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首页> 外文期刊>Journal of Neurophysiology >Transplants of NGF-secreting fibroblasts restore stimulus-evoked activity in barrel cortex of basal-forebrain-lesioned rats.
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Transplants of NGF-secreting fibroblasts restore stimulus-evoked activity in barrel cortex of basal-forebrain-lesioned rats.

机译：分泌NGF的成纤维细胞的移植恢复了基底前脑病变大鼠的桶皮质的刺激诱发活性。

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摘要

Cholinergic nuclei in the basal forebrain supply the cerebral cortex with acetylcholine (ACh). Depletion of cholinergic fibers following basal forebrain lesion results in reduced stimulus-evoked functional activity in rat barrel cortex in response to whisker stimulation. We showed previously that exogenous delivery of nerve growth factor (NGF) to the lateral ventricle restores reduced functional activity toward normal despite persistent reductions in cortical cholinergic activity. Gene transfer of therapeutic peptides using genetically engineered cells allows for localized and biological delivery of compounds to the CNS, circumventing systemic administration or repetitive invasive surgery. In this study, we grafted genetically engineered fibroblasts that secrete NGF (NGF+) into three CNS loci of rats with unilateral basal forebrain lesions, along with control fibroblasts (NGF-) that did not secrete NGF. Only NGF+ fibroblasts grafted into ACh-depleted somatosensory cortex resulted in improvement of functional activity following cholinergic depletion. NGF+ fibroblast transplants into the lateral ventricle or basal forebrain did not improve functional activity nor did NGF- fibroblasts in any site. Similar to our previous experiments using intraventricular NGF injections, despite improvements in functional activity, the affected barrel cortex remained depleted of acetylcholinesterase-stained fibers following insertion of NGF+ fibroblasts. These data support the idea that NGF can act directly on the cerebral cortex following reductions in cholinergic innervation. The mechanism of NGF action is elusive, however, since the presence of its high-affinity receptor, trkA, in the cerebral cortex is controversial.
机译：基底前脑的胆碱能核为大脑皮层提供乙酰胆碱（ACh）。基底前脑病变后胆碱能纤维的耗竭导致大鼠晶须皮中的晶须刺激引起的刺激诱发的功能活性降低。我们先前显示，尽管皮质胆碱能活性持续降低，但神经生长因子（NGF）向侧脑室的外源性递送可恢复正常的功能活性。使用基因工程细胞进行治疗性肽的基因转移，可将化合物局部和生物递送至CNS，从而避免了全身性给药或重复性侵入性手术。在这项研究中，我们将分泌NGF（NGF +）的基因工程成纤维细胞与不分泌NGF的对照成纤维细胞（NGF-）移植到了具有单侧基底前脑病变的大鼠的三个CNS基因座中。胆碱能耗竭后，仅将NGF +成纤维细胞移植到ACh缺乏的体感皮层中可以改善功能活性。 NGF +成纤维细胞移植到侧脑室或基底前脑中并没有改善功能活性，NGF-成纤维细胞也没有改善任何部位。与我们先前使用脑室内NGF注射的实验相似，尽管功能活性有所改善，但在插入NGF +成纤维细胞后，受影响的桶状皮质仍缺乏乙酰胆碱酯酶染色的纤维。这些数据支持了NGF在胆碱能神经支配减少后可以直接作用于大脑皮层的想法。但是，NGF作用的机制尚不清楚，因为它在大脑皮层中的高亲和力受体trkA的存在是有争议的。

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