Key result
Repeated administration of desipramine decreased [3H]nisoxetine binding by 20-40% in 8 of 17 rat brain regions, whereas chronic electroconvulsive shock had minimal effects.
Desipramine downregulates NET binding in select rat brain regions unlike ECS; hypothesis-generating for mechanisms, requires human validation before clinical relevance.
To determine if repeated administration of desipramine (DMI) or electroconvulsive shock (ECS) regulate uptake sites for norepinephrine (NE) in rat brain, the binding of [3H]nisoxetine ([3H]NIS) was measured using quantitative autoradiography. Groups of animals were given DMI intraperitoneally, either a single injection or repeated doses of 10 mg/kg once daily for 21 days and were killed 48 h after the last injection. Another group of rats received ECS daily for 12 days (150 mA, 300 ms, 60 Hz) and was killed 24 h after the last shock. Repeated administration of DMI caused statistically significant decreases (20-40%) in the binding of [3H]NIS in 8 out of 17 brain regions measured; these areas included the hippocampus, thalamus and the amygdala. Acute treatment with DMI had no effect on the binding of [3H]NIS in any of the regions analyzed except the centrolateral nucleus of the amygdala. By contrast, except for the paraventricular nucleus of the thalamus where ECS caused a modest (20%) increase in binding, no other brain region was affected by ECS. Thus it appears that repeated administration of DMI and chronic ECS treatment have different effects on the binding of [3H]NIS to uptake sites for NE in rat brain.
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Bauer et al. (1992) studied this question. Desipramine (DMI) or electroconvulsive shock (ECS) was evaluated on Binding of [3H]nisoxetine ([3H]NIS) to norepinephrine uptake sites. Repeated administration of desipramine decreased [3H]nisoxetine binding by 20-40% in 8 of 17 rat brain regions, whereas chronic electroconvulsive shock had minimal effects.
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