Abstract：
:Amyloid beta protein (A beta), has been reported to be toxic to neurons in vitro. However, the molecular mechanism leading to neuronal death remains unknown. Here we report protective effects of phenothiazines, a class of neuroleptic agent, against A beta toxicity in primary cultures of rat cortical neurons and PC12 cells. beta(25-35), an active sequence of A beta, showed dose-dependent reduction of the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide dye (MTT) reductivity, and chlorpromazine (CPZ), promethazine or trifluoperazine restored it at micromolar concentration. The significant increase in Ca2+ uptake by chronic treatment of beta(25-35) was reduced not only by nimodipine but also by CPZ. These results suggest that phenothiazines attenuate beta(25-35) toxicity possibly by reducing of Ca2+ influx through L-type Ca2+ channels.
journal_name
Brain Resjournal_title
Brain researchauthors
Ueda K,Yagami T,Asakura K,Kawasaki Kdoi
10.1016/s0006-8993(96)01300-5subject
Has Abstractpub_date
1997-02-14 00:00:00pages
184-8issue
1-2eissn
0006-8993issn
1872-6240pii
S0006-8993(96)01300-5journal_volume
748pub_type
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