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Durch die Hemmung von TREK-1 verstärkt PE-22-28 die serotonerge Neurotransmission und fördert die BDNF-Expression , die hippocampale Neurogenese sowie die synaptische Plastizität, wodurch in Forschungsmodellen rasche antidepressivumartige Effekte erzielt werden, ohne die kardiale TREK-1-Aktivität zu beeinflussen
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