Ma W, Höhmann C F, Coyle J T, Juliano S L
Department of Anatomy, USUHS, Bethesda, Maryland 20814.
J Comp Neurol. 1989 Oct 15;288(3):414-27. doi: 10.1002/cne.902880305.
The role that acetylcholine plays in processing sensory stimuli is beginning to be characterized; however, morphological correlates of cholinergic effects on activity patterns in sensory cortex are not available. To study this problem, unilateral neurotoxic lesions that depleted the necortex of acetylcholine were made in the basal forebrains of mice. The aim of these experiments was to study the effect of cholinergic depletion on stimulus-evoked activity in the barrel field of the mouse somatosensory cortex. One month following the lesion, 2-deoxyglucose (2DG) experiments were conducted on the lesioned and on normal mice while the animal received bilateral stimulation to the C3 whisker. The tissue was processed for acetylcholinesterase and cytochrome oxidase histochemistry and 2DG autoradiography. Evaluation of the column-like 2DG label evoked in the somatosensory cortex revealed that the activity on the lesioned side was significantly reduced in dimension and intensity from that in the normal hemisphere. On the normal side, the activated barrels averaged 641 microns in tangential width, were 76.5% above background in density, and extended from lamina I-V. On the lesioned side, the activated barrels were 485 microns in tangential width, 65.4% above background in density, and extended from lamina II-V. In other cortical regions, outside the stimulus-evoked barrel field, 2DG activity values were similar on the normal and lesioned side. Additionally, both the pattern and intensity of the cytochrome oxidase staining within the barrel field displayed no differences in either hemisphere. These studies suggest that acetylcholine plays a significant role in the processing of somatosensory information. Neurotoxic lesions that diminish cortical cholinergic innervation cause a reduction of stimulus-evoked activity levels, while underlying metabolic activity is either not affected or recovers over time.
乙酰胆碱在处理感觉刺激中所起的作用正开始得到描述；然而，胆碱能效应对感觉皮层活动模式的形态学关联尚不清楚。为研究此问题，在小鼠基底前脑制作了使新皮质乙酰胆碱耗竭的单侧神经毒性损伤。这些实验的目的是研究胆碱能耗竭对小鼠体感皮层桶状区刺激诱发活动的影响。损伤后一个月，在损伤小鼠和正常小鼠身上进行2-脱氧葡萄糖（2DG）实验，同时对动物的C3胡须进行双侧刺激。对组织进行乙酰胆碱酯酶和细胞色素氧化酶组织化学以及2DG放射自显影处理。对体感皮层诱发的柱状2DG标记的评估显示，损伤侧的活动在维度和强度上均显著低于正常半球。在正常侧，激活的桶状结构切向宽度平均为641微米，密度比背景高76.5%，并从I - V层延伸。在损伤侧，激活的桶状结构切向宽度为485微米，密度比背景高65.4%，并从II - V层延伸。在刺激诱发的桶状区之外的其他皮质区域，正常侧和损伤侧的2DG活性值相似。此外，桶状区内细胞色素氧化酶染色的模式和强度在两个半球均无差异。这些研究表明，乙酰胆碱在体感信息处理中起重要作用。减少皮质胆碱能神经支配的神经毒性损伤会导致刺激诱发活动水平降低，而潜在的代谢活动要么不受影响，要么随时间恢复。
