Brain Computation Laboratory, Program in Biomedical Engineering, University of Nevada Reno, NV, USA.
Front Neural Circuits. 2010 Nov 18;4:122. doi: 10.3389/fncir.2010.00122. eCollection 2010.
Hippocampal "place cells" and the precession of their extracellularly recorded spiking during traversal of a "place field" are well-established phenomena. More recent experiments describe associated entorhinal "grid cell" firing, but to date only conceptual models have been offered to explain the potential interactions among entorhinal cortex (EC) and hippocampus. To better understand not only spatial navigation, but mechanisms of episodic and semantic memory consolidation and reconsolidation, more detailed physiological models are needed to guide confirmatory experiments. Here, we report the results of a putative entorhinal-hippocampal circuit level model that incorporates recurrent asynchronous-irregular non-linear (RAIN) dynamics, in the context of recent in vivo findings showing specific intracellular-extracellular precession disparities and place field destabilization by entorhinal lesioning. In particular, during computer-simulated rodent maze navigation, our model demonstrate asymmetric ramp-like depolarization, increased theta power, and frequency (that can explain the phase precession disparity), and a role for STDP and K(AHP) channels. Additionally, we propose distinct roles for two entorhinal cell populations projecting to hippocampus. Grid cell populations transiently trigger place field activity, while tonic "suppression-generating cell" populations minimize aberrant place cell activation, and limit the number of active place cells during traversal of a given field. Applied to place-cell RAIN networks, this tonic suppression explains an otherwise seemingly discordant association with overall increased firing. The findings of this circuit level model suggest in vivo and in vitro experiments that could refute or support the proposed mechanisms of place cell dynamics and modulating influences of EC.
海马体“位置细胞”及其在穿越“位置场”时细胞外记录的放电脉冲的进动是已确立的现象。最近的实验描述了相关的内嗅皮层“网格细胞”放电，但迄今为止，仅提出了概念模型来解释内嗅皮层（EC）和海马体之间的潜在相互作用。为了更好地理解空间导航，以及情景和语义记忆巩固和再巩固的机制，需要更详细的生理模型来指导验证实验。在这里，我们报告了一个假设的内嗅-海马体回路水平模型的结果，该模型结合了递归异步不规则非线性（RAIN）动力学，该模型是在最近的体内发现的基础上提出的，这些发现显示了特定的细胞内-细胞外进动差异以及内嗅皮层损伤导致的位置场失稳。特别是，在计算机模拟的啮齿动物迷宫导航过程中，我们的模型表现出不对称的斜坡状去极化、增加的θ功率和频率（可以解释相位进动差异），以及 STDP 和 K(AHP)通道的作用。此外，我们提出了两个投射到海马体的内嗅细胞群体的不同作用。网格细胞群体短暂地触发位置场活动，而紧张的“抑制生成细胞”群体最小化异常的位置细胞激活，并限制给定场穿越过程中活跃的位置细胞数量。将该紧张抑制应用于位置细胞 RAIN 网络，可以解释与整体增加的放电之间看似不一致的关联。该回路水平模型的发现表明，体内和体外实验可以反驳或支持所提出的位置细胞动力学机制以及 EC 的调节影响。
