BIOCHEMICAL STUDIES OF NEURONS AND OTHER CELL TYPES

九氨基酸核心肽（ADNF-9）的神经营养特性 来源于活动依赖性神经营养因子的研究， 从大鼠大脑皮层产生的细胞培养物。比较研究 ADNF-9在混合（胶质细胞+神经元）与胶质细胞缺失的 神经元培养表明ADNF-9可直接作用于神经元， 尽管在混合的情况下肽的效力是10,000倍 cultures. 动力学研究表明，暴露于ADNF-9， 小时足以产生针对细胞的四天保护 河豚毒素的杀灭作用。 巴弗洛霉素A1治疗2例 小时阻止了这种ADNF-9介导的神经保护作用。 ADNF抗血清 增加大脑皮层培养物中凋亡神经元的数量 降低脊髓胆碱乙酰转移酶活性 cultures. ADNP是一种具有共同表位和生物活性的克隆蛋白， 与ADNF的活性，定位于胚胎和成人中枢神经系统上， 小鼠原位杂交。滋养层细胞中检测到ADNP mRNA 和胎盘，在底板上有强烈的标记。 成人 脑中，ADNP mRNA在嗅球，丘脑， 海马和小脑。 妊娠小鼠抗ADNF给药 显著抑制胚胎生长并产生小头畸形。 来自抗ADNF治疗的母亲的后代表现出显著降低， 测试时，增量DRL时间表学习范例的性能 作为成年人 VIP是ADNF的促泌剂。 在妊娠小鼠中， 在E6时，滋养层细胞中VIP mRNA的瞬时增加 在E7。 VIP结合位点在E6滋养层细胞和E7滋养层细胞中丰富。 胚胎神经上皮和整个妊娠期的蜕膜。 VIP mRNA 直到E11-12才在小鼠胚胎中检测到。 早孕因子 (EPF)mRNA在成年小鼠的大脑中被检测到，但这 怀孕期间丘脑核和皮质的强度更大。 EPF mRNA也存在于胚胎神经上皮和胚胎神经细胞中。 从E6到E12的羊膜和滋养层细胞膜周围。 一个 EPF的活性肽被证明可以阻止生长抑制 人类免疫缺陷病毒包膜蛋白gp 120的作用 病毒

The neurotrophic properties of a nine amino acid core peptide (ADNF-9) derived from activity dependent neurotrophic factor was investigated in cell cultures produced from the rat cerebral cortex. Comparative studies of ADNF-9 action in mixed (glia plus neurons) versus glia-depleted neuronal cultures indicated that ADNF-9 can act directly on neurons, although the potency of the peptide was 10,000-fold greater in mixed cultures. Kinetic studies showed that exposure to ADNF-9 for only two hours was sufficient to produce a four day protection against the cell killing action of tetrodotoxin. Treatment with bafilomycin A1 for two hours prevented this ADNF-9-mediated neuroprotection. Antiserum to ADNF increased the number of apoptotic neurons in cerebral cortical cultures and decreased the activity of choline acetyltransferase in spinal cord cultures. ADNP, a cloned protein with shared epitopes and biological activity with ADNF, was localized in the embryonic and adult CNS on the mouse by in situ hybridization. ADNP mRNA was detected in the trophoblast and the placenta, with intense labeling in the floor plate. In adult brain, ADNP mRNA was especially intense in the olfactory bulb, thalamus, hippocampus and cerebellum. Administration of anti-ADNF to pregnant mice significantly inhibited embryonic growth and produced microcephaly. Progeny from anti-ADNF-treated mothers exhibited significant decreases in performance on an incremental DRL schedule learning paradigm when tested as adults. VIP is a secretagogue of ADNF. In the pregnant mouse, a transient increase in mRNA for VIP was found in the trophoblast at E6 and E7. VIP binding sites were abundant in the E6 trophoblast and in the embryonic neuroepithelium and decidua throughout pregnancy. VIP mRNA was not detected in the mouse embryo until E11-12. Early pregnancy factor (EPF) mRNA was detected throughout the brains of adult mice, but this greater intensity in the thalamic nuclei and cortex during pregnancy. EPF mRNA was also present in the embryonic neuroepithelium and the surrounding amniotic and trophoblastic membranes from E6 to E12. An active peptide from EPF was shown to prevent the growth-inhibitory effects of gp120, the envelope protein from the human immunodeficiency virus.