Thyronamine induces TRPM8 channel activation in human conjunctival epithelial cells

In the brain of mice, 3-iodothyronamine (T1AM) is converted into 3-iodothyroacetic acid (TA1) and it is included within the signaling network connecting thyroid hormone metabolites with histamine

“…Instead, T1AM could i) stimulate a target on histaminergic neurons inducing the release of the amine ii) be transported intracellular and converted into TA1, which might work intracellular inducing vesicle docking or extruded in the synaptic cleft where it could act on auto receptors positively controlling histamine release. In light of recent reports, TRPM8 was found to be a novel target for T1AM (Khajavi et al, 2014). The activation of these channels might account for the rapid effects and for the non-linear dose response often observed when injecting T1AM.…”

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca2+Influx Dysfunction in Human Pterygial Cells

“…45 Similarly, TRPM8 expression may contribute to the pterygial transition, as this channel plays a role in cancer diseases concerning by modulating proliferation and cell cycle progression. 55 Notably, TRPM8 is functionally expressed at higher levels in hPtEC (data not shown) compared with human corneal epithelial cells and conjunctival epithelial cells, 41,56 whereas TRPM8 mRNA expression was not significantly different (Fig. 2).…”

“…Such a strategy is tenable, as TRPM8 activation by a thyroid hormone analogue (3-T 1 AM) inhibited through crosstalk CAP-and hypertonic-induced increases in TRPV1 channel activity in both HCjEC and HCEC. 41,56 …”

“…The I-V response patterns were generated by imposing voltages in 10 mV steps from À60 mV to þ130 mV. 41 The holding potential was set to 0 mV to eliminate any possible contribution of voltage-dependent Ca 2þ channels.…”

Trace Amines and Their Receptors

“…This has subsequently been verified by numerous laboratories (Mühlhaus et al, 2014;Cöster et al, 2015;Chiellini et al, 2017), with 3IT also shown to act as an agonist at TAAR2 (Babusyte et al, 2013;Cichero and Tonelli, 2017) and as an inverse agonist at TAAR5 (Dinter et al, 2015c). 3IT is promiscuous, however, and also interacts with high affinity at a 2 -adrenoceptors (Regard et al, 2007;Dinter et al, 2015b), b-adrenergic receptors (Meyer and Hesch, 1983;Kleinau et al, 2011;Dinter et al, 2015a), muscarinic acetylcholine receptors (Laurino et al, 2016), transient receptor potential cation channel subfamily M member 8 ion channels (Khajavi et al, 2015;Lucius et al, 2016), various monoamine and organic anion transporters (Snead et al, 2007;Panas et al, 2010), and molecular target(s) within mitochondria, including the F 1 -F 0 ATP synthase (Cumero et al, 2012) and possibly complex III (Venditti et al, 2011). 3IT also tightly binds to the plasma protein apolipoprotein B-100 .…”