Myles-Worsley Marina, Ord Lisa, Blailes Francisca, Ngiralmau Hilda, Freedman Robert
Department of Psychiatry, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA.
Biol Psychiatry. 2004 Apr 1;55(7):663-7. doi: 10.1016/j.biopsych.2003.12.006.
Gating or inhibition of the P50 auditory evoked potential is a heritable neurobiological trait that has shown strong potential to serve as an endophenotype for schizophrenia. P50 sensory gating deficits have been found repeatedly in schizophrenic patients and in their unaffected first-degree relatives. P50 sensory gating has not yet been studied in high-risk (HR) offspring nor in prodromal adolescents.
A paired-stimulus auditory event-related potential paradigm was used to examine P50 sensory gating in 44 genetically HR adolescent offspring and 43 clinically HR prodromal adolescents with the same low genetic liability as a comparison group of 39 normal adolescents.
Auditory sensory gating, as measured by the P50 ratio, was impaired in both genetically HR offspring and also in the clinically HR prodromal adolescents with no close affected relatives. In the genetically HR group, abnormal P50 sensory gating was found only in offspring who met criteria for the schizophrenia prodrome.
Our findings suggest that P50 deficits are associated with the presence of prodromal symptoms, regardless of genetic risk. The results are consistent with the hypothesis that genetic liability in HR offspring increases risk for prodromal symptoms, and prodromal symptoms, in turn, increase risk for impaired sensory gating.
P50听觉诱发电位的门控或抑制是一种可遗传的神经生物学特征，已显示出作为精神分裂症内表型的强大潜力。在精神分裂症患者及其未受影响的一级亲属中反复发现P50感觉门控缺陷。尚未对高危（HR）后代和前驱期青少年的P50感觉门控进行研究。
采用配对刺激听觉事件相关电位范式，对44名具有遗传高危因素的青少年后代和43名临床高危前驱期青少年进行P50感觉门控检查，并与39名正常青少年组成的对照组进行比较，后两组遗传易感性较低。
通过P50比率测量的听觉感觉门控在具有遗传高危因素的后代以及无近亲患病的临床高危前驱期青少年中均受损。在具有遗传高危因素的组中，仅在符合精神分裂症前驱期标准的后代中发现异常的P50感觉门控。
我们的研究结果表明，无论遗传风险如何，P50缺陷都与前驱症状的存在有关。这些结果与以下假设一致，即具有遗传高危因素的后代的遗传易感性增加了前驱症状的风险，而前驱症状反过来又增加了感觉门控受损的风险。
