Abstract
Neuronal uptake recognition sites in norepinephrine neurons have been labeled with the antidepressant [3H]desipramine. A high-affinity component of [3H]desipramine binding to rat cerebral cortex membranes is abolished selectively by 6-hydroxydopamine lesions, which destroy central catecholamine neurons. The high-affinity [3H]desipramine binding has a nanomolar affinity constant for desipramine and is inhibited by tricyclic antidepressants with potencies that correlate with their ability to inhibit the neuronal uptake of norepinephrine. [3H]Desipramine binding to the uptake sites is markedly stimulated by sodium, with potassium, lithium, and choline being much less effective. The ability to monitor norepinephrine neuronal uptake "receptors" in simple binding studies should permit a differential analysis of drug influences on the norepinephrine recognition site and the translocation mechanism. The regulation of [3H]desipramine binding by sodium may help clarify how sodium influences neurotransmitter uptake.