Matin Meisam Habibi, Xiao Shulan, Jayant Krishna
Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN, USA, 47907.
Purdue Institute for Integrative Neuroscience, Purdue University, West Lafayette, IN, USA, 47907.
bioRxiv. 2024 Nov 3:2024.11.02.621672. doi: 10.1101/2024.11.02.621672.
Focal cooling is a powerful technique to temporally scale neural dynamics. However, the underlying cellular mechanisms causing this scaling remain unresolved. Here, using targeted focal cooling (with a spatial resolution of 100 micrometers), dual somato-dendritic patch clamp recordings, two-photon calcium imaging, transmitter uncaging, and modeling we reveal that a 5°C drop can enhance synaptic transmission, plasticity, and input-output transformations in the distal apical tuft, but not in the basal dendrites of intrinsically bursting L5 pyramidal neurons. This enhancement depends on N-methyl-D-aspartate (NMDA) and Kv4.2, suggesting electrical structure modulation. Paradoxically, and despite the increase in tuft excitability, we observe a reduced rate of recovery from inactivation for apical Na+ channels, thereby regulating back-propagating action potential invasion, coincidence detection, and overall burst probability, resulting in an "apparent" slowing of somatic spike output. Our findings reveal a differential temperature sensitivity along the basal-tuft axis of L5 neurons analog modulates cortical output.
局灶性冷却是一种在时间上调节神经动力学的强大技术。然而，导致这种调节的潜在细胞机制仍未得到解决。在这里，我们使用靶向局灶性冷却（空间分辨率为100微米）、双体树突膜片钳记录、双光子钙成像、递质解笼和建模，揭示了5°C的温度下降可以增强内在爆发性L5锥体神经元远端顶端树突簇中的突触传递、可塑性和输入-输出转换，但在其基底树突中则不然。这种增强依赖于N-甲基-D-天冬氨酸（NMDA）和Kv4.2，提示电结构调制。矛盾的是，尽管树突簇兴奋性增加，但我们观察到顶端钠通道失活后的恢复速率降低，从而调节反向传播动作电位的侵入、重合检测和整体爆发概率，导致体细胞动作电位输出出现“明显”减慢。我们的研究结果揭示了L5神经元沿基底-树突簇轴的不同温度敏感性，类似物调节皮层输出。
