ABSTRACT
The growing number of cognitive dysfunction patients is bringing heavy mental and financial burdens to the society and families.Voltage-gated potassium channels (Kv), which consist of delayed rectifier potassium channels and transient outward po -tassium channels , are involved in the incidence of cognitive dysfunction .This review summarized the role of Kv channels in cognitive dysfunction and their relationship with N-methyl-D-aspartic acid receptors ( NMDARs) that play an important role in the process of learning and memory .
ABSTRACT
Objective To investigate the effects of docosahexaenoic acid (DHA) on action potential (AP)and transient outward potassium channel (Ito) in rat ventricular myocytes in order to evaluate the anti-arrhythmia mechanism of DHA. Method The rat ventricular myocytes were isolated by using enzyme digestion method. AP and Ito of individual ventricular myocyte were recorded by using patch-clamp technique in whole-cell configuration at room temperature. The effects of DHA on AP and Ito were observed when it was applied in 0 μmol/L, 20 μmol/L, 40 μmol/L, 60 μmol/L, 80 μmol/L, 100 μmol/L and 120μmol/L separaterly. Results The 25%,50% and 90% of action potential duration (APD25, APD50 and APD90) were gradually prolonged with the escalation of concentration of DHA ( P ＜ 0.05, n= 20). The effects of DHA of different concentrations on AP maximal velocity (Vmax), AP amplitude (APA) and AP overshoot (OS) did not produce significantly different results (P ＞ 0.05, n= 20). The degree of blockade of Ito was concentration-dependent as different concentrations of DHA were applied, and as the concentration of DHA was escalated, the I-V curves went downwards, the stably inactivated curves shifted to the lift, and the time taken for recovery from inactivation prolonged ( P ＜ 0.05, n =20). However, the different concentrations of DHA did not produce different effects on stably activated curves ( P＞ 0.05). The Itos were blocked to (2.61 ± 0.26)%, (21.79±4.85)%, (63.11 ± 6.57)%, 75.52±7.26 ) %, (81.82 ± 7.63) % and (84.33 ± 8.25) % by the above given concentrations of DHA respectively under given potential equaling to + 70 mV( P ＜ 0.05, n = 20), and the half-effect concentration (EC50) of DHA on Ito was(49.11±2.68) umol/L. Conclusions The effects of DHA on APD and Ito may be one of the anti-arrhythmia mechanism of DHA.
ABSTRACT
Objective To investigate the effects of unaggregated amyloid ? protein(A?25～35) on transient outward potassium channel(IA) in Rat Hippocampal CA3 Pyramidal Neurons.Methods Patch-clamp technique with whole cell recording was used.Results Unaggregated A?25～35 inhibited IA in neonatal rat hippocampal CA3 pyramidal neurons and displayed a time-,concentration- and voltage-dependent manner;the dynamic characteristics of IA were influenced:shifted the steady-state activation and inactivation curves to left significantly.Conclusion These results suggest that the inhibition of unaggregated A?25-35 on transient outward potassium channel in acutely isolated hippocampal CA3 pyramidal neurons may be an important mechanism of its toxicity,which participates in pathological changes of AD.