Desipramine binding: relationship to central and sympathetic noradrenergic activity.

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.

journal_name

J Neurochem

authors

Swann AC,Duman R,Hewitt L

doi

10.1111/j.1471-4159.1985.tb05455.x

subject

Has Abstract

pub_date

1985-02-01 00:00:00

pages

611-5

issue

2

eissn

0022-3042

issn

1471-4159

journal_volume

44

pub_type

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