EFFECTS OF CHRONIC EXPOSURE TO BETA-AMYLOID PEPTIDE_25-35 ON VOLTAGE-GATED POTASSIUM OUTWARD CURRENT IN CULTURED RAT HIPPOCAMPAL NEURONS

AIM To investigate the effects of chronic exposure to beta amyloid peptide _25-35 (β-AP_25-35) on transient outward (I_A) and delayed rectifying (I_K) current in cultured rat hippocampal neurons. METHODS Voltage gated potassium outward current was recorded using whole cell patch clamp techniques in the cultured rat hippocampal neurons. RESULTS Cells were exposed to β-AP_25-35 3 μmol·L^-1 for 24 h. The I_K current amplitude was increased by (44±5)% (n=10, P<0.05), current density increased from (30±6) pA·PF^-1 to (44±5) pA·PF^-1 (n=10, P<0.05) at the membrane potential of 40 mV. When β-AP_25-35 was 10 μmol·L^-1, I_K was increased by (70±4)% (n=10, P<0.01), current density increased by (52±8) pA·pF^-1 (n=10, P<0.01), The effect of β-AP_25-35 was shown to be in a dosage dependent manner. The increment of I_K current by β-AP_25-35 was sensitive to 5 mmol·L^-1 TEA. The increase of I_K mainly happened within 48 h after exposure to β-AP_25-35. I_A did not change obviously after exposure to β-AP_25-35 (n=10, P>0.05). CONCLUSION Beta-amyloid peptide enhanced I_K current selectively. This may be related to β-AP induced neurotoxicity in the hippocampal neurons.