Wei Chun-ling, Liu Yi-hui, Yang Ming-hao, Liu Zhi-qiang, Ren Wei
Key Laboratory of MOE for Modern Teaching Technology and College of Life Sciences, Shaanxi Normal University, Xi'an, China.
Neurosignals. 2013;21(3-4):150-9. doi: 10.1159/000342435. Epub 2012 Sep 27.
The efficiency of neural circuits is modified by changes not only in synaptic strength, but also in intrinsic excitability of neurons. In CA1 hippocampal pyramidal neurons, bidirectional changes in the intrinsic excitability are often presented after induction of synaptic long-term potentiation or depression. This plasticity of intrinsic excitability has been identified as a cellular correlate of learning. Besides, behavioral learning often involves action of reinforcement or rewarding mediated by dopamine (DA). Here, we examined how DA influences the intrinsic plasticity of CA1 hippocampal pyramidal neurons when high-frequency stimulation (HFS) was applied to Schaffer collaterals. The results showed that DA inhibits the decrease in rheobase and increase in mean firing rate of pyramidal neurons induced by HFS, and that this inhibition was abolished by the D1-like receptor antagonist SCH23390 but not by the D2-like receptor antagonist sulpiride. The results suggest that DA inhibits the potentiation of excitability induced by presynaptic HFS, and that this inhibition depends on the activation of D1-like receptors.
神经回路的效率不仅会因突触强度的变化而改变，还会因神经元的内在兴奋性变化而改变。在CA1海马锥体神经元中，内在兴奋性的双向变化常在突触长时程增强或抑制诱导后出现。这种内在兴奋性的可塑性已被确定为学习的细胞相关物。此外，行为学习通常涉及多巴胺（DA）介导的强化或奖赏作用。在此，我们研究了在对海马体CA1锥体神经元的Schaffer侧支施加高频刺激（HFS）时，多巴胺如何影响其内在可塑性。结果表明，多巴胺抑制了由高频刺激诱导的锥体神经元阈强度的降低和平均放电率的增加，并且这种抑制作用可被D1样受体拮抗剂SCH23390消除，但不能被D2样受体拮抗剂舒必利消除。结果表明，多巴胺抑制了突触前高频刺激诱导的兴奋性增强，并且这种抑制作用依赖于D1样受体的激活。
