Mechanisms underlying short-term synaptic plasticity between identified neurons

神经系统的所有功能都依赖于神经元通过称为突触的特殊结构进行的交流。电活动诱导的神经递质在突触间隙的扩散，以及它对受体细胞上并列受体的激活，使信息能够在所有大脑回路中流动。这种神经元通讯的失败会导致大脑功能失调。尽管在神经科学领域进行了广泛的研究，但调控各种突触通讯模式的确切细胞和分子机制仍然很大程度上是未知的。此外，人们对神经元能够增加或减少其突触强度(突触可塑性)以应对环境变化的机制知之甚少。我们已经开发了一个简单的模型，由蜗牛的功能定义神经元组成。这个模型不仅让我们能够定义突触传递的潜在机制，还帮助设计了可以与脑细胞连接的硅芯片。使用这个模型，我们现在将定义细胞和分子通路，这些通路不仅调节突触传递，而且还调节构成学习和记忆基础的短期突触可塑性。神经元网络将在细胞培养中重建，并使用几种最先进的神经科学技术，我们将识别在正常条件下和在形成学习和记忆基础的短期突触可塑性后调节神经元通信的机制。我们将试图确定钙离子如何进入神经元激活一系列第二信使，从而在工作记忆过程中影响神经元的输出。

All nervous system functions rely upon neuronal communications through specialized structure, termed synapse. Diffusion of electrical activity-induced, neurotransmitters across the synaptic cleft and its activation of juxtaposed receptors on the recipient cell enable the flow of information across all brain circuits. Failure of this neuronal communication renders the brain dysfunctional. Despite extensive research in the field of neuroscience, the precise cellular and molecular mechanisms that regulate various modes of synaptic communications remain, however, largely unknown. Moreover, even less is known about the mechanisms that enable neurons to either increase or decrease their synaptic strength (synaptic plasticity) in response to a changing environment. We have developed a simple model comprising of functionally defined neurons from the snail. This model has not only allowed us to define mechanisms underlying synaptic transmission, but has also helped design silicon chips that can be interfaced with brain cells. Using this model, we will now define both cellular and molecular pathways that regulate not only the synaptic transmission, but also the short-term synaptic plasticity that forms the basis for learning and memory. Neuronal networks will be reconstructed in cell culture and using several state-of-the-art neuroscience techniques, we will identify mechanisms that regulate neuronal communication under normal conditions and after short-term synaptic plasticity that form the basis for learning and memory. We will seek to determine how calcium entry into neurons activates a cascade of second messengers that in turn affect neuronal output during working memory.