Delayed rectifier potassium currents and Kv2.1 mRNA increase in hippocampal neurons of scopolamine-induced memory-deficient rats

To explore the ionic mechanisms of memory deficits induced by cholinergic lesion, whole-cell patch clamp recording techniques in combination with single-cell RT-PCR were used to characterize delayed rectifier potassium currents ( I K) in acutely isolated hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. Scopolamine could induce deficits in spatial memory of rats. The peak amplitude and current density of I K measured in hippocampal pyramidal neurons were increased from 1.2 ± 0.6 nA and 38 ± 19 pA/pF of the control group ( n = 12) to 1.8 ± 0.5 nA and 62 ± 24 pA/pF ( n = 48, P < 0.01) of the scopolamine-treated group. The steady-state activation curve of I K was shifted about 8 mV ( P < 0.01) in the direction of hyperpolarization in scopolamine-treated rats. The mRNA level of Kv2.1 was increased ( P < 0.01) in the scopolamine-treated group, but there was no significant change of Kv1.5 mRNA level. The present study demonstrated for the first time that I K was enhanced significantly in hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. The increase of Kv2.1 mRNA expression in hippocampal pyramidal cells might be responsible for the enhancement of I K and could be the ionic basis of the memory deficits induced by scopolamine.