Desipramine Binding: Relationship to Central and Sympathetic Noradrenergic Activity
Article first published online: 5 OCT 2006
Journal of Neurochemistry
Volume 44, Issue 2, pages 611–615, February 1985
How to Cite
Swann, A. C., Duman, R. and Hewitt, L. (1985), Desipramine Binding: Relationship to Central and Sympathetic Noradrenergic Activity. Journal of Neurochemistry, 44: 611–615. doi: 10.1111/j.1471-4159.1985.tb05455.x
- Issue published online: 5 OCT 2006
- Article first published online: 5 OCT 2006
- Received April 10, 1984; accepted July 28, 1984.
- Desipramine binding;
- Norepinephrine uptake;
- Noradrenergic lesions;
- Soleus muscle
Abstract: 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.