ATTENTION, CORTICAL ACH RELEASE AND NEURONAL ACTIVITY

说明： 本研究的目的是为了确定大脑的认知功能 皮质乙酰胆碱(ACh)。大脑皮层ACh被假设为调节 注意力的过程，特别是持续的注意力。建议数 实验将评估大脑皮层ACh的注意功能 测定大鼠皮层ACh释放量和单位活动 执行为持续的测量设计和验证的任务 请注意。我们的初步实验表明，需求的增加 关于持续的注意力，由分心的东西和 由特定的表现障碍表示，与 内侧前额叶皮质ACh释放增加。另外， 观察到与注意力相关的神经元活动增加，并 被移除到记录区的胆碱能输入所阻断(产生 通过向录音中注入胆碱毒素192免疫球蛋白 字段)。拟议的研究将确定大脑皮层ACh在 持续关注：1)开发一系列分心装置，用于 系统地改变对注意力的要求；2)证明 在课税条件下的注意力表现主要取决于 皮质胆碱能传入系统的完整性；3)证明 注意力需求的增加与内科疾病的增加有关 前额叶ACh释放和单个单位活动的可预测变化；4) 证明与注意力相关的神经元活动增加 由于失去对记录区的胆碱能输入而受阻；以及5) 证明输注苯二氮卓类受体激动剂和 反向激动剂分别阻断和增强注意 大脑皮层ACh外流和神经元的表现相关增加 活动。总的来说，突触前(即ACh释放)和 注意相关变化的突触后(单单位活动)测量 大脑皮层ACh将产生一个关于大脑皮层作用的特定假说 集中注意力。特定认知功能的确定 皮质酸痛将导致对灾难性认知的更好理解 皮质胆碱能神经元完整性偏离的后果 传入器。

DESCRIPTION: The goal of this research is to determine the cognitive functions of cortical acetylcholine (ACh). Cortical ACh is hypothesized to mediate attentional processes, specifically sustained attention. The proposed experiments will assess the attentional functions of cortical ACh by measuring cortical ACh release and single unit activity in rats while they perform a task designed and validated for the measurement of sustained attention. Our preliminary experiments demonstrated that increased demands on sustained attention, caused by the presentation of distractors and indicated by specific impairments in performance, are associated with increases in ACh release in the medial prefrontal cortex. Additionally, attention-associated increases in neuronal activity were observed and blocked by the removal of cholinergic inputs to the recording area (produced by an infusion of the cholinotoxin 192 IgG-saporin into the recording field). The proposed research will determine the role of cortical ACh in sustained attention by : 1) developing a series of distractors which serve to systematically vary the demands on attention; 2) demonstrating that the attentional performance under taxing conditions depends critically on the integrity of the cortical cholinergic afferent system; 3) demonstrating that increased demands on attention are associated with increases in medial prefrontal ACh release and predictable shifts in single unit activity; 4) demonstrating that the attention-associated increases in neuronal activity are blocked by loss of cholinergic inputs to the recording area; and 5) demonstrating that infusions of a benzodiazepine receptor agonist and an inverse agonist block and augment, respectively, the attentional performance-associated increases in cortical ACh efflux and neuronal activity. Collectively, the presynaptic (i.e., ACh release) and postsynaptic (single unit activity) measures of attention-associated changes in cortical ACh will yield a specific hypothesis about the role of cortical ACh in attention. The determination of the specific cognitive functions of cortical ACh will lead to a better understanding of the disastrous cognitive consequences of deviations in the integrity of cortical cholinergic afferents.