5-Fluorowillardiine is a selective agonist for the AMPA receptor,[1][2][3] with only limited effects at the kainate receptor.[4] It is an excitotoxicneurotoxin when used in vivo and so is rarely used in intact animals, but it is widely used to selectively stimulate AMPA receptors in vitro.[5][6][7]
It is structurally similar to the compound willardiine, which is also an agonist for the AMPA and kainate receptors. Willardiine occurs naturally in Mariosousa willardiana and Acacia sensu lato.[8][9]
The name is unusual as it has two successive i's. This is not a typo.
Toxicity
(S)-5-Fluorowillardiine activity has been studied in vitro in a variety of neural tissues. In mouse embryo hippocampal neurons, it was found to desensitize AMPA/kainate receptors with an EC50 of 1.5 μM –— 7 times more potent than racemic AMPA (EC50 of 11 μM).[10] In another study, (S)-5-Fluorowillardiine showed biphasic dose-dependent neurotoxicity in cultural rodent cortical neurons, with EC50 values of 0.70 and 170 μM.[11]
While in vivo research is sparse, a study in 5-day-old mice injected with the closely related AMPA/kainate agonist (S)-5-Bromowillardiine showed cortical and white matter damage. AMPA antagonists reduced the extent of the damage in a dose-dependent fashion.[12]
Applications in research
Radiolabeled 5-fluorowillardiine has been used to study the distribution of ionotropic glutamate receptors in rodent brains.[13] It has also been used to evaluate the effects of various allosteric modulators of the AMPA receptor.[14]
Chemistry
Structure and activity
5-fluorowillardiine is derived from the nitrogenous base uracil found in RNA. It is one member of a family of willardiine compounds, which share uracil or a substituted uracil as an amino acid side chain.
5-Fluorowillardiine exists as two distinct isomers:
(2R) or D
(2S) or L
The particularly high affinity of 5-fluorowillardiine for the AMPA receptor is attributed to its fluorine substituent at the 5-position of the ring, which is electron-withdrawing and small enough to not interfere with binding. By contrast, related willardiine derivatives with larger nonpolar electron withdrawing groups exhibit greater affinity for kainate receptors than 5-fluorowillardiine, and less affinity for AMPA receptors.[15]
The binding of 5-fluorowillardiine to the AMPA receptor is driven by entropy when its ring is uncharged. When the ring is deprotonated and has a negative charge, a favorable change in enthalpy primarily drives binding. Because the pKa values of halogenated willardiine derivates are approximately 8 (7.98 for 5-Fluorowillardiine), binding is mostly driven by an increase in entropy at physiological pH.[16]
^Klaassen, C. D.; John Barr Watkins (2010). "Toxic Agents"(PDF). Casarett and Doull's essentials of toxicology. USA: McGraw-Hill Prof Med/Tech. p. 374. ISBN978-0-07-176651-7.
^Larm, Jari A.; Cheung, Nam Sang; Beart, Philip M. (October 1996). "(S)-5-Fluorowillardiine-mediated neurotoxicity in cultured murine cortical neurones occurs via AMPA and kainate receptors". European Journal of Pharmacology. 314 (1–2): 249–254. doi:10.1016/S0014-2999(96)00633-4. PMID8957243.
^Gressens, Pierre; Spedding, Michael; Gigler, Gabor; Kertesz, Szabolcs; Villa, Pascal; Medja, Fadia; Williamson, Toni; Kapus, Gabor; Levay, Gyorgy; Szenasi, Gabor; Barkoczy, Jozsef; Harsing, Laszlo G. (September 2005). "The effects of AMPA receptor antagonists in models of stroke and neurodegeneration". European Journal of Pharmacology. 519 (1–2): 58–67. doi:10.1016/j.ejphar.2005.06.031. PMID16112106.
^Jane, David E.; Hoo, Ken; Kamboj, Raj; Deverill, Michele; Bleakman, David; Mandelzys, Allan (October 1997). "Synthesis of Willardiine and 6-Azawillardiine Analogs: Pharmacological Characterization on Cloned Homomeric Human AMPA and Kainate Receptor Subtypes". Journal of Medicinal Chemistry. 40 (22): 3645–3650. doi:10.1021/jm9702387. PMID9357531.
^Dewar, J. H.; Shaw, G. (1962). "110. Purines, pyrimidines, and imidazoles. Part XVII. A synthesis of willardiine". Journal of the Chemical Society (Resumed): 583. doi:10.1039/JR9620000583.