Although lithium possesses neuropro- tective functions, the molecular mechanism underly- ing its actions has not been fully elucidated. In the present paper, the effects of lithium chloride on volt- age-dependent potassium currents in the CA1 py- ramidal neurons acutely isolated from rat hippocam- pus were studied using the whole-cell patch-clamp technique. Depolarizing test pulses activated two components of outward potassium currents: a rapidly activating and inactivating component, IA and a de- layed component, IK. Results showed that lithium chloride increased the amplitude of IA in a concentra- tion-dependent manner. Half enhancement concen- tration (EC50) was 22.80±5.45 μmol?L?1. Lithium chloride of 25 μmol?L?1 shifted the steady-state acti- vation curve and inactivation curve of IA to more negative potentials, but mainly affected the activation kinetics. The amplitude and the activation processes of IK were not affected by lithium chloride. The effects of lithium chloride on potassium channel appear to possess neuroprotective properties by Ca2+-lowing effects modulate neuronal excitability by activating IA in rat hippocampal neurons.
The [2] pseudorotaxane of cucurbit[6]uril(CB[6]) with guest molecule 1,6-bis(imidazol-1-yl)hexane dihydrochloride(BIMH-Cl) made pBR322 DNA hydrolyzed efficiently in physiological environment. The cleavage mechanism was proposed that was a cooperation process of the CB[6] molecule and the guest BIMH molecule. In this mechanism, the protonated imidazole might bind DNA via the electrostatic interactions and the CB[6] glycoluril carbonyl oxygen atoms activated a water molecule to attack the phosphorus atom.
