Mousseau D D, Rao V L, Butterworth R F
Neuroscience Research Unit, Hôpital Saint-Luc (University of Montreal), Canada.
Eur J Pharmacol. 1996 Dec 19;317(2-3):263-7. doi: 10.1016/s0014-2999(96)00842-4.
Experimental and clinical studies indicate that catecholamines play an important role in the neurobehavioural symptomatology of thiamine deficiency. Given the cerebral region-selective vulnerability and the behavioural impairment commonly encountered in thiamine deficiency, we undertook to investigate regional catecholamine metabolism in the brains of pyrithiamine-induced thiamine-deficient rats. Dopamine metabolism was unaffected in the striatum. In contrast, other regions also known to be involved in sensory processing and intellectual function (e.g., frontal cortex, hypothalamus, thalamus), but having a greater noradrenergic input, had increased levels of 3,4-dihydroxyphenylacetic acid (DOPAC) and decreased levels of other dopaminergic metabolites including noradrenaline. In these regions levels of the vesicular amine transporter, defined by tetrabenazine-sensitive [3H]ketanserin binding, were also decreased. Our data suggest a region-selective vesicular dysfunction resulting in intraneuronal release, and subsequent degradation, of dopamine. These disruptions of dopamine and consequently noradrenaline metabolism may account for certain neurobehavioural deficits commonly encountered in thiamine deficiency.
实验和临床研究表明，儿茶酚胺在硫胺素缺乏的神经行为症状学中起重要作用。鉴于硫胺素缺乏时常见的脑区选择性易损性和行为损害，我们着手研究吡硫胺诱导的硫胺素缺乏大鼠脑内区域儿茶酚胺代谢情况。纹状体内多巴胺代谢未受影响。相比之下，其他已知参与感觉处理和智力功能的区域（如额叶皮质、下丘脑、丘脑），但去甲肾上腺素能输入较多，其3,4-二羟基苯乙酸（DOPAC）水平升高，包括去甲肾上腺素在内的其他多巴胺能代谢产物水平降低。在这些区域，由丁苯那嗪敏感的[3H]酮色林结合定义的囊泡胺转运体水平也降低。我们的数据表明存在区域选择性囊泡功能障碍，导致多巴胺在神经元内释放并随后降解。多巴胺以及由此导致的去甲肾上腺素代谢的这些破坏可能是硫胺素缺乏时常见的某些神经行为缺陷的原因。
