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Potent TREK-1 channel blocker (IC50 = 71 nM). Enhances dorsal raphe nucleus 5-HT neurotransmission in mice. Induces hippocampal CREB activation and neurogenesis in adult mice. Exhibits antidepressant effects in mouse models of depression. Brain penetrant.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solubility||Soluble to 2 mg/ml in water|
References are publications that support the biological activity of the product.
Mazella et al (2010) Spadin, a sortilin-derived peptide, targeting rodent TREK-1 channels: a new concept in the antidepressant drug design. PLoS Biol. 8 e1000355 PMID: 20405001
Borsotto et al (2015) Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept. Br.J.Pharmacol. 172 771 PMID: 25263033
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Keywords: Spadin, Spadin supplier, potent, TREK-1, channels, inhibits, inhibitors, depression, antidepressants, CREB, neurotensin, receptors, NTSR3, gp95, sortilin, K2P, KCNK2, Two-P, Potassium, Channels, 5594, Tocris Bioscience
1 Citation for Spadin
Citations are publications that use Tocris products. Selected citations for Spadin include:
Fernandez-Fernandez et al (2018) Activation of TREK currents by riluzole in three subgroups of cultured mouse nodose ganglion neurons. PLoS One 13 e0199282 PMID: 29928032
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Reviews for Spadin
Average Rating: 5 (Based on 1 Review.)
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A very potent K2p channel blocker which was used to figure out the blocking activity as concentration of the blocker molecule increased. Spadin is a great antagonist molecule which shows channel blocking properties which is concentration dependent.
Literature in this Area
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Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.