ATTENTION, CORTICAL ACH RELEASE AND NEURONAL ACTIVITY

产品说明： 这项研究的目的是确定认知功能， 皮质乙酰胆碱（ACh）。 假设皮质ACh介导 注意力过程，特别是持续的注意力。 拟议 实验将通过以下方式评估皮质ACh的注意力功能： 测量大鼠皮层ACh释放和单个单位活性， 执行一项为衡量持续的 关注 我们的初步实验表明， 持续的注意力，由干扰物的呈现引起， 表现出的具体损害，与 内侧前额叶皮层的乙酰胆碱释放增加。 此外，本发明还 观察到与注意力相关的神经元活动增加， 通过移除记录区域的胆碱能输入（产生 通过将胆碱毒素192 IgG-皂草素输注到记录中， field）。 这项拟议的研究将确定皮质ACh在 通过以下方式保持注意力：1）开发一系列分散注意力的东西， 系统地改变对注意力的要求; 2）证明， 在繁重的条件下，注意力的表现主要取决于 皮质胆碱能传入系统的完整性; 3）证明， 对注意力的需求增加与媒体的增加有关。 前额叶ACh释放和单个单位活动的可预测变化; 4） 证明了与注意力相关的神经元活动的增加 被记录区胆碱能输入的损失所阻断;以及5） 这表明，苯二氮卓受体激动剂和 反向激动剂分别阻断和增强注意力， 与成绩相关的皮质ACh流出和神经元 活动 总的来说，突触前（即，乙酰胆碱释放）和 注意力相关变化的突触后（单个单位活动）测量 在皮质ACh的作用将产生一个特定的假设， 注意。 特定认知功能的确定 皮质ACh将导致更好地理解灾难性的认知 皮质胆碱能神经系统完整性偏差的后果 传入神经

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.