Swann A C, Duman R, Hewitt L
J Neurochem. 1985 Feb;44(2):611-5. doi: 10.1111/j.1471-4159.1985.tb05455.x.
We examined the effects of treatments affecting norepinephrine release on the number of norepinephrine reuptake recognition sites as reflected by desipramine binding. To do this, we used manipulations having similar presynaptic but contrasting postsynaptic effects. Presynaptic inhibition by 6-hydroxydopamine lesion or by clonidine, and postsynaptic receptor stimulation by isoproterenol, reduced desipramine binding. Presynaptic stimulation by d-amphetamine and postsynaptic receptor blockade by prazosin increased desipramine binding. Similar effects and binding properties were seen in cerebral cortex, heart, and soleus muscle. After unilateral noradrenergic lesions, reduction in desipramine binding correlated with reduction in norepinephrine uptake. These results show that norepinephrine reuptake appears to be regulated by transmitter release regardless of effects on postsynaptic transmission, and that this regulation is analogous in the central and sympathetic nervous systems.
我们研究了影响去甲肾上腺素释放的处理对以地昔帕明结合反映的去甲肾上腺素再摄取识别位点数量的影响。为此，我们采用了具有相似突触前但相反突触后效应的操作方法。用6-羟基多巴胺损伤或可乐定进行突触前抑制，以及用异丙肾上腺素进行突触后受体刺激，均可降低地昔帕明结合。用d-苯丙胺进行突触前刺激，并用哌唑嗪进行突触后受体阻断，可增加地昔帕明结合。在大脑皮层、心脏和比目鱼肌中观察到了类似的效应和结合特性。单侧去甲肾上腺素能损伤后，地昔帕明结合的减少与去甲肾上腺素摄取的减少相关。这些结果表明，无论对突触后传递的影响如何，去甲肾上腺素再摄取似乎受递质释放的调节，并且这种调节在中枢和交感神经系统中是相似的。
