ArticleBiochemical and biophysical research communications2012
Desipramine selectively potentiates norepinephrine-elicited ERK1/2 activation through the α2A adrenergic receptor.
Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Compromised trigemino-coerulean coupling in migraine sensitization can be prevented by blocking beta-receptors in the locus coeruleus.The journal of headache and pain · 2023Article
- Tricyclic antipsychotics promote adipogenic gene expression to potentiate preadipocyte differentiation in vitro.Human cell · 2020Article
- Norepinephrine upregulates the expression of tyrosine hydroxylase and protects dopaminegic neurons against 6-hydrodopamine toxicity.Neurochemistry international · 2019Article
- Noradrenergic Modulation on Dopaminergic Neurons.Neurotoxicity research · 2018Review
- Diverse arrestin-recruiting and endocytic profiles of tricyclic antipsychotics acting as direct αNeuropharmacology · 2017Article
- Effects of anti-depressant treatments on FADD and p-FADD protein in rat brain cortex: enhanced anti-apoptotic p-FADD/FADD ratio after chronic desipramine and fluoxetine administration.Psychopharmacology · 2016Article
- Activation of α2A-adrenergic signal transduction in chondrocytes promotes degenerative remodelling of temporomandibular joint.Scientific reports · 2016Article
- Hypertension overrides the protective effect of female hormones on the development of aortic aneurysm secondary to Alk5 deficiency via ERK activation.American journal of physiology. Heart and circulatory physiology · 2015Article
- Tricyclic antidepressants exhibit variable pharmacological profiles at the α(2A) adrenergic receptor.Biochemical and biophysical research communications · 2014Article
- Rare Genomic Variants Link Bipolar Disorder with Anxiety Disorders to CREB-Regulated Intracellular Signaling Pathways.Frontiers in psychiatry · 2013Article
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3 authors.
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Abstract
The precise physiological effects of antidepressant drugs, and in particular their actions at non-monoamine transporter targets, are largely unknown. We have recently identified the tricyclic antidepressant drug desipramine (DMI) as a direct ligand at the α(2A) adrenergic receptor (AR) without itself driving heterotrimeric G protein/downstream effector activation [5]. In this study, we report our novel finding that DMI modulates α(2A)AR signaling in response to the endogenous agonist norepinephrine (NE). DMI acted as a signaling potentiator, selectively enhancing NE-induced α(2A)AR-mediated ERK1/2 MAPK signaling. This potentiation of ERK1/2 activation was observed as an increase in NE response sensitivity and a prolongation of the activation kinetics. DMI in a physiologically relevant ratio with NE effectively turned on ERK1/2 signaling that is lacking in response to physiological NE alone. Further, the DMI-induced ERK1/2 potentiation relied on heterotrimeric G(i/o) proteins and was arrestin-independent. This modulatory effect of DMI on NE signaling provides novel insight into the effects of this antidepressant drug on the noradrenergic system which it regulates, insight which enhances our understanding of the therapeutic mechanism for DMI.
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