PE-22-28

TREK1 channel blockade induces an antidepressant-like response synergizing with 5-HT1A receptor signaling

Shortened Spadin Analogs Display Better TREK-1 Inhibition, In Vivo Stability and Antidepressant Activity

Spadin, a sortilin-derived peptide, targeting rodent TREK-1 channels: a new concept in the antidepressant drug design.

Spadin as a new antidepressant: absence of TREK-1-related side effects.

Retroinverso analogs of spadin display increased antidepressant effects.

The peptidic antidepressant spadin interacts with prefrontal 5-HT(4) and mGluR(2) receptors in the control of serotonergic function.

Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept.

In vitro and in vivo regulation of synaptogenesis by the novel antidepressant spadin.

Serum sortilin-derived propeptides concentrations are decreased in major depressive disorder patients.

Increased serum levels of sortilin-derived propeptide after electroconvulsive therapy in treatment-resistant depressed patients.

Fighting against depression with TREK-1 blockers: Past and future. A focus on spadin.

The Involvement of Sortilin/NTSR3 in Depression as the Progenitor of Spadin and Its Role in the Membrane Expression of TREK-1.

First evidence of protective effects on stroke recovery and post-stroke depression induced by sortilin-derived peptides.

Genetic and pharmacological inhibition of two-pore domain potassium channel TREK-1 alters depression-related behaviors and neuronal plasticity in the hippocampus in mice.

Blocking Two-Pore Domain Potassium Channel TREK-1 Inhibits the Activation of A1-Like Reactive Astrocyte Through the NF-κB Signaling Pathway in a Rat Model of Major Depressive Disorder.

Serum sortilin-derived propeptide concentrations as markers of depression in chronic stroke.