Investigating the effects of antipsychotic drugs as a treatment for improving the activity of the unc-33 /Dpysl2 gene in C. elegans.

microPublication biology Pub Date : 2024-07-31 eCollection Date: 2024-01-01 DOI:10.17912/micropub.biology.001063
Maria C Miranda, Jessica Hyde, Kaylee Salazar, Balyssa Bell, Andrea Holgado
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Abstract

Prenatal stress is hypothesized to contribute to the development of schizophrenia. Lee and colleagues determined that prenatal stress in rats decreases levels of Dpysl2, which is found to be inactivated in schizophrenic patients. UNC-33 , the homolog to Dpysl2 in C. elegans , is important for axonal outgrowth and synapse formation. Herein, we study the effects of antipsychotic drugs on developing C.elegans exposed to stress through high temperatures. Results indicate that the unc-33 promoter was not impacted by antipsychotic drug treatment, but the lifespan was decreased.

研究抗精神病药物作为一种治疗方法对提高优雅小鼠 unc-33 /Dpysl2 基因活性的影响。
产前压力被认为是导致精神分裂症的原因之一。Lee及其同事发现,大鼠产前压力会降低Dpysl2的水平,而精神分裂症患者体内的Dpysl2会失活。UNC-33是优雅类动物中Dpysl2的同源物,对轴突生长和突触形成非常重要。在此,我们研究了抗精神病药物对暴露于高温胁迫下的发育中的秀丽隐杆线虫的影响。结果表明,unc-33启动子没有受到抗精神病药物的影响,但寿命却缩短了。
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