Batchelor A M, Garthwaite J
The Cruciform Project, University College London, UK.
Nature. 1997 Jan 2;385(6611):74-7. doi: 10.1038/385074a0.
In the classical view, a central neuron integrates incoming synaptic information by simple algebraic summation of the resultant bioelectrical signals that coincide in time. The voltage dependence of the NMDA (N-methyl-D-aspartate) type of ionotropic glutamate receptor endows neurons with an additional tool that allows one synaptic input to influence another, providing, again, that the two are active simultaneously. Here we identify a new mechanism by which non-coincident signals generated by different synaptic inputs are integrated. The device serves to regulate neuronal excitation through G-protein-coupled, metabotropic glutamate receptors (mGluRs) in a powerful and specific manner. We show that, in cerebellar Purkinje cells, a single activation of the climbing-fibre input markedly potentiates mGluR-mediated excitation at parallel-fibre synapses. The potentiation results from a transient rise in cytosolic Ca2+ which is 'memorized' in such a way that it promotes excitation through mGluRs for about two minutes. A Ca2+-transient is also effective if imposed up to two seconds after parallel-fibre stimulation. By allowing temporally and spatially dispersed synaptic signals to be assimilated, this mechanism adds a new element to the computational power of central neurons.
在传统观点中,中枢神经元通过对同时出现的生物电信号进行简单代数求和来整合传入的突触信息。离子型谷氨酸受体的NMDA(N-甲基-D-天冬氨酸)亚型的电压依赖性赋予神经元一种额外的机制,使得一个突触输入能够影响另一个突触输入,条件是这两个输入同时处于激活状态。在此,我们发现了一种新机制,不同突触输入产生的非同步信号可借此进行整合。该机制通过G蛋白偶联的代谢型谷氨酸受体(mGluRs)以强大且特异的方式调节神经元兴奋。我们发现,在小脑浦肯野细胞中,单一次攀缘纤维输入的激活能显著增强平行纤维突触处mGluR介导的兴奋。这种增强源于胞质Ca2+的短暂升高,其以一种能促进通过mGluRs兴奋约两分钟的方式被“记忆”下来。如果在平行纤维刺激后两秒内施加Ca2+瞬变,其同样有效。通过允许在时间和空间上分散的突触信号被整合,该机制为中枢神经元的计算能力增添了新元素。