The therapeutic potential of berberine against the altered intrinsic properties of the CA1 neurons induced by Aβ neurotoxicity.

It was demonstrated that treatment with beta amyloid (Aβ) led to extreme alterations in the intrinsic electrophysiological properties of CA1 pyramidal neurons. Also, malfunction of the cholinergic system is correlated to the memory and cognitive impairments. Several new studies have suggested that Berberis vulgaris can act as a cholinesterase inhibitor. The present study aimed to investigate the effects of berberine (BER) on the Aβ-induced impairments in learning and memory. The male Wistar rats were divided into 4 groups of Sham, BER, Aβ and Aβ+BER. The administration of BER or its vehicle started immediately after the injection of Aβ and followed by 13 days. Then, the animals were tested for learning and memory performance using the Morris water maze (MWM) and passive avoidance tests. Then, they were sacrificed for the whole cell patch clamp recording. The results of the MWM and passive avoidance tasks indicated that administration of the BER in the Aβ+BER group prevented the memory impairment induced by Aβ. The results of the whole cell patch clamp also showed that administration of the BER restored the Aβ-induced impairments in the firing frequency, half-width and rebound action potential. These results suggested that administration of the BER could ameliorate neurotoxicity induced by Aβ. However, this neuroprotection impact could be resulted from the balance effect of the Ca(2+) entry. The optimal level of Ca(2+) entry by BER could be a major factor that modified the function of the Ca(2+)-activated K(+) channels and decreased the half-width in the Aβ treated rats.