REGULATION OF SYNAPTIC AMINO ACID RECEPTORS

对单个突触强度的控制对于精细- 调整神经电路的性能。突触强度可能是 高频突触前神经元在短期内的调节 在许多突触上导致短期突触的动作电位 抑郁症。利用雏鸡耳蜗区的大突触 核(核)，或nMAG，我们将进行 基于以下假设的实验：我们建议 有多种形式的短期抑郁，每一种都有 独特的性质，这些人会在特定的地点被招募 神经活动的频率。通过独立监管这些 抑郁症的形式，神经元可能在突触强度上产生变化 特定的频率范围，而不是在其他频率范围。这个概念，我们 抑郁症一词复杂，会提供一种强大而老练的 控制神经回路的手段，并将进行全面测试 在拟议的研究中。这些将使用膜片钳记录和 突触前和突触后信号的直接测量 抑郁症的病程，测试关于类型的特定假设， 抑郁症的起源和功能。具体地说，我们将首先记录 抑郁有不同的成分，以及每种成分是如何 有助于控制特定频率下的突触强度 突触活动。然后，我们将确定可能的细胞 不同形式的抑郁症背后的机制。此外，我们 将研究如何通过递质摄取来调节抑郁 系统和活动模式。最后，我们将确定 突触转化为神经元时抑郁的功能后果 单一目标单元格。分析的结果将提供新的见解 中决定信号光传输的因素 大脑，并将有助于理解感官或 认知缺陷。

The control of the strength of individual synapses is essential to fine- tuning the performance of neural circuits. Synaptic strength may be regulated in the short term by trains of high frequency pre-synaptic action potential which at many synapses leads to short-term synaptic depression. Using the large calyceal synapses of the chick cochlear nucleus (nucleus magnocellularis, or nMAG), we will carry out experiments which are based upon the following hypothesis: We propose that there are multiple forms of short-term depression, each with distinctive properties, and that these become recruited at specific frequencies of neural activity. By the independent regulation of these forms of depression, neurons may produce changes in synaptic strength at specific ranges of frequencies and not at others. This concept, which we term complex depression, would provide a powerful and sophisticated means for control of neural circuits, and will be comprehensively tested in the proposed studies. These will employ patch clamp recordings and the direct measurement of pre- and postsynaptic signals during the course of depression, testing specific hypotheses about the types, origins and function of depression. Specifically, we will first document that there are different components to depression and how each contributes to the control of synaptic strength at specific frequencies of synaptic activity. Then, we will identify the probable cellular mechanisms that underlie different forms of depression. Moreover, we will examine how depression can be regulated by transmitter uptake systems and by patterns of activity. Finally, we will determine the functional consequences of depression when synapses converse onto a single target cell. The results of the analyses will give new insight into the factors that determine the optical transmission of signals in the brain, and will contribute to an understanding of sensory or cognitive deficits.