Johnston M V, McKinney M, Coyle J T
Exp Brain Res. 1981;43(2):159-72. doi: 10.1007/BF00237760.
Electrothermic lesion of the peri-pallidal region of the rat caused a marked reduction in the activity of choline acetyltransferase in the ipsilateral fronto-parietal cortex without affecting the activity of glutamate decarboxylase. Only lesions that involved the ventral globus pallidus significantly reduced cortical choline acetyltransferase activity; and lesions limited to the thalamus, internal capsule, pyriform cortex or zone incerta were ineffective. Excito-toxin lesions of the ventral globus pallidus caused 45-5% reductions in all presynaptic markers for cholinergic neurons but did not significantly decrease presynaptic markers for noradrenergic, serotonergic or histaminergic neurons in the cortex. The maximal reductions in cortical choline acetyltransferase activity achieved with the pallidal lesion was 70%; and enzyme activity reached its nadir by four days after placement of the lesion. The pallidal lesion, which ablated the large isodendritic acetylcholinesterase positive neuronal perikarya, resulted in a profound loss in histochemically stained acetylcholinesterase-reactive fibers in the fronto-parietal cortex but not in the cingulate, pyriform and occipital cortex or hippocampal formation; analysis of the subregions in choline acetyltransferase activity. The kainate lesion of the parietal cortex to ablate intrinsic neurons did not reduce the activity of tyrosine hydroxylase, a marker for noradrenergic terminals, but depressed glutamate decarboxylase by 68%; in contrast choline acetyltransferase activity fell only 29%. The results indicate that approximately 70% of the cholinergic innervation in the fronto-parietal cortex is derived from acetylcholinesterase positive neurons in the peripallidal nucleus basalis, whereas the remainder appears to be localized in cortical intrinsic neurons.
大鼠苍白球周围区域的电热损伤导致同侧额顶叶皮质中胆碱乙酰转移酶的活性显著降低，而谷氨酸脱羧酶的活性未受影响。只有累及腹侧苍白球的损伤才会显著降低皮质胆碱乙酰转移酶的活性；而仅限于丘脑、内囊、梨状皮质或未定带的损伤则无效。腹侧苍白球的兴奋性毒素损伤导致胆碱能神经元所有突触前标志物减少45%-5%，但并未显著降低皮质中去甲肾上腺素能、5-羟色胺能或组胺能神经元的突触前标志物。苍白球损伤导致皮质胆碱乙酰转移酶活性最大降低70%；损伤后四天酶活性降至最低点。苍白球损伤破坏了大的异树突状乙酰胆碱酯酶阳性神经元胞体，导致额顶叶皮质中组织化学染色的乙酰胆碱酯酶反应性纤维大量丧失，但扣带回、梨状皮质、枕叶皮质或海马结构中未出现这种情况；对胆碱乙酰转移酶活性亚区域的分析。顶叶皮质的海藻酸损伤以破坏内在神经元，但并未降低去甲肾上腺素能终末标志物酪氨酸羟化酶的活性，却使谷氨酸脱羧酶降低了68%；相比之下，胆碱乙酰转移酶活性仅下降了29%。结果表明，额顶叶皮质中约70%的胆碱能神经支配来自苍白球周围基底核中的乙酰胆碱酯酶阳性神经元，而其余部分似乎定位于皮质内在神经元。
