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Discontinued Product(-)-Cotinine (Cat. No. 3110) has been withdrawn from sale for commercial reasons.
Major metabolite of nicotine. Shown to activate a subpopulation of α3/α6β2 nAChRs in monkey striatum. Displays cognition-enhancing effects in vivo; reduces amyloid β (Aβ) aggregation and improves memory in an Alzheimer's disease mouse model.
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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.
References are publications that support the biological activity of the product.
Buccafusco and Terry (2003) The potential role of cotinine in the cognitive and neuroprotective actions of nicotine. Life Sci. 72 2931 PMID: 12706481
Terry et al (2005) Cotinine, a neuroactive metabolite of nicotine: potential for treating disorders of impaired cognition. CNS Drug Rev. 11 229 PMID: 16389292
O'Leary et al (2008) Cotinine selectively activates a subpopulation of α3/α6β2 nicotinic receptors in monkey striatum. 325 646 PMID: 18305015
Echeverria et al (2011) Cotinine reduces amyloid-β aggregation and improves memory in Alzheimer's disease mice. J.Alzheimers Dis. 23 1 PMID: 20930295
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Keywords: Cotinine, Cotinine supplier, metabolite, nicotine, Acetylcholine, Nicotinic, Receptors, Non-Selective, Subtypes, nAChR, (Non-selective), 3110, Tocris Bioscience
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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.