Research Applications
Rapid-onset antidepressant research. TREK-1 channel pharmacology. Non-monoaminergic depression treatment. Treatment-resistant depression.
Mechanism of Action
Spadin selectively blocks TREK-1 potassium channels, increasing neuronal excitability in hippocampus and cortex. TREK-1 blockade enhances serotonergic neurotransmission, increases BDNF expression and hippocampal neurogenesis, and activates CREB signaling — effects similar to chronic SSRI treatment but occurring within days.
Dosage Information
Calculation Results
Syringe Fill Level (100u syringe)
Protocols
No protocols featuring this peptide yet.
Browse All ProtocolsResearch Studies
Spadin: A Novel Antidepressant Targeting TREK-1
Mazella J, Petrault O, Lucas G, et al.
Frequently Asked Questions
Spadin is a 17-amino acid peptide derived from the propeptide of sortilin (a neuronal sorting receptor) that acts as a selective antagonist of the TREK-1 potassium channel. TREK-1 is a two-pore domain potassium channel involved in mood regulation — TREK-1 knockout mice display a depression-resistant phenotype. Spadin blocks TREK-1, producing rapid antidepressant effects in animal models within 4 days (versus 2-4 weeks for SSRIs). It represents a novel, non-monoaminergic approach to depression treatment.
Spadin selectively blocks TREK-1 potassium channels, increasing neuronal excitability in hippocampus and cortex. TREK-1 blockade enhances serotonergic neurotransmission, increases BDNF expression and hippocampal neurogenesis, and activates CREB signaling — effects similar to chronic SSRI treatment but occurring within days.
Rapid-onset antidepressant research. TREK-1 channel pharmacology. Non-monoaminergic depression treatment. Treatment-resistant depression.
