Inhibitory effect of unaggregated amyloid beta protein (25-35) on delayed rectifier potassium current in rat hippocampal CA3 pyramidal neurons.
- Author:
Lin LI
1
;
Zhen-Zhai LIU
;
Bing-Jun HE
;
Yu QI
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; metabolism; Amyloid beta-Peptides; chemistry; pharmacology; Animals; Animals, Newborn; Cells, Cultured; Female; Hippocampus; cytology; Male; Mice; Neurons; drug effects; metabolism; Patch-Clamp Techniques; Potassium; metabolism; Rats; Rats, Wistar
- From: Acta Academiae Medicinae Sinicae 2008;30(3):301-304
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of unaggregated Abeta(25.35) on delayed rectifier potassium current (I(K)) in neonatal rat hippocampal CA3 pyramidal neurons.
METHODSThe rat hippocampal neurons were enzymatically isolated from 10-11-day-old Wistar rat. The I(K) was recorded using whole-cell patch clamp technique.
RESULTSThe inhibitory effect of unaggregated Abeta(25-35) on I(K) was time-dependent, because I(K) significantly decreased from (6.987 +/- 1.152) nA to (2.540 +/- 0.349) nA after adding unaggregated Abeta(25-35) and reached a stabilized level after 5-7 min (n = 8, P <0.01). However, the inhibitory effect was not concentration-dependent, because the decrease of the I(K) amplitude in different concentration groups were all around 60%. Unaggregated Abeta(25-35) also remarkably affected the half-activation potential, which was (4.114 +/- 0.730) mV and (-5.463 +/- 0.950) mV before and after its application (n = 15, P <0.05); however, the slope factor of activation curve was not significantly changed.
CONCLUSIONThe inhibitory effect of unaggregated Abeta(25-35) on I(K) may be a possible mechanism involved in the pathogenesis of Alzheimer's disease.
