多不饱和脂肪酸
突触小泡
秀丽隐杆线虫
神经传递
神经科学
生物
神经递质
突触裂
小泡
脂肪酸
生物化学
中枢神经系统
基因
受体
膜
作者
Esther Marza,Giovanni M. Lesa
出处
期刊:Biochemical Society Transactions
[Portland Press]
日期:2006-01-20
卷期号:34 (1): 77-80
被引量:20
摘要
Changes in PUFA (polyunsaturated fatty acid) metabolism can cause mental retardation and cognitive impairment. However, it is still unclear why altered levels of PUFAs result in neuronal dysfunction. Recent studies on the nematode Caenorhabditis elegans suggest that PUFA depletion may cause cognitive impairment by compromising communication among neurons. Pharmacological and electrophysiological experiments showed that animals devoid of most PUFAs release abnormally low levels of neurotransmitters. In addition, ultrastructural analysis revealed that synapses in these mutants are severely depleted of synaptic vesicles. The conclusion of these studies is that PUFAs are required to maintain a normal pool of synaptic vesicles at pre-synaptic sites, thus ensuring efficient neurotransmission.
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