Effects of presenilins and beta-amyloid precursor protein on delayed rectifier potassium channels in cultured rat hippocampal neurons
Abstract
AIM:
To study the effects of presenilin-1 (PS-1), presenilin-2 (PS-2), and amyloid beta-protein precursor (APP695) on delayed rectifier potassium channels (IK) in the cultured rat hippocampal neurons.
METHODS:
PS-1, PS-2, and APP695 were transfected into the cultured rat hippocampal neurons by transient transfection techniques. The IK current was observed by the whole cell patch-clamp techniques.
RESULTS:
IK was increased in cultured rat hippocampal neurons, after transient transfection of PS-1, PS-2, and APP695. IK amplitudes and densities were significantly increased from (1689 +/- 412) pA, (48 +/- 18) pA/pF (mock cells, GFP alone, n=17) to (5565 +/- 1403) pA, (252 +/- 107) pA/pF (PS-1/GFP, n=22, P<0.01), (3804 +/- 1651) pA, (120 +/- 58) pA/pF (PS-2/GFP, n=16, P<0.01), and (4978 +/- 904) pA, (218 +/- 70) pA/pF (APP695, n=22, P<0.01). But PS-1, PS-2, and APP695 did not alter the activation curve of IK (P>0.05).
CONCLUSION:
Overexpression of PS-1, PS-2, and APP695 increased IK in the cultured rat hippocampal neurons. The upregulation of IK may be related to neuronal apoptosis after PS-1, PS-2, and APP695 were transfected.
Keywords:
To study the effects of presenilin-1 (PS-1), presenilin-2 (PS-2), and amyloid beta-protein precursor (APP695) on delayed rectifier potassium channels (IK) in the cultured rat hippocampal neurons.
METHODS:
PS-1, PS-2, and APP695 were transfected into the cultured rat hippocampal neurons by transient transfection techniques. The IK current was observed by the whole cell patch-clamp techniques.
RESULTS:
IK was increased in cultured rat hippocampal neurons, after transient transfection of PS-1, PS-2, and APP695. IK amplitudes and densities were significantly increased from (1689 +/- 412) pA, (48 +/- 18) pA/pF (mock cells, GFP alone, n=17) to (5565 +/- 1403) pA, (252 +/- 107) pA/pF (PS-1/GFP, n=22, P<0.01), (3804 +/- 1651) pA, (120 +/- 58) pA/pF (PS-2/GFP, n=16, P<0.01), and (4978 +/- 904) pA, (218 +/- 70) pA/pF (APP695, n=22, P<0.01). But PS-1, PS-2, and APP695 did not alter the activation curve of IK (P>0.05).
CONCLUSION:
Overexpression of PS-1, PS-2, and APP695 increased IK in the cultured rat hippocampal neurons. The upregulation of IK may be related to neuronal apoptosis after PS-1, PS-2, and APP695 were transfected.