Synergistic interactions between independent synaptic input streams may fundamentally change the action potential (AP) output. Using partial information decomposition, we demonstrate here a substantial contribution of synergy between somatic and apical dendritic inputs to the information in the AP output of L5b pyramidal neurons. Activation of dendritic GABA B receptors (GABA B Rs), known to decrease APs in vivo, potently decreased synergy and increased somatic control of AP output. Synergy was the result of the voltage-dependence of the transfer resistance between dendrite and soma, which showed a two-fold increase per 28.7 mV dendritic depolarization. GIRK channels activated by dendritic GABA B Rs decreased voltage-dependent transfer resistances and AP output. In contrast, inhibition of dendritic L-type Ca2+ channels prevented high-frequency bursts of APs, but did not affect dendro-somatic synergy. Finally, we show that NDNF-positive neurogliaform cells effectively control somatic AP via synaptic activation of dendritic GIRK channels. These results uncover a novel inhibitory mechanism that powerfully gates cellular information flow in the cortex.

中文翻译：

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GABA B 受体介导的第 5 层锥体神经元树突-体细胞协同作用的调节。

独立突触输入流之间的协同相互作用可能会从根本上改变动作电位 (AP) 输出。使用部分信息分解，我们在这里证明了体细胞和顶端树突输入之间的协同作用对 L5b 锥体神经元 AP 输出中的信息的实质性贡献。已知可在体内减少 APs 的树突状 GABA B 受体 (GABA B Rs) 的激活有效地降低了协同作用并增加了对 AP 输出的体细胞控制。协同作用是树突和体细胞之间转移电阻的电压依赖性的结果，每 28.7 mV 树突去极化显示两倍增加。由树突状 GABA B Rs 激活的 GIRK 通道降低了电压依赖性转移电阻和 AP 输出。相比之下，树突状 L 型 Ca2+ 通道的抑制阻止了 AP 的高频爆发，但不影响树状体协同作用。最后，我们表明 NDNF 阳性神经胶质细胞通过树突 GIRK 通道的突触激活有效控制体细胞 AP。这些结果揭示了一种新的抑制机制，可以有力地控制皮层中的细胞信息流。