Effects of chronic exposure to beta-amyloid-peptide25-35 on the mRNA expressions of voltage-gated outward potassium channel subunits in cultured rat hippocampal neurons.
- Author:
Hong-wei JIN
1
;
Wei ZHANG
;
Xiao-liang WANG
Author Information
- Publication Type:Journal Article
- MeSH: Amyloid beta-Peptides; toxicity; Animals; Animals, Newborn; Cell Division; drug effects; Cells, Cultured; Delayed Rectifier Potassium Channels; Female; Gene Expression; drug effects; Hippocampus; cytology; Male; Neurons; drug effects; metabolism; Peptide Fragments; toxicity; Potassium Channels; biosynthesis; genetics; Potassium Channels, Voltage-Gated; RNA, Messenger; biosynthesis; drug effects; Rats; Rats, Wistar; Shab Potassium Channels
- From: Acta Pharmaceutica Sinica 2002;37(8):598-602
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate mRNA expression changes of voltage-gated outward potassium channel subtypes in cultured rat hippocampal neurons after chronic exposure to beta-amyloid-petitde25-35 (beta-AP25-35).
METHODSmRNA expression was detected by RT-PCR, comparative expression levels were determined by imaging densitometer.
RESULTSDelayed rectifying (Kv2.1, Kv1.5), transient outward (Kv1.4, Kv4.2) and large conductance calcium-activated (rSlo) potassium channel mRNA were expressed in cultured rat hippocampal. In the presence of beta-AP25-35 3 mumol.L-1 for 24 h, the relative expression level of Kv2.1 was significantly increased (n = 3, P < 0.05); the other subtypes were not changed obviously (n = 3, P > 0.05). The increase of Kv2.1 mRNA mainly happened between 24 and 36 h after exposure to beta-AP25-35. After exposure to beta-AP25-35 for 60 h, Kv2.1 mRNA decreased significantly (n = 3, P < 0.01).
CONCLUSIONThe upregulation of Kv2.1 on transcription levels may be involved in the enhancement of delayed rectifying outward potassium (Ik) current induced by beta-AP25-35.
