Title : Brain-derived tumor necrosis factor-alpha and its involvement in noradrenergic neuron functioning involved in the mechanism of action of an antidepressant.

Pub. Date : 2004 Sep

PMID : 15082752






6 Functional Relationships(s)
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1 The present study documents a role for brain-derived tumor necrosis factor-alpha (TNF) in the mechanism of action of the antidepressant drug desmethylimipramine (desipramine). Desipramine tumor necrosis factor Rattus norvegicus
2 The present study documents a role for brain-derived tumor necrosis factor-alpha (TNF) in the mechanism of action of the antidepressant drug desmethylimipramine (desipramine). Desipramine tumor necrosis factor Rattus norvegicus
3 Chronic desipramine administration transforms TNF-mediated inhibition of NE release to facilitation, dependent upon alpha2-adrenergic receptor activation. Desipramine tumor necrosis factor Rattus norvegicus
4 To determine whether this transformation is due to desipramine-induced inhibition of TNF bioactivity in the brain, rats were i.c.v. Desipramine tumor necrosis factor Rattus norvegicus
5 Although simultaneous microinfusion of rrTNF with chronic desipramine administration prevents the transformation induced by desipramine, microinfusion of rrTNF enhances TNF inhibition of NE release. Desipramine tumor necrosis factor Rattus norvegicus
6 microinfusion of rrTNF with concomitant desipramine administration opposes decreases in neuron-associated TNF levels, required to transform presynaptic sensitivity to TNF, which is necessary for the drug to be efficacious. Desipramine tumor necrosis factor Rattus norvegicus