Vickroy T W, Johnson K M
Neuropharmacology. 1983 Jul;22(7):839-42. doi: 10.1016/0028-3908(83)90129-6.
The effect of phencyclidine (PCP) on the release and synthesis of [3H]-dopamine ( [3H]-DA) newly synthesized from [3,5-3H]-L-tyrosine was studied under both basal and potassium-stimulated conditions in slices from the rat striatum. Phencyclidine (3-100 microM) stimulated the release of [3H]-DA during superfusion with low level potassium (4.5 mM) buffer, but had no effect on the release of [3H]-DA elicited by superfusion with buffer containing 40 mM potassium. On the other hand, phencyclidine had no effect (except at 100 microm) on the spontaneous release of [3H]-H2O (formed as a result of the hydroxylation of [3,5-3H]-L-tyrosine), but inhibited the increase in formation of [3H]-H2O normally associated with potassium-induced depolarization. These data are discussed in relation to results obtained with phencyclidine on other in vitro and in vivo models of dopaminergic function.
在基础条件和钾刺激条件下，研究了苯环己哌啶（PCP）对大鼠纹状体切片中由[3,5 - 3H] - L - 酪氨酸新合成的[3H] - 多巴胺（[3H] - DA）释放和合成的影响。苯环己哌啶（3 - 100 microM）在低水平钾（4.5 mM）缓冲液灌流期间刺激了[3H] - DA的释放，但对含40 mM钾的缓冲液灌流引发的[3H] - DA释放没有影响。另一方面，苯环己哌啶对[3H] - H2O（由[3,5 - 3H] - L - 酪氨酸羟基化形成）的自发释放没有影响（100 microM除外），但抑制了通常与钾诱导的去极化相关的[3H] - H2O生成增加。结合苯环己哌啶在其他多巴胺能功能的体外和体内模型中获得的结果对这些数据进行了讨论。
