Traub R D
IBM Research Division, T.J. Watson Research Center, Yorktown Heights, NY 10598, USA.
J Comput Neurosci. 1995 Dec;2(4):283-9. doi: 10.1007/BF00961440.
We constructed a computer model of 128 interneurons, each with multiple dendritic branches and an axonal segment. The model neurons were interconnected by gap junctions between dendritic compartments, as are known to occur in rat and guinea-pig hilar interneurons. The model contained no excitatory synapses. In the presence of low-frequency spontaneous action potentials, the model generated synchronized population bursts, when gap junction resistance was 50 M omega and there were at least two gap junctions per neuron on average. Population bursts occurred only when the dendrites of model neurons were electrically excitable. Consistent with experiment, somatic hyperpolarization during the population burst uncovered partial spikes. In the model, partial spikes originated in electrically active dendrites driven by coupled dendrites. This model may account for population bursts in hilar interneurons that occur in 4-aminopyridine (4AP) together with blockers of GABAA and excitatory amino acid (EAA) receptors.
我们构建了一个包含128个中间神经元的计算机模型，每个中间神经元都有多个树突分支和一个轴突节段。模型神经元通过树突隔室之间的缝隙连接相互连接，正如在大鼠和豚鼠海马门区中间神经元中所发现的那样。该模型不包含兴奋性突触。在存在低频自发动作电位的情况下，当缝隙连接电阻为50兆欧且每个神经元平均至少有两个缝隙连接时，模型会产生同步的群体爆发。群体爆发仅在模型神经元的树突具有电兴奋性时发生。与实验一致，群体爆发期间的体细胞超极化揭示了部分尖峰。在模型中，部分尖峰起源于由耦合树突驱动的电活动树突。该模型可能解释了在4-氨基吡啶（4AP）以及GABAA和兴奋性氨基酸（EAA）受体阻滞剂存在时海马门区中间神经元中出现的群体爆发。
