Decynium has been shown to have a very high affinity to organic cation transporters in a variety of species, including human,[3][4] rat,[5] and pig.[6]Decynium-22 has been shown to block the uptake of the neurotoxin1-methyl-4-phenylpyridinium (MPP) via theOCT3 transporter in ratastrocytes.[7]
Decynium-22 emits a lowfluorescence yield (around 0.001), and in its monomeric form is a weakly fluorescent. However, aggregated decynium-22 emits a strongsuperradiant emission with a maximum near 570–580 nm.[8][9] 480 nm light falls near a short wavelength peak of theexcitation spectrum of these aggregates. Decynium-22 fluorescence caused by aggregation can be observed in astrocytes.[2]
Decynium-22 has recently been investigated for its role in increasingextracellularserotonin in the brain in neuropharmacology research. The transportation of the neurotransmitter serotonin is often disrupted in psychiatric disorders characterized by social impairment, such asschizophrenia anddepression. Serotonin is primarily taken up by the5-HT transporter (SERT), although it is also taken up by auxiliary transporters, known as "uptake 2", which include OCT and PMAT.
The most commonly prescribed antidepressant drugs are theselective serotonin reuptake inhibitors (SSRIs), which act by blocking the high affinity SERT. A proposed explanation for the limited efficacy of SSRIs is the presence of the low affinity transporters OCT and PMAT, which limit the ability of SSRIs to increaseextracellular serotonin. Decynium-22 blocked serotonin uptake via these auxiliary transporters, and when used in conjunction with SSRIs, decynium-22 enhanced the effects of SSRIs to inhibit serotonin clearance.[10] A similar effect was seen in SERTknock-out mice, which resulted in an improvement of social behavior.[11] When OCT3 was knocked out in mice, however, decynium-22 was ineffectual, indicating that the anti-depressant effects of decynium-22 are dependent upon its blockage of the OCT3.[10]
