the New York Academy of Sciences Vol. 1003, No. 1 ( 2003-11), p. 169-175
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1003, No. 1 ( 2003-11), p. 169-175
    Abstract: A bstract : A variety of data point to the possibility that neuroadaptations in glutamate transmission are produced by repeated exposure to cocaine that result in the expression of behaviors characteristic of addiction, such as craving and relapse. Using the reinstatement model of relapse in rats, glutamate release in the projection from the prefrontal cortex to the nucleus accumbens has been shown to underlie cocaine‐ and stress‐primed reinstatement. In this report, four adaptations produced by withdrawal from repeated cocaine are described that may regulate the release of glutamate underlying reinstatement of drug‐seeking resulted. (1) Neurons in the prefrontal cortex have increased levels of activator of G protein signaling 3 (AGS3) that causes reduced signaling through Gi coupled receptors, and normalization of AGS3 blocked cocaine‐primed reinstatement. (2) The activity of the cystine‐glutamate exchanger is reduced resulting in decreased extracellular glutamate in the nucleus accumbens, and normalization of exchanger activity prevented cocaine‐primed reinstatement. (3) Metobotropic glutamate receptor function is diminished after repeated cocaine administration that results in reduced regulation of glutamate release. (4) Homer1 protein is reduced in the nucleus accumbens, and Homer2 knockout mice show enhanced responsiveness to cocaine. Taken together, there appears to be both pre‐ and postsynaptic changes in glutamate transmission that dysregulates the glutamatergic projection from the prefrontal cortex to the nucleus accumbens. These adaptations are hypothesized to facilitate glutamate release in response to a cocaine injection or acute stress and lead to the reinstatement of drug‐seeking behavior.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2003
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2019
    In:  Annals of the New York Academy of Sciences Vol. 1452, No. 1 ( 2019-09), p. 18-33
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1452, No. 1 ( 2019-09), p. 18-33
    Abstract: Myasthenia gravis (MG) is an acquired autoimmune disease affecting the postsynaptic membrane of neuromuscular junctions and characterized by antibody‐mediated T cell dependence and complement involvement. Cholinesterase inhibitors (e.g., pyridostigmine bromide), glucocorticoids, and azathioprine are currently recommended as first‐line treatments for MG, though they have limitations, including potential toxicity and ineffectiveness in patients with refractory MG. In recent years, owing to an increasing understanding of MG pathogenesis the development and execution of clinical trials with novel biologics, including monoclonal antibodies (mAbs) that have demonstrated higher safety and more specificity, provide new opportunities for the treatment of MG. In this article, we review recent advances in MG pathogenesis and the mAbs that have been used for target‐specific MG therapy.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
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