Barrionuevo G, Rinaldi P, Kessler M, Lynch G, Tewari S
Brain Res. 1984 Jul 30;307(1-2):1-7. doi: 10.1016/0006-8993(84)90453-0.
The effect of chronic lithium exposure on the electrophysiological responses of the Schaffer collateral-commissural (SCC) input to the CA1 pyramidal neurons in the in vitro hippocampus was investigated. Experimental animals were intubated intragastrically with lithium carbonate (150 mg/kg) for 3-4 weeks. This treatment produced lithium levels in serum and hippocampus of 0.3-1.3 mM. During the recording period, the hippocampal slice retained a stable lithium concentration of 53% of the initial value. Chronic lithium exposure had a depressive effect on input/output relationships, paired-pulse facilitation and strength of orthodromic inhibition. The antidromic inhibition was virtually intact. No obvious differences were found between control and lithium slices in amplitude, latency or waveforms, of synaptic and antidromic extracellular potentials. These findings are compatible with a major action of lithium on the excitability of SCC axons and synaptic terminals.
研究了慢性锂暴露对体外海马体中Schaffer侧支-连合(SCC)输入至CA1锥体神经元的电生理反应的影响。实验动物通过胃内插管给予碳酸锂(150 mg/kg),持续3 - 4周。该处理使血清和海马体中的锂水平达到0.3 - 1.3 mM。在记录期间,海马切片保持了初始值53%的稳定锂浓度。慢性锂暴露对输入/输出关系、双脉冲易化和正向抑制强度有抑制作用。逆向抑制基本完好。在对照切片和锂处理切片之间,突触和逆向细胞外电位的幅度、潜伏期或波形未发现明显差异。这些发现与锂对SCC轴突和突触终末兴奋性的主要作用相符。