Gribkoff V K, Bauman L A, VanderMaelen C P
Bristol-Myers Squibb Pharmaceutical Research Institute, Wallingford, Connecticut 06492.
Neuropharmacology. 1990 Nov;29(11):1001-9. doi: 10.1016/0028-3908(90)90105-z.
The effects of the substituted pyrrolidinone, BMY 21502, on the properties of cell membranes, synaptic transmission and synaptic plasticity, were assessed in area CA1 of hippocampal slices from the rat. Application of the compound to the bath had no consistent direct effects on parameters of the cell membrane or evoked synaptic potentials, at concentrations of less than 30 microM. In a blind experimental design, BMY 21502 at 1.0 and 10 microM, but not 25 microM, significantly delayed the decay of long-term potentiation in slices obtained from young animals; in slices obtained from very old rats (2.5-3.2 yr), 10 microM BMY 21502 significantly delayed decay of long-term potentiation. Therefore BMY 21502 was active in a physiological model that may predict of cognitive enhancement.
在大鼠海马切片的CA1区评估了取代吡咯烷酮BMY 21502对细胞膜特性、突触传递和突触可塑性的影响。在浓度低于30微摩尔时，将该化合物应用于浴液对细胞膜参数或诱发的突触电位没有一致的直接影响。在一项盲法实验设计中，1.0和10微摩尔的BMY 21502（而非25微摩尔）显著延迟了幼年动物切片中长时程增强的衰减；在非常年老的大鼠（2.5 - 3.2岁）的切片中，10微摩尔的BMY 21502显著延迟了长时程增强的衰减。因此，BMY 21502在一个可能预测认知增强的生理模型中具有活性。
