Lapchak P A, Araujo D M
Department of Neurogerontology, University of Southern California, Los Angeles 90089-0191.
Brain Res. 1994 Aug 15;654(1):1-7. doi: 10.1016/0006-8993(94)91564-4.
The present study determined whether chronic intracerebroventricular (i.c.v.) nerve growth factor (NGF) treatment alters the hippocampal content of vasoactive intestinal peptide (VIP) or neuropeptide Y (NPY) in rats with unilateral fimbrial transections. In addition, effects of chronic NGF treatment on cortical VIP and NPY levels were determined. Following partial and full fimbrial transections, hippocampal choline acetyltransferase (ChAT) activity was reduced by 41% and 60% ipsilateral to the lesioned side, respectively. Chronic NGF treatment partially attenuated (by 48%) the reduction of ChAT following partial lesions, but not full lesions. Neither the hippocampal contents of VIP or NPY were altered by partial or full fimbrial transections nor by chronic NGF treatment. However, in the NGF-treated rats, significant increases not only in cortical ChAT activity (by 28%), but also cortical VIP levels (by 68%) were observed. Cortical NPY levels remained unchanged following chronic NGF administration. In summary, the results suggest that the increases in cortical VIP levels observed in chronic NGF-treated rats may be specific to this tissue and consequent to the enhanced cholinergic tone exerted by this neurotrophin in the basalocortical pathway. Additionally, it appears that NGF when administered in pharmacological doses is not involved in the regulation of NPY synthesis in the hippocampus or cortex despite the presence of an NGF-responsive element associated with the rat NPY gene.
本研究确定了慢性脑室内（i.c.v.）注射神经生长因子（NGF）治疗是否会改变单侧海马伞横断大鼠海马中血管活性肠肽（VIP）或神经肽Y（NPY）的含量。此外，还确定了慢性NGF治疗对皮质VIP和NPY水平的影响。部分和完全海马伞横断后，损伤侧同侧海马胆碱乙酰转移酶（ChAT）活性分别降低了41%和60%。慢性NGF治疗部分减轻了（48%）部分损伤后ChAT的降低，但对完全损伤无效。部分或完全海马伞横断以及慢性NGF治疗均未改变海马中VIP或NPY的含量。然而，在接受NGF治疗的大鼠中，不仅观察到皮质ChAT活性显著增加（28%），还观察到皮质VIP水平显著增加（68%）。慢性给予NGF后，皮质NPY水平保持不变。总之，结果表明，在慢性NGF治疗的大鼠中观察到的皮质VIP水平升高可能是该组织特有的，并且是由于这种神经营养因子在基底皮质通路中增强胆碱能张力所致。此外，尽管大鼠NPY基因存在NGF反应元件，但以药理剂量给药的NGF似乎不参与海马或皮质中NPY合成的调节。
