文献检索，用中文搜 PubMed

Suppr 超能文献

核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Higashida H, Hoshi N, Knijnik R, Zadina J E, Kastin A J

Department of Biophysics, Kanazawa University School of Medicine, Kanazawa 920, Japan.

J Physiol. 1998 Feb 15;507 ( Pt 1)(Pt 1):71-5. doi: 10.1111/j.1469-7793.1998.071bu.x.

Extracellular application of the novel brain peptides endomorphin 1 (EM1) and endomorphin 2 (EM2) inhibited high-threshold Ca2+ channel currents in NGMO-251 cells, a daughter clone of NG108-15 mouse neuroblastoma x rat glioma hybrid cells, in which mu-opioid receptors are overexpressed. 2. In contrast, EM1 and EM2 did not induce this inhibition in the parental NG108-15 cells that predominantly express endogenous delta-receptors. 3. The IC50 for EM1 and EM2 was 7.7 and 23.1 nM, respectively. 4. EM-induced Ca2+ channel current inhibition was blocked by treatment or pretreatment of the cells with 100 microM N-methylmaleimide or 100 ng ml-1 pertussis toxin. 5. These results show that a decrease in conductance of Ca2+ channels results following interaction of EMs with cloned mu-receptors, which couple via Gi/Go-type G proteins, and that EMs fulfill one of the necessary synaptic conditions for them to be identified as neurotransmitters.

新型脑肽内吗啡肽1（EM1）和内吗啡肽2（EM2）在细胞外应用时，可抑制NGMO - 251细胞（NG108 - 15小鼠神经母细胞瘤x大鼠胶质瘤杂交细胞的子代克隆，其中μ - 阿片受体过表达）中的高阈值Ca2 +通道电流。2. 相比之下，EM1和EM2在主要表达内源性δ受体的亲代NG108 - 15细胞中未诱导这种抑制作用。3. EM1和EM2的IC50分别为7.7和23.1 nM。4. 用100 microM N - 甲基马来酰亚胺或100 ng/ml百日咳毒素处理或预处理细胞可阻断EM诱导的Ca2 +通道电流抑制。5. 这些结果表明，EMs与克隆的μ受体相互作用后，Ca2 +通道的电导降低，这些受体通过Gi/Go型G蛋白偶联，并且EMs满足将它们鉴定为神经递质的必要突触条件之一。

Higashida H, Hoshi N, Knijnik R, Zadina J E, Kastin A J

Department of Biophysics, Kanazawa University School of Medicine, Kanazawa 920, Japan.

J Physiol. 1998 Feb 15;507 ( Pt 1)(Pt 1):71-5. doi: 10.1111/j.1469-7793.1998.071bu.x.

Extracellular application of the novel brain peptides endomorphin 1 (EM1) and endomorphin 2 (EM2) inhibited high-threshold Ca2+ channel currents in NGMO-251 cells, a daughter clone of NG108-15 mouse neuroblastoma x rat glioma hybrid cells, in which mu-opioid receptors are overexpressed. 2. In contrast, EM1 and EM2 did not induce this inhibition in the parental NG108-15 cells that predominantly express endogenous delta-receptors. 3. The IC50 for EM1 and EM2 was 7.7 and 23.1 nM, respectively. 4. EM-induced Ca2+ channel current inhibition was blocked by treatment or pretreatment of the cells with 100 microM N-methylmaleimide or 100 ng ml-1 pertussis toxin. 5. These results show that a decrease in conductance of Ca2+ channels results following interaction of EMs with cloned mu-receptors, which couple via Gi/Go-type G proteins, and that EMs fulfill one of the necessary synaptic conditions for them to be identified as neurotransmitters.

新型脑肽内吗啡肽1（EM1）和内吗啡肽2（EM2）在细胞外应用时，可抑制NGMO - 251细胞（NG108 - 15小鼠神经母细胞瘤x大鼠胶质瘤杂交细胞的子代克隆，其中μ - 阿片受体过表达）中的高阈值Ca2 +通道电流。2. 相比之下，EM1和EM2在主要表达内源性δ受体的亲代NG108 - 15细胞中未诱导这种抑制作用。3. EM1和EM2的IC50分别为7.7和23.1 nM。4. 用100 microM N - 甲基马来酰亚胺或100 ng/ml百日咳毒素处理或预处理细胞可阻断EM诱导的Ca2 +通道电流抑制。5. 这些结果表明，EMs与克隆的μ受体相互作用后，Ca2 +通道的电导降低，这些受体通过Gi/Go型G蛋白偶联，并且EMs满足将它们鉴定为神经递质的必要突触条件之一。