Three subdivisions of the auditory midbrain in chicks (Gallus gallus) identified by their afferent and commissural projections

The auditory midbrain is a site of convergence of multiple auditory channels from the brainstem. In birds, two separate ascending channels have been identified, through which time and intensity information is sent to the nucleus mesencephalicus lateralis, pars dorsalis (MLd), the homologue of the central nucleus of the mammalian inferior colliculus. Using in vivo anterograde and retrograde tracing techniques, the current study provides two lines of anatomical evidence supporting the presence of a third ascending channel to the chick MLd. First, three non‐overlapping zones of the MLd receive inputs from three distinct cell groups in the caudodorsal brainstem. The projections from the nucleus angularis (NA) and nucleus laminaris (NL) are predominantly contralateral and may correspond to the time and intensity channels. A rostromedial portion of the MLd receives bilateral projections mainly from the regio intermedius, an interposed region of cells lying at a caudal level between the NL and NA, as well as scattered neurons embedded in the 8th nerve tract, and probably a very ventral region of the NA. Second, the bilateral zones of the MLd on two sides of the brain are reciprocally connected and do not interact with other zones of the MLd via commissural connections. In contrast, the NL‐recipient zone projects contralaterally upon the NA‐recipient zone. The structural separation of the third pathway from the NA and NL projections suggests a third information‐processing channel, in parallel with the time and intensity channels. Neurons in the third channel appear to process very low frequency information including infrasound, probably utilizing different mechanisms than that underlying higher frequency processing. J. Comp. Neurol. 518:1199–1219, 2010. © 2009 Wiley‐Liss, Inc.     

血管内皮生长因子在次声作用后的表达及其与血-视网膜屏障破坏的关系

目的探讨血管内皮生长因子(VEGF)在次声暴露后大鼠视网膜的表达及其与次声暴露的关系.方法免疫组织化学法研究不同时间次声暴露VEGF在视网膜各层的表达情况.结果各实验所有视网膜组织中,VEGF的表达随次声暴露的延长而有一定程度的加深.表现为棕黄色阳性染色弥漫分布于神经节细胞层和内核层内.血管分布的区域阳性染色分布较集中.可见表达于内皮细胞的细胞浆内和(或)细胞膜上呈棕黄色圆形,环状分布或不规则分布的颗粒.阴性对照未见阳性染色.结论次声作用导致大鼠视网膜组织VEGF表达不同程度地升高,与次声所致血-视网膜屏障的损害密切相关.     

8 Hz、90 dB次声引起的心肌细胞超微结构变化及相关机制的探讨

目的:观察次声多次暴露后大鼠心肌细胞超微结构的变化,并分析其机制。方法:用8Hz、90dB的次声连续作用大鼠1、7、14、21和28d,每天2h,使用透射电镜观察心肌细胞超微结构改变。结果:在次声暴露期间,与对照组比较,1d无显著变化,7d开始出现少数线粒体肿胀,14d开始出现较多线粒体肿胀,21d肌浆网扩张,28d有血栓形成。结论:8Hz、90dB次声可引起心肌细胞超微结构的轻微变化,这些变化和次声暴露时间和量有关。     

胶质纤维酸性蛋白及生长相关蛋白-43在低声压次声治疗颅脑外伤大鼠过程中的变化

目的:探讨低声压级次声对大鼠颅脑外伤后胶质纤维蛋白(GFAP)及生长相关蛋白-43(GAP-43)表达的影响。方法:采用Feeney法制作颅脑外伤模型。将30只SD大鼠随机分为假手术组、模型组、次声60min组、次声90min组和次声120min组共5组,其中次声3组分别予次声干预60min、90min和120min,连续7天;模型组干预过程中除不开机外,其余过程同次声组。假手术组只打开颅窗,不损伤脑组织,不进行次声干预。7天后处死前行改良神经功能缺损评分(m NSS),然后断头取脑、免疫组化观察损伤脑组织周围GFAP及GAP-43表达变化。结果:次声3组与模型组的m NSS评分均存在显著差异(P0.05),次声3组间的m NSS评分无显著差异(P0.05)。免疫组化结果:15组间的GFAP表达存在显著性差异(P0.05),3个次声组与模型组比较均存在显著差异(P0.05),3个次声组间GFAP表达无明显差异(P0.05);25组间的GAP-43表达存在显著性差异(P0.05),3个次声组与模型组比较均存在显著差异(P0.05),3个次声组间GAP-43表达无明显差异(P0.05)。结论:低声压级次声能提高大鼠脑外伤后脑组织GFAP及GAP-43的表达,改善脑外伤大鼠神经功能。     

On the biological plausibility of Wind Turbine Syndrome

An emerging environmental health issue relates to potential ill-effects of wind turbine noise. There have been numerous suggestions that the low-frequency acoustic components in wind turbine signals can cause symptoms associated with vestibular system disorders, namely vertigo, nausea, and nystagmus. This constellation of symptoms has been labeled as Wind Turbine Syndrome, and has been identified in case studies of individuals living close to wind farms. This review discusses whether it is biologically plausible for the turbine noise to stimulate the vestibular parts of the inner ear and, by extension, cause Wind Turbine Syndrome. We consider the sound levels that can activate the semicircular canals or otolith end organs in normal subjects, as well as in those with preexisting conditions known to lower vestibular threshold to sound stimulation.     

Infrasound-induced hemodynamics, ultrastructure, and molecular changes in the rat myocardium

Recent interest in adverse effects of infrasound on organisms arises from health concerns. We assessed the association between infrasound exposure of 5 Hz at 130 dB and changes of cardiac ultrastructure and function in rats. Thirty-two Sprague-Dawley rats were randomized into control, 1, 7, and 14 days groups for 2 h of infrasound once daily according to planned schedules. Changes of cardiac ultrastructure, hemodynamics indices, intracellular Ca(2+) concentrations ([Ca(2+)](i)), and sarcoplasmic reticulum Ca(2+)-ATPase 2 (SERCA2) were detected. Heart rates in 1 day group were significantly increased compared with control group and no significant changes in other groups. Left ventricular systolic pressures were significantly increased with time. Left ventricular diastolic end pressure and maximum rising rates of left ventricular pressure (+dl/dt) were significantly increased in 7 and 14 days groups and not changed in 1 day group, compared with control group. Maximum dropping rates of left ventricular pressure (-dl/dt) were significantly decreased in 7 and 14 days groups and not changed in 1 day group, compared with control group. In heart cells, there were several swelled mitochondria in 1 day group, more swelled mitochondria in 7 days group, platelet aggregation in the intercellular substance in 14 days group. [Ca(2+)](i) were significantly increased with time. There was a significant increase in SERCA2 in 1 day group, while a significant decrease in 7 and 14 days groups, compared with control group. Infrasound of 5 Hz at 130 dB can damage cardiac ultrastructure and function. Changes of [Ca(2+)](i) and SERCA2 play an important role in the secondary cardiac damage.     

次声作用后大鼠下丘脑HSP70的表达

研究大鼠经次声作用后下丘脑中ＨＳＰ７０的表达。方法ＳＤ大鼠先经８Ｈｚ,１２０ｄＢ次声作用２ｈ,然后分为８组,每组３只。分别于次声作用后０．５,１,２,３,４,５,６和７ｈ后取下丘脑,通过Ｗｅｓｔｅｒｎｂｌｏｔｔｉｎｇ技术检测ＳＨＰ７０的表达。结论ＨＳＰ７０参与了次声应激后机体的反应机制。     

次声作用下大鼠脑皮质内谷氨酸及其代谢型受体1亚型mRNA的变化

目的：探讨8Hz130dB次声作用对大鼠脑皮质内谷氨酸（glutamic acid,Glu)水平和代谢性谷氨酸受体1亚型（mGluR1)mRNA表达的影响。方法：SD大鼠60只随机分为对照组及次声作用1,7和14次组,次声作用组动物采用自制的次声压力仓用8Hz,130dB的次声按规定次数,每次作2h。通过氨基酸分析仪测定各组脑皮质Glu的含量。利用地高辛标记寡聚核苷酸探针原位杂交技术与计算机图像分析系统,在光镜下分别观察mGluR1在大鼠脑皮质阳性神经元的表达以及相应皮质的病理变化。结果：次声作用1次组,脑皮质内Glu 的含量开始升高,7次组显高于对照组（P＜0．01）,14次组低于正常值;次声作用1次组,mGluR1mRNA阳性神经元数量增加;7次组至峰值（P＜0．01）,14次组数目基本恢复到正常水平。结论：形态学研究表明次声作用7次组皮质浅层有部分神经元损伤,次声脑损伤过程中,脑皮质内Glu含量的升高曲线与mGluR1表达合成增加趋势基本吻合,提示Glu可能通过其受体mGluR1产生的神经毒作用参与了次声对中枢神经系统的损害作用。     

次声信号数据采集系统的研制

次声信号数据采集系统所采集的是0-20Hz的次声信号。该信号通过传声器转换为相应的电压信号。计算机实时采集、处理次声信号,分析次声信号的各主要频率成分和强度大小、对分析结果进行图形显示,曲线自动输出,并生长、打印最终结果。     

次声治疗对Raji细胞的影响

目的 研究次声治疗对人B淋巴瘤细胞株Raji细胞的影响.方法 Raji细胞分为次声组和对照组.以hfrasound 8TM次声治疗仪作为处理因素,分别处理15、30、60、90、120min.对照组关闭次卢治疗仪电源,余同次声组.各组细胞经相应时间的次声处理或对照处理后培养24,48 h后m采用MTT法测试细胞增殖活性,采用流式细胞术观察细胞凋亡情况,应用扫描电镜和透射电镜观察细胞超微结构的变化.结果 MTT法检测结果显示.各次声组的OD值与相应对照组比较差异均无统计学意义(P>0.05);流式细胞仪检测结果显示各组总体无显著差异(P>0.05);扫描电镜观察结果显示,经次声处理后培养24 h的Raji突起明显变短、凹陷变浅,细胞表面突起和微绒毛减少或变短明显,细胞表面光滑.透射电镜观察结果示,次声组细胞表面微绒毛有明显减少,细胞核呈均质化,胞质呈出芽脱落.结论 本实验采用的次声处理(次声信号声强级均小于90 dB)对Raji细胞的生长及凋亡影响不明显:但改变细胞膜的突起,可对细胞膜的超微结构产生直接作用.