Publikation: Wide spectrum modulation by KP-544 in models relevant for neuronal survival
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2007
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Neuroreport. 2007, 18(6), pp. 571-575. ISSN 0959-4965. eISSN 1473-558X. Available under: doi: 10.1097/WNR.0b013e328012475c
Zusammenfassung
Reduced neurotrophic signalling has been proposed as a part of the pathophysiology behind neuronal death and dysfunction. The small molecule KP-544 was developed with the intention to enhance nerve growth factor signalling. To characterize the actions of KP-544 pharmacologically, we used four diverse models with relevance for neuronal function and survival. We found that 300-1000 nM KP-544 enhanced the neurite outgrowth in PC12 cells in response to a suboptimal concentration of nerve growth factor. KP-544 also protected the cerebellar granule cells from excitotoxicity apoptosis induced by the mitochondrial toxin methyl-phenyl-pyridinium, and modulated inflammation by inhibiting interleukin-6 production in primary astrocytes. Chronic treatment of rats with KP-544 prevented the hyper-responsiveness to amphetamine of animals treated with methylazoxymethanol acetate, a recently described neurodevelopmental model of schizophrenia.
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570 Biowissenschaften, Biologie
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GEIST, Marie A., Christiane VOLBRACHT, Jana PODHORNA, Jeppe FALSIG, Marcel LEIST, 2007. Wide spectrum modulation by KP-544 in models relevant for neuronal survival. In: Neuroreport. 2007, 18(6), pp. 571-575. ISSN 0959-4965. eISSN 1473-558X. Available under: doi: 10.1097/WNR.0b013e328012475cBibTex
@article{Geist2007-04-16spect-40776,
year={2007},
doi={10.1097/WNR.0b013e328012475c},
title={Wide spectrum modulation by KP-544 in models relevant for neuronal survival},
number={6},
volume={18},
issn={0959-4965},
journal={Neuroreport},
pages={571--575},
author={Geist, Marie A. and Volbracht, Christiane and Podhorna, Jana and Falsig, Jeppe and Leist, Marcel}
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<dcterms:abstract xml:lang="eng">Reduced neurotrophic signalling has been proposed as a part of the pathophysiology behind neuronal death and dysfunction. The small molecule KP-544 was developed with the intention to enhance nerve growth factor signalling. To characterize the actions of KP-544 pharmacologically, we used four diverse models with relevance for neuronal function and survival. We found that 300-1000 nM KP-544 enhanced the neurite outgrowth in PC12 cells in response to a suboptimal concentration of nerve growth factor. KP-544 also protected the cerebellar granule cells from excitotoxicity apoptosis induced by the mitochondrial toxin methyl-phenyl-pyridinium, and modulated inflammation by inhibiting interleukin-6 production in primary astrocytes. Chronic treatment of rats with KP-544 prevented the hyper-responsiveness to amphetamine of animals treated with methylazoxymethanol acetate, a recently described neurodevelopmental model of schizophrenia.</dcterms:abstract>
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