SEROTONIN-DEFICIENT MUTANTS AND MALE MATING-BEHAVIOR IN THE NEMATODE CAENORHABDITIS-ELEGANS
SEROTONIN-DEFICIENT MUTANTS AND MALE MATING-BEHAVIOR IN THE NEMATODE CAENORHABDITIS-ELEGANS
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DOI：
10.1523/jneurosci.13-12-05407.1993
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发表时间：
1993-12-01
影响因子：
5.3
通讯作者：
KENYON, CJ
中科院分区：
文献类型：
--
作者：
LOER, CM;KENYON, CJ
在自由生活的秀丽隐杆线虫（Caenorhabditis elegans）中定义一种需要特定神经元功能的行为，可以让人们筛选破坏这些神经元规范或功能的突变。我们确定了秀丽隐杆线虫雄性在交配期间表现出的尾巴卷曲或“转向”行为所需的血清素免疫反应神经元。减少血清素表达的三种不同基因（cat-1、cat-4和bas-1）的雄性突变，在转向行为上表现出与这些神经元被切除的野生型雄性相似的缺陷。外源性血清素挽救了4型雄性猫的转向缺陷，这与它们的行为缺陷是由缺乏血清素引起的观点一致。虽然我们分析的血清素缺乏突变体有某些共同的行为特征，但它们在不同的步骤中被血清素合成阻断。对这些和其他5 -羟色胺缺乏突变体的分析可能有助于我们理解神经元如何控制5 -羟色胺能表型的表达。
Defining a behavior that requires the function of specific neurons in the free-living nematode Caenorhabditis elegans can allow one to screen for mutations that disrupt the specification or function of those neurons. We identified serotonin-immunoreactive neurons required for tail curling or ''turning'' behavior exhibited by C. elegans males during mating. Males mutant in three different genes that reduce serotonin expression, cat-1, cat-4, and bas-1, exhibited defects in turning behavior similar to those of wild-type males in which these neurons were ablated. The turning defect of cat-4 males was rescued by exogenous serotonin, consistent with the idea that their behavioral defect is caused by a lack of serotonin. While the serotonin-deficient mutants we analyzed shared certain behavioral traits, they were blocked for serotonin synthesis at different steps. Analysis of these and additional serotonin-deficient mutants may help us understand how a neuron controls the expression of a serotonergic phenotype.