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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Prefrontal Corticotropin-Releasing Factor (CRF) Neurons Act Locally to Modulate Frontostriatal Cognition and Circuit Function
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Prefrontal Corticotropin-Releasing Factor (CRF) Neurons Act Locally to Modulate Frontostriatal Cognition and Circuit Function

机译：前甲基皮质脂素 - 释放因子（CRF）神经元在本地起作用以调节前叉子认知和电路功能

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摘要

The PFC and extended frontostriatal circuitry support higher cognitive processes that guide goal-directed behavior. PFC-dependent cognitive dysfunction is a core feature of multiple psychiatric disorders. Unfortunately, a major limiting factor in the development of treatments for PFC cognitive dysfunction is our limited understanding of the neural mechanisms underlying PFC-dependent cognition. We recently demonstrated that activation of corticotropin-releasing factor (CRF) receptors in the caudal dorsomedial PFC (dmPFC) impairs higher cognitive function, as measured in a working memory task. Currently, there remains much unknown about CRF-dependent regulation of cognition, including the source of CRF for cognition-modulating receptors and the output pathways modulated by these receptors. To address these issues, the current studies used a viral vector-based approach to chemogenetically activate or inhibit PFC CRF neurons in working memory-tested male rats. Chemogenetic activation of caudal, but not rostral, dmPFC CRF neurons potently impaired working memory, whereas inhibition of these neurons improved working memory. Importantly, the cognition-impairing actions of PFC CRF neurons were dependent on local CRF receptors coupled to protein kinase A. Additional electrophysiological recordings demonstrated that chemogenetic activation of caudal dmPFC CRF neurons elicits a robust degradation of task-related coding properties of dmPFC pyramidal neurons and, to a lesser extent, medium spiny neurons in the dorsomedial striatum. Collectively, these results demonstrate that local CRF release within the caudal dmPFC impairs frontostriatal cognitive and circuit function and suggest that CRF may represent a potential target for treating frontostriatal cognitive dysfunction.
机译：PFC和扩展frontostriatal电路支持更高的认知过程使得导向目标导向的行为。 PFC相关的认知功能障碍是多种精神疾病的核心功能。不幸的是，在治疗的发展为PFC认知功能障碍的主要限制因素是我们有限的潜在PFC相关的认知神经机制的理解。我们最近证实，尾背内侧PFC（dmPFC）也妨碍促肾上腺皮质激素释放因子（CRF）受体更高级的认知功能，如在工作记忆测量任务激活。目前，仍然存在对认知的CRF依赖性调节，包括CRF的用于认知调节受体和这些受体调制的输出途径的源多未知。为了解决这些问题，目前的研究中使用的基于病毒载体的方法chemogenetically激活或抑制PFC CRF神经元在工作记忆测试雄性大鼠。尾的Chemogenetic激活，但不喙，dmPFC CRF神经元有效地受损工作存储器，而这些神经元的抑制提高工作存储器。重要的是，PFC CRF神经元的认知损害行动是依赖于耦合到蛋白激酶A.附加电生理记录本地CRF受体表明尾部dmPFC CRF神经元的chemogenetic活化引起dmPFC锥体神经元的任务相关的编码属性的健壮降解和，在较小程度上，中型多棘神经元在背内侧纹状体。总的来说，这些结果表明尾dmPFC也妨碍frontostriatal认知和电路功能内的本地CRF释放和建议，CRF可能是一个潜在的目标治疗frontostriatal认知功能障碍。

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