Adrenergic β receptor activation reduces amyloid β1-42-mediated intracellular Zn2+ toxicity in dentate granule cells followed by rescuing impairment of dentate gyrus LTP.

Neurotoxicology
Haruna TamanoAtsushi Takeda

Abstract

Adrenergic β receptor activation prevents human soluble amyloid β (Aβ)-induced impairment of long-term potentiation (LTP) in slices. On the basis of the evidence that human Aβ1-42-induced impairment of LTP is due to Aβ1-42-mediated Zn2+ toxicity, we postulated that adrenergic β receptor activation reduces Aβ1-42-mediated intracellular Zn2+ toxicity followed by rescuing Aβ1-42 toxicity. To test the effect of adrenergic β receptor activation, LTP was recorded at perforant pathway-dentate granule cell synapses of anesthetized rats 60 min after Aβ1-42 injection into the dentate granule cell layer. Human Aβ1-42-induced impairment of LTP was rescued by co-injection of isoproterenol, an adrenergic β receptor agonist, but not by co-injection of phenylephrine, an adrenergic α1 receptor agonist. Isoproterenol did not reduce Aβ1-42 uptake into dentate granule cells, but reduced increase in intracellular Zn2+ in dentate granule cells induced by Aβ1-42. In contrast, phenylephrine did not reduce both Aβ1-42 uptake and increase in intracellular Zn2+ by Aβ1-42. In the case of human Aβ1-40 and rat Aβ1-42, which do not increase intracellular Zn2+, human Aβ1-40- and rat Aβ1-42-induced impairments of LTP were not rescued by co-injection of isoprot...Continue Reading

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Jun 9, 2021·Seminars in Cell & Developmental Biology·Mara Mather
Jan 23, 2022·Biometals : an International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine·Yuya KawanoAtsushi Takeda

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