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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

The neuropharmacology of a novel gamma-aminobutyric acid analog, kojic amine.

Kojic amine (KA; 2-aminomethyl-5-hydroxy-4H-pyran-4-one), a compound which shares some structural features with gamma-aminobutyric acid (GABA) and muscimol, has been examined in a variety of test systems for GABAmimetic activity. In several in vitro central nervous system receptor binding assays employing rat brain membrane preparations, KA exhibited selective activity to displace 3H-muscimol but with a relatively high IC50 of 4.4 muM. KA did not alter the binding of 3H-diazepam. Iontophoretically applied KA exerted a pronounced (comparable to GABA on the basis of ejection currents)i inhibition of the firing of cerebellar Purkinje cells and spontaneously active or glutamate-activated neurons in the cerebral cortex. The inhibitory effects of KA, which were longer lasting than those of GABA, were antagonized by bicuculline and enhanced in the presence of 2,4-diaminobutyric acid. On the isolated amphibian (Bufo marinus) spinal cord, KA was less than 1/3 as potent as GABA in depolarizing primary afferent terminals. In this preparation KA caused a marked decrease in the dorsal and ventral root potentials evoked by electrical stimulation of an adjacent or corresponding dorsal root. KA is a poor substrate for GABA uptake systems into rat brain synaptosomes, has no effect on GABA release in vitro, and does not inhibit GABA transaminase activity. Altogether, these data suggest that KA does have some GABAmimetic actions (which are perhaps restricted to hyperpolarizing post-synaptic GABA receptors) but also exerts other pharmacological effects as well.[1]

References

  1. The neuropharmacology of a novel gamma-aminobutyric acid analog, kojic amine. Yarbrough, G.G., Williams, M., Haubrich, D.R. Archives internationales de pharmacodynamie et de thérapie. (1979) [Pubmed]
 
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