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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Lapchak P A, Hefti F

Andrus Gerontology Center, University of Southern California, Los Angeles.

Prog Neuropsychopharmacol Biol Psychiatry. 1991;15(6):851-60. doi: 10.1016/0278-5846(91)90013-q.

Partial transection of the septo-hippocampal pathway decreased measures of presynaptic cholinergic function in the rat hippocampal formation. 2. Chronic intraventricular treatment with recombinant human nerve growth factor attenuated lesioned-induced deficits in cholinergic function. Following nerve growth factor treatment measures of choline acetyltransferase activity, acetylcholine synthesis and release were significantly increased compared to cytochrome c-treated lesioned animals. 3. Single injections of nerve growth factor were ineffective in altering lesioned-induced deficits in cholinergic function. 4. Chronic nerve growth factor treatment was ineffective in increasing presynaptic cholinergic function if administered 3 or more weeks following fimbrial transections. 5. The nerve growth factor-induced increases of presynaptic cholinergic function persisted for 3 weeks following the cessation of chronic 3 week nerve growth factor treatment.

隔海马通路的部分横断降低了大鼠海马结构中突触前胆碱能功能的指标。2. 用重组人神经生长因子进行慢性脑室内治疗可减轻损伤诱导的胆碱能功能缺陷。与细胞色素c处理的损伤动物相比，神经生长因子治疗后胆碱乙酰转移酶活性、乙酰胆碱合成和释放的指标显著增加。3. 单次注射神经生长因子对改变损伤诱导的胆碱能功能缺陷无效。4. 如果在纤维横断后3周或更长时间给予慢性神经生长因子治疗，则对增加突触前胆碱能功能无效。5. 在持续3周的慢性神经生长因子治疗停止后，神经生长因子诱导的突触前胆碱能功能增加持续了3周。

Lapchak P A, Hefti F

Andrus Gerontology Center, University of Southern California, Los Angeles.

Prog Neuropsychopharmacol Biol Psychiatry. 1991;15(6):851-60. doi: 10.1016/0278-5846(91)90013-q.

Partial transection of the septo-hippocampal pathway decreased measures of presynaptic cholinergic function in the rat hippocampal formation. 2. Chronic intraventricular treatment with recombinant human nerve growth factor attenuated lesioned-induced deficits in cholinergic function. Following nerve growth factor treatment measures of choline acetyltransferase activity, acetylcholine synthesis and release were significantly increased compared to cytochrome c-treated lesioned animals. 3. Single injections of nerve growth factor were ineffective in altering lesioned-induced deficits in cholinergic function. 4. Chronic nerve growth factor treatment was ineffective in increasing presynaptic cholinergic function if administered 3 or more weeks following fimbrial transections. 5. The nerve growth factor-induced increases of presynaptic cholinergic function persisted for 3 weeks following the cessation of chronic 3 week nerve growth factor treatment.

隔海马通路的部分横断降低了大鼠海马结构中突触前胆碱能功能的指标。2. 用重组人神经生长因子进行慢性脑室内治疗可减轻损伤诱导的胆碱能功能缺陷。与细胞色素c处理的损伤动物相比，神经生长因子治疗后胆碱乙酰转移酶活性、乙酰胆碱合成和释放的指标显著增加。3. 单次注射神经生长因子对改变损伤诱导的胆碱能功能缺陷无效。4. 如果在纤维横断后3周或更长时间给予慢性神经生长因子治疗，则对增加突触前胆碱能功能无效。5. 在持续3周的慢性神经生长因子治疗停止后，神经生长因子诱导的突触前胆碱能功能增加持续了3周。