Information Routing in the Hippocampus via Gamma Oscillations

大脑能够通过跨不同功能的大脑区域进行交流来执行复杂的过程。神经振荡或脑电波/节律，包括伽马频率范围(~25？140赫兹)内的那些，可能在这种形式的交流中发挥关键作用。神经振荡代表着大群神经元之间的周期性、同步活动。当一个区域的振荡与另一个区域的振荡同步时，它们的神经元活动在时间上是一致的，从而促进了区域间的交流。通过这种方式，振荡同步性可能会关闭大脑特定区域之间的信息流，创建特定大脑过程独有的瞬时集合。重要的是，这种连接调制是快速、可逆的，并且与底层电路的物理变化无关。最近的证据表明，记忆功能的中心区域--海马体，可能以这种方式利用伽马振荡。海马体中的伽马振荡以两种形式发生：慢伽马形式(~25？55赫兹)和快速伽马形式(~65？140赫兹)。每个变异发生在不同的时间，并同步解剖上不同的海马子区域。具体地说，慢伽马连接CA3和CA1区，这是一个与记忆提取有关的电路，而快伽马连接内侧内嗅皮层(MEC)和CA1，这是记忆编码所必需的电路。因此，我们假设慢伽马同步增强CA1？CA3通信并且对于正确的记忆提取是必需的，而快速伽马同步增强MEC？CA1通信并且对于正确的记忆编码是必需的。这一假说将通过检测在每个记忆功能(提取和编码)过程中海马体振荡和单细胞活动的差异来检验。我们期望在记忆编码过程中看到快速伽马活动增强，在记忆提取过程中看到慢伽马活动增强。具体目标1将通过测量位置细胞的活动在细胞水平上检验这一假说，位置细胞代表记忆的位置成分。这些细胞在记忆编码与记忆提取过程中表现出独特的激发特性，为确定慢和快伽马对不同记忆功能的影响提供了一种方便的方法。《特定目标2》将通过测量简单学习任务中的快伽马活动和慢伽马活动，在行为水平上检验这一假说。拟议中的实验结果有望为振荡活动和复杂的大脑功能之间的联系提供洞察力，并有助于更深入地理解异常振荡在认知功能障碍产生中的作用。

The brain is able to perform complex processes through communication across functionally distinct brain regions. Neural oscillations, or brain waves/rhythms, including those in the gamma frequency range (~25 ¿ 140 Hz), may play a critical role in this form of communication. Neural oscillations represent periodic, synchronous activity across large groups of neurons. When oscillations in one region are synchronous with oscillations in another, their neuronal activity is temporally aligned, and thus region-to-region communication is facilitated. In this way, oscillatory synchrony may gate the flow of information between specific regions of the brain, creating transient ensembles unique to given brain processes. Importantly, this modulation of connectivity is rapid, reversible, and independent of physical changes to the underlying circuitry. Recent evidence suggests that the hippocampus, a region central to memory function, may utilize gamma oscillations in this way. Gamma oscillations in the hippocampus occur as two variants ¿ a slow gamma form (~25 ¿ 55 Hz) and a fast gamma form (~65 ¿ 140 Hz). Each variant occurs at separate times and synchronizes anatomically distinct hippocampal sub-regions. Specifically, slow gamma links areas CA3 and CA1, a circuit implicated in memory retrieval, while fast gamma links the medial entorhinal cortex (MEC) and CA1, a circuit thought necessary for memory encoding. We therefore hypothesize that slow gamma synchrony enhances CA1 ¿ CA3 communication and is necessary for proper memory retrieval, while fast gamma synchrony enhances MEC ¿ CA1 communication and is necessary for proper memory encoding. This hypothesis will be tested by examining differences in oscillatory and single cell activity in the hippocampus during each memory function (retrieval and encoding). We expect to see enhanced fast gamma activity during memory encoding and enhanced slow gamma activity during memory retrieval. Specific Aim 1 will examine this hypothesis at the cellular level by measuring the activity of place cells, which represent the ¿where¿ component of memory. These cells exhibit unique firing properties during memory encoding vs. memory retrieval, providing a convenient method for determining the effects of slow and fast gamma on different memory functions. Specific Aim 2 will examine this hypothesis at the behavioral level by measuring fast and slow gamma activity during a simple learning task. The results of the proposed experiments are expected to provide insights into the link between oscillatory activity and complex brain function, and lead to a deeper understanding of the role of aberrant oscillations in the generation of cognitive dysfunction.