Rancz Ede A, Häusser Michael
Wolfson Institute for Biomedical Research, Department of Physiology, University College London, London WC1E 6BT, United Kingdom.
J Neurosci. 2006 May 17;26(20):5428-37. doi: 10.1523/JNEUROSCI.5284-05.2006.
Understanding the relationship between dendritic excitability and synaptic plasticity is vital for determining how dendrites regulate the input-output function of the neuron. Dendritic calcium spikes have been associated with the induction of long-term changes in synaptic efficacy. Here we use direct recordings from cerebellar Purkinje cell dendrites to show that synaptically activated local dendritic calcium spikes are potent triggers of cannabinoid release, producing a profound and short-term reduction in synaptic efficacy at parallel fiber synapses. Enhancing dendritic excitability by modulating dendritic large-conductance calcium-activated potassium (BK) channels improves the spread of dendritic calcium spikes and enhances cannabinoid release at the expense of spatial specificity. Our findings reveal that dendritic calcium spikes provide a local and tunable coincidence detection mechanism that readjusts synaptic gain when synchronous activity reaches a threshold, and they reveal a tight link between the regulation of dendritic excitability and the induction of synaptic plasticity.
了解树突兴奋性与突触可塑性之间的关系对于确定树突如何调节神经元的输入-输出功能至关重要。树突钙峰与突触效能的长期变化诱导有关。在这里，我们通过对小脑浦肯野细胞树突进行直接记录，表明突触激活的局部树突钙峰是大麻素释放的有效触发因素，在平行纤维突触处产生突触效能的深刻且短期的降低。通过调节树突大电导钙激活钾（BK）通道来增强树突兴奋性，可改善树突钙峰的传播，并以空间特异性为代价增强大麻素释放。我们的研究结果表明，树突钙峰提供了一种局部且可调谐的巧合检测机制，当同步活动达到阈值时可重新调整突触增益，并且揭示了树突兴奋性调节与突触可塑性诱导之间的紧密联系。
