Effect of antidepressant drugs in mice lacking the norepinephrine transporter

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology
Marta Dziedzicka-WasylewskaHeinz Bönisch


One of the main theories concerning the mechanism of action of antidepressant drugs (ADs) is based on the notion that the neurochemical background of depression involves an impairment of central noradrenergic transmission with a concomitant decrease of the norepinephrine (NE) in the synaptic gap. Many ADs increase synaptic NE availability by inhibition of the reuptake of NE. Using mice lacking NE transporter (NET-/-) we examined their baseline phenotype as well as the response in the forced swim test (FST) and in the tail suspension test (TST) upon treatment with ADs that display different pharmacological profiles. In both tests, the NET-/- mice behaved like wild-type (WT) mice acutely treated with ADs. Autoradiographic studies showed decreased binding of the beta-adrenergic ligand [3H]CGP12177 in the cerebral cortex of NET-/- mice, indicating the changes at the level of beta-adrenergic receptors similar to those obtained with ADs treatment. The binding of [3H]prazosin to alpha1-adrenergic receptors in the cerebral cortex of NET-/- mice was also decreased, most probably as an adaptive response to the sustained elevation of extracellular NE levels observed in these mice. A pronounced NET knockout-induced shortening of the immobi...Continue Reading


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