Possible involvement of thiamine in acetylcholine release

Ultracytochemical Localization of Thiamine Monophosphatase Activity in the Substantia Gelatinosa of the Rat Spinal Cord

“…The above observations suggest that the fluoride resistant AcPase activity reflects that of TMPase. It was also been reported (4,5,15,16) that activities of phosphatase related to thiamine are located in the neuronal membrane (perikaryon and processes), the synapse (membrane and synaptic vesicle), and the Golgi apparatus in neurons, except for TMPase activity at pH 9.2 and pH 6.8 (15). In spite of the divergence of incubation pH used, the localization of the reaction products coincides largely with those observed in the present experiment.…”

Biological functions of thiamine derivatives: Focus on non-coenzyme roles

“…These results suggest a coenzyme-independent effect of thiamine on neurotransmitter release, affecting at least three different neurotransmitters (acetylcholine 28,34,35 , dopamine 36 and noradrenaline 35 ) in different preparations ranging from fish electric organ to mammalian brain. This suggests a rather conserved mechanism.…”

“…Synaptosomes prepared from Torpedo electric organ are enriched in thiamine and its phosphate esters, while synaptic vesicle are not, suggesting that they are localized in the axoplasm 28 . Another study suggested that thiamine is an integral component of synaptomal membranes 29 .…”

“…While there is presently no convincing evidence that thiamine has physiologically relevant effects on axonal conductance, it has been reported consistently that thiamine (and/or some of its phosphate esters) facilitates neurotransmission in various preparations, probably by potentiation of the release of the neurotransmitters acetylcholine 28,34,35 , dopamine 36 and noradrenaline 35 . Here, we are exclusively interested in direct (rapid) effects on neurotransmission, as in chronic experiments (for instance after administration of thiamine for several weeks in animals) it is very difficult to discriminate between putative coenzyme-independent and coenzymedependent effects: for instance, increased pyruvate dehydrogenase activity could lead to increased acetyl-CoA production which in turn could increase acetylcholine synthesis.…”

New Considerations on the Neuromodulatory Role of Thiamine

“…Depressed ganglionic transmission after incubation with pyrithiamine and oxythiamine has been reported, presumptively because of inhibited synthesis of acetylcholine [16] . However, this effect occurred after hours of incubation and stands in marked contrast to the body of research which shows that either or both drugs have excitatory effects on nervous tissue, especially with much shorter lengths of exposure [8,11,13,14,17,18] . Enhanced neurotransmitter release of acetylcholine has been observed in peripheral [13][14][15] and central nervous system tissues [16] .…”