Plaitakis A, Nicklas W J, Berl S
Neurology. 1978 Jul;28(7):691-8. doi: 10.1212/wnl.28.7.691.
To explore the role of thiamine deficiency in synaptic transmission, the high-affinity uptake and release systems for putative neurotransmitters were studied in synaptosomal preparations isolated from the telencephalon, hypothalamus, and cerebellum of rats made thiamine deficient by diet or pyrithiamine. There was significant decrease in the uptake of serotonin by the synaptosomal preparations of the cerebellum. Although thiamine and its phosphorylated forms added in vitro did not restore the decreased serotonin uptake, the administration of the vitamin in vivo resulted in a significant reversibility of the inhibition of serotonin uptake, coinciding with dramatic clinical improvement. The study supports the possibility of an important serotonergic innervation of the cerebellum and suggests a selective involvement of this system in the pathogenesis of some of the neurologic manifestations of thiamine deficiency.
为探讨硫胺素缺乏在突触传递中的作用,我们对从经饮食或吡硫胺诱导造成硫胺素缺乏的大鼠的端脑、下丘脑和小脑中分离出的突触体进行了研究,观察了假定神经递质的高亲和力摄取和释放系统。小脑突触体对血清素的摄取显著下降。虽然体外添加硫胺素及其磷酸化形式并不能恢复血清素摄取的下降,但体内给予该维生素可使血清素摄取抑制显著逆转,这与临床症状的显著改善相一致。该研究支持小脑存在重要的血清素能神经支配的可能性,并提示该系统选择性地参与了硫胺素缺乏某些神经学表现的发病机制。