白噪声对听觉脑干电反应(ABR)和耳蜗电图(ECochG)的影响

本文通过20例听力正常人和10例听力正常豚鼠研究了白噪声对耳蜗电图(ECochG)和听觉脑干电反应(ABR)的干涉作用。实验结果表明,白噪声比短声(信号)的声强级低30dB(SL)以上时,ECochG和ABR的振幅仅轻微减小。白噪声与短声的声强级相等时,ECochG与ABR的振幅和出现率会明显受到干涉而减小,甚至完全消失。但是,此时的耳蜗微音器电位(CM)并未观察到有明显的变化。这意味着白噪声对ECochG和ABR的干涉作用主要与围绕毛细胞基底部的突触产生的抑制密切相关。由于白噪声对ABR各波的干涉有些差异,所以认为这种抑制,可能既包括脑中抑制也包括侧方抑制。     

Dynamic changes in hair cell stereocilia and cochlear transduction after noise exposure

The structures of cochlear transduction include stereocilia at the apical surface of hair cells and their connection to the tectorial membrane. The transduction site is one of the loci for noise-induced cochlear damage. Although stereocilia are susceptible to noise, it has been found that in the inner ears of avians, this fragile structure is largely self-repairing and is associated with recovery of hearing sensitivity after noise exposure, as observed in the difference between the temporal threshold shift (TTS) and the permanent threshold shift (PTS). In the mammalian cochleae, however, threshold shifts measured in the auditory brainstem responses (ABR) did not parallel the chronological changes in the stereocilia on hair cells. It is unclear how the morphological recovery of the stereocilia on the mammalian hair cells is correlated with the changes in cochlear transduction that can be assessed by measuring receptor potential. In the present study, guinea pigs were exposed to a broadband noise of 110 dB SPL for 2 h. Auditory sensitivity was evaluated using ABR and cochlear transduction was assessed using cochlear microphonics (CM). Stereocilia morphology was quantified at different time points after the noise and compared with the control. The noise produced a TTS of 55.69 ± 14.13 dB in frequency-averaged ABR thresholds. The threshold shift was reduced to 9.58 ± 11.75 dB SPL 1 month later with virtually no loss of hair cells. Damage to the stereocilia immediately after noise exposure was found to be associated with depression of CM amplitude. Virtually no abnormal stereocilia were observed 1 month after the noise in association with a fully recovered CM.     

卡那霉素致聋豚鼠耳蜗电极植入模型的建立及意义

目的:探讨人工耳蜗电极的插入对耳蜗功能的影响,为研究人工耳蜗植入建立相应的动物模型。方法:取听力正常的豚鼠8只,4只注射卡那霉素联合呋塞米致聋,为致聋组;4只仅注射生理盐水,为对照组。对两组动物行听性脑干反应(ABR)及耳声发射(DPOAE)检查后,将耳蜗电极植入左侧耳蜗。结果:致聋组术侧4个频率段ABR阈移随着时间的推移逐渐减小,术后24 h、48 h、72 h时间段比较无显著性差异(P0.05);对照组术侧ABR阈移随着时间的推移逐渐减小,32 kHz频率的三个时间段比较有显著性差异(P0.05),其余3个频率无显著性差异。此外,致聋组与对照组术侧耳ABR阈移比较均无显著性差异(P0.05)。致聋组术前5个频率的DPOAE无法引出,术后DPOAE仍无法引出;对照组术前DPOAE均可引出,术后术侧的DPOAE均无法引出。术后72 h可见电极周围有组织包绕,固定良好,局部未见明显炎症反应。结论:本实验成功建立了卡那霉素致聋的豚鼠耳蜗电极植入模型,可为人工耳蜗植入术后颞骨病理改变的研究提供实验基础。     

Auditory function in the Tc1 mouse model of down syndrome suggests a limited region of human chromosome 21 involved in otitis media

Down syndrome is one of the most common congenital disorders leading to a wide range of health problems in humans, including frequent otitis media. The Tc1 mouse carries a significant part of human chromosome 21 (Hsa21) in addition to the full set of mouse chromosomes and shares many phenotypes observed in humans affected by Down syndrome with trisomy of chromosome 21. However, it is unknown whether Tc1 mice exhibit a hearing phenotype and might thus represent a good model for understanding the hearing loss that is common in Down syndrome. In this study we carried out a structural and functional assessment of hearing in Tc1 mice. Auditory brainstem response (ABR) measurements in Tc1 mice showed normal thresholds compared to littermate controls and ABR waveform latencies and amplitudes were equivalent to controls. The gross anatomy of the middle and inner ears was also similar between Tc1 and control mice. The physiological properties of cochlear sensory receptors (inner and outer hair cells: IHCs and OHCs) were investigated using single-cell patch clamp recordings from the acutely dissected cochleae. Adult Tc1 IHCs exhibited normal resting membrane potentials and expressed all K(+) currents characteristic of control hair cells. However, the size of the large conductance (BK) Ca(2+) activated K(+) current (I(K,f)), which enables rapid voltage responses essential for accurate sound encoding, was increased in Tc1 IHCs. All physiological properties investigated in OHCs were indistinguishable between the two genotypes. The normal functional hearing and the gross structural anatomy of the middle and inner ears in the Tc1 mouse contrast to that observed in the Ts65Dn model of Down syndrome which shows otitis media. Genes that are trisomic in Ts65Dn but disomic in Tc1 may predispose to otitis media when an additional copy is active.     

The endolymphatic sac: its roles in the inner ear

The endolymphatic sac is a non-sensory organ of the inner ear. It is connected to the endolymphatic compartment that is filled with endolymph, a potassium-rich fluid that bathes the apical side of inner ear sensory cells. The main functions ascribed to the endolymphatic sac are the regulation of the volume and pressure of endolymph, the immune response of the inner ear, and the elimination of endolymphatic waste products by phagocytosis. Functional alteration of these functions, leading to deficient endolymph homeostasis and/or altered inner ear immune response, may participate to the pathophysiology of Ménière's disease, an inner ear pathology that causes episodes of vertigo, sensorineural hearing loss and tinnitus, and is characterized by an increase in volume of the cochleo-vestibular endolymph (endolymphatic hydrops).     

谷氨酸受体在噪声所致豚鼠螺旋神经节细胞损伤中的作用

本文旨在研究谷氨酸及其受体在噪声致豚鼠螺旋神经节细胞损伤中的作用。实验分为在体和离体两部分。（1）在体实验：豚鼠分为生理盐水（NS,10μL）组,NS（10μL）＋噪声组和犬尿喹啉酸（kynurenic acid,KYNA,5mmol／L,10μL）＋噪声组,每组15只。用微量注射器经完整圆窗膜表面给予NS或KYNA：暴露于白噪声110dBSPL,1h。在圆窗给药前及噪声暴露后测试听觉脑干诱发电位（auditory brainstem response,ABR）阈值及Ⅲ波幅值,听神经复合动作电位（compound action potential,CAP）阈值及N1波幅值和潜伏期,测试后取基底膜进行透射电镜观察。（2）离体实验：观察高浓度谷氨酸对急性分离的豚鼠螺旋神经节细胞的影响。结果显示,NS＋噪声组豚鼠ABR及CAP阈移显著高于KYNA＋噪声组,且Ⅲ波和NI波幅值明显降低,潜伏期明显延长。NS＋噪声组豚鼠毛细胞及传入神经末梢急性水肿和线粒体结构破坏：KYNA＋噪声组豚鼠的毛细胞和传入神经末梢无明显变化。离体胞外施加谷氨酸可引起螺旋神经节细胞逐渐出现水肿、变性,最后死亡。本实验提示,噪声暴露可引起豚鼠听功能损伤,毛细胞／传入神经突触的结构破坏和螺旋神经节细胞变性、死亡：这种损伤可能与噪声暴露引起谷氨酸的过度释放有关;谷氨酸通过其受体介导致使螺旋神经节细胞损伤,谷氨酸受体的广谱拮抗剂KYNA可减轻噪声对螺旋神经节细胞的损伤。     

Different regulation of connexin26 and ZO-1 in cochleas of developing rats and of guinea pigs with endolymphatic hydrops.

Using confocal microscopy and morphometry, we analyzed the expression of connexin26 (Cx26) and ZO-1 in rat cochlea during the postnatal period to elucidate spatiotemporal changes in gap junctions and tight junctions during auditory development. We also studied changes in these junctions in experimental endolymphatic hydrops in the guinea pig. In the adult rat cochlear lateral wall, Cx26 was detected in fibrocytes in the spiral ligament and in the basal cell layer of the stria vascularis, whereas ZO-1 was detected in the apical surfaces of marginal cells and in the basal cell layer. During postnatal development, Cx26 expression increased mainly in the spiral ligament, whereas ZO-1 expression increased in the basal cell layer. The morphometry of Cx26 showed a sigmoid time course with a rapid increase on postnatal day (PND) 14, whereas that of ZO-1 showed a marked increase on PND 7. In experimental endolymphatic hydrops, the expression of Cx26 significantly decreased, whereas there were no obvious changes in the expression of ZO-1. These results indicate that gap junctions and tight junctions in the cochlea increase in a different spatiotemporal manner during the development of auditory function and that gap junctions and tight junctions in the cochlea are differentially regulated in experimental endolymphatic hydrops. (J Histochem Cytochem 49:573-586, 2001)     

刺五加注射液对豚鼠庆大霉素耳毒性拮抗作用的实验研究

目的：探讨中药刺五加注射液（ASS）对庆大霉素（GM）耳毒性作用的影响及其机制。方法：豚鼠随机分成对照组、GM组、ASS4-GM组和ASS组。采用听性脑干反应（ABR）、透射电镜技术（TEM）、Western blot方法观察用药前后豚鼠的ABR阈值、形态学变化及caspase-3的表达情况。结果：用药后GM组ABR阈值明显升高;ASS组ABR阈值与对照组相比无显著性差异,与GM组和ASS4-GM组相比明显降低。透射电镜观察用药后GM组毛细胞损伤严重,出现了凋亡的形态学特征,而ASS4-GM组损伤较轻。Western blot结果表明用药后GM组豚鼠caspase-3表达明显增加;ASS4-GM组caspase-3的表达稍有升高。结论：刺五加注射液对庆大霉素耳毒性具有拮抗作用,其机制可能是通过抑制caspase-3的表达来实现的。     

豚鼠庆大霉素耳中毒后HSP70 mRNA的表达

为探讨热休克蛋白(heatshockprotein,HSP)70mRNA在庆大霉素(gentamicin,GM)耳中毒中的意义,本实验选用耳廓反射灵敏的健康白色红目豚鼠(200~250g)20只,雌雄不拘,随机分成两组,每组10只。实验组动物每日腹腔注射GM100mg/kg;对照组动物每日腹腔注射与GM等量的生理盐水2.5ml/kg。两组动物混合饲养,均连续用药10d。在用药前1天和停药后第1天进行听脑干反应(auditorybrainstemresponse,ABR)测试。各组豚鼠在行第二次ABR检测后,应用原位杂交及图像分析技术观察GM耳中毒后HSP70mRNA在豚鼠耳蜗中表达。结果显示:实验组耳蜗ABR阈值明显高于对照组,有显著性差异(P<0.01);实验组豚鼠耳蜗血管纹、螺旋韧带、螺旋神经节细胞HSP70mRNA表达呈强阳性,其平均灰度值较正常对照组明显减小(P<0.001),即GM能显著增强耳蜗HSP70mRNA的表达。结果提示,GM中毒后,动物可能通过增加HSP70mRNA在耳蜗的表达,起保护听力的作用。     

Ectopic expression of ROR1 prevents cochlear hair cell loss in guinea pigs with noise‐induced hearing loss

Noise‐induced hearing loss (NIHL) is one of the most frequent disabilities in industrialized countries. Evidence shows that hair cell loss in the auditory end organ is responsible for the majority of various ear pathological conditions. The functional roles of the receptor tyrosine kinase ROR1 have been underscored in various tumours. In this study, we evaluated the ability of ROR1 to influence cochlear hair cell loss of guinea pigs with NIHL. The NIHL model was developed in guinea pigs, with subsequent measurement of the auditory brainstem response (ABR). Gain‐of‐function experiments were employed to explore the role of ROR1 in NIHL. The interaction between ROR1 and Wnt5a and their functions in the cochlear hair cell loss were further analysed in response to alteration of ROR1 and Wnt5a. Guinea pigs with NIHL demonstrated elevated ABR threshold and down‐regulated ROR1, Wnt5a and NF‐κB p65. The up‐regulation of ROR1 was shown to decrease the cochlear hair cell loss and the expression of pro‐apoptotic gene (Bax, p53) in guinea pig cochlea, but promoted the expression of anti‐apoptotic gene (Bcl‐2) and the fluorescence intensity of cleaved‐caspase‐3. ROR1 interacted with Wnt5a to activate the NF‐κB signalling pathway through inducing phosphorylation and translocation of p65. Furthermore, Wnt5a overexpression decreased the cochlear hair cell loss. Collectively, this study suggested the protection of overexpression of ROR1 against cochlear hair cell loss in guinea pigs with NIHL via the Wnt5a‐dependent NF‐κB signalling pathway.     

Mechanisms of Hearing Loss in Neurofibromatosis Type 2

Introduction

Patients with neurofibromatosis type 2 (NF2) develop bilateral cochleovestibular schwannomas (CVSs) that cause binaural deafness in most individuals. Hearing loss occurs in an unpredictable manner and the underlying mechanisms are not known. To gain insight into the pathophysiologic basis for hearing loss in NF2, we performed a prospective cross-sectional study of untreated ears in NF2 patients.

Methods

One hundred consecutive NF2 patients in a prospective natural history study were included. Clinical and audiometric data were analyzed for treatment naïve ears. In addition to standard MR-imaging sequences, alterations in intralabyrinthine protein content were determined utilizing high resolution FLAIR, the presence of cochlear aperture obstruction was determined by examining 3D T2 sequences, and endolymphatic hydrops was identified on delayed post-contrast FLAIR sequences.

Results

Eighty-nine ears harboring 84 untreated CVSs in 56 consecutive NF2 patients (age 30±16 years) were analyzed. Thirty-four (38%) ears had varying degrees of hearing loss. Elevated intralabyrinthine protein was identified in 70 (75%) ears by FLAIR MR-imaging and was strongly associated with the presence of hearing loss (32/34 hearing loss ears; 94%)(Fisher''s exact test; P = .005). Elevated intralabyrinthine protein was associated with the presence of CVS-associated cochlear aperture obstruction (64 of 67 ears with elevated protein; 96%)(Fisher''s exact test; P<0.0001) in both normal and hearing loss ears. Elevated intralabyrinthine protein was not identified in ears without CVS (5 ears). While larger tumor size was associated with hearing loss (P = 0.006), 16 hearing loss ears (47%) harbored CVSs less than 0.5 cm³, including 14 ears (88%) with block of the cochlear aperture and elevated protein.

Discussion

These findings are consistent with a model in which hearing loss develops as a result of cochlear aperture obstruction and accumulation of intralabyrinthine protein. MRI based identification of elevated intralabyrinthine protein may help identify the ear at-risk for developing hearing loss.     

Reduced acoustic startle response and peripheral hearing loss in the 5xFAD mouse model of Alzheimer's disease

Hearing dysfunction has been associated with Alzheimer's disease (AD) in humans, but there is little data on the auditory function of mouse models of AD. Furthermore, characterization of hearing ability in mouse models is needed to ensure that tests of cognition that use auditory stimuli are not confounded by hearing dysfunction. Therefore, we assessed acoustic startle response and pre‐pulse inhibition in the double transgenic 5xFAD mouse model of AD from 3–4 to 16 months of age. The 5xFAD mice showed an age‐related decline in acoustic startle as early as 3–4 months of age. We subsequently tested auditory brainstem response (ABR) thresholds at 4 and 13–14 months of age using tone bursts at frequencies of 2–32 kHz. The 5xFAD mice showed increased ABR thresholds for tone bursts between 8 and 32 kHz at 13–14 months of age. Finally, cochleae were extracted and basilar membranes were dissected to count hair cell loss across the cochlea. The 5xFAD mice showed significantly greater loss of both inner and outer hair cells at the apical and basal ends of the basilar membrane than wild‐type mice at 15–16 months of age. These results indicate that the 5xFAD mouse model of AD shows age‐related decreases in acoustic startle responses, which are at least partially due to age‐related peripheral hearing loss. Therefore, we caution against the use of cognitive tests that rely on audition in 5xFAD mice over 3–4 months of age, without first confirming that performance is not confounded by hearing dysfunction.     

线粒体毒素诱导突发性耳聋模型血管纹损伤机制的研究

目的研究线粒体毒素诱导豚鼠突发性耳聋模型血管纹损伤的机制。方法20只杂色豚鼠随机分为3-硝基丙酸（3-NP）组和磷酸盐缓冲液（PBS）对照组,分别经圆窗膜给予0.3 mmol/L 3-NP或PBS 10min。分别检测两组豚鼠的听性脑干反应测听（ABR）,血管纹丙二醛（MDA）、超氧化物歧化酶（SOD）及边缘细胞超微结构变化。结果与PBS对照组相比较,3-NP组ABR阈移增大、幅值减小;血管纹MDA含量增高（P〈0.05）,SOD活性降低（P〈0.05）;边缘细胞超微结构改变,尤以线粒体肿胀,空泡变最为显著。结论线粒体毒素通过氧化应激反应损伤突发性耳聋豚鼠的血管纹。     

Semi-Quantitative vs. Volumetric Determination of Endolymphatic Space in Menière’s Disease Using Endolymphatic Hydrops 3T-HR-MRI after Intravenous Gadolinium Injection

Magnetic resonance imaging enhances the clinical diagnosis of Menière''s disease. This is accomplished by in vivo detection of endolymphatic hydrops, which are graded using different semi-quantitative grading systems. We evaluated an established, semi-quantitative endolymphatic hydrops score and with a quantitative method for volumetric assessment of the endolymphatic size. 11 patients with Menière''s disease and 2 healthy subjects underwent high resolution endolymphatic hydrops 3 Tesla MRI with highly T2 weighted FLAIR and T2DRIVE sequences. The degree of endolymphatic hydrops was rated semi-quantitatively and compared to the results of 3D-volumetry. Moreover, the grade of endolymphatic hydrops was correlated with pure tone audiometry. Semi-quantitative grading and volumetric evaluation of the endolymphatic hydrops are in accordance (r = 0.92) and the grade of endolymphatic hydrops correlates with pure tone audiometry. Patients with a sickness duration of ≥ 30 months showed a significant higher total labyrinth fluid volume (p = 0.03). Fast, semi-quantitative evaluation of endolymphatic hydrops is highly reliable compared to quantitative/volumetric assessment. Endolymphatic space is significantly higher in patients with longer sickness duration.     

Surgical Induction of Endolymphatic Hydrops by Obliteration of the Endolymphatic Duct

Surgical induction of endolymphatic hydrops (ELH) in the guinea pig by obliteration and obstruction of the endolymphatic duct is a well-accepted animal model of the condition and an important correlate for human Meniere''s disease. In 1965, Robert Kimura and Harold Schuknecht first described an intradural approach for obstruction of the endolymphatic duct (Kimura 1965). Although effective, this technique, which requires penetration of the brain''s protective covering, incurred an undesirable level of morbidity and mortality in the animal subjects. Consequently, Andrews and Bohmer developed an extradural approach, which predictably produces fewer of the complications associated with central nervous system (CNS) penetration.(Andrews and Bohmer 1989) The extradural approach described here first requires a midline incision in the region of the occiput to expose the underlying muscular layer. We operate only on the right side. After appropriate retraction of the overlying tissue, a horizontal incision is made into the musculature of the right occiput to expose the right temporo-occipital suture line. The bone immediately inferio-lateral the suture line (Fig 1) is then drilled with an otologic drill until the sigmoid sinus becomes visible. Medial retraction of the sigmoid sinus reveals the operculum of the endolymphatic duct, which houses the endolymphatic sac. Drilling medial to the operculum into the area of the endolymphatic sac reveals the endolymphatic duct, which is then packed with bone wax to produce obstruction and ultimately ELH. In the following weeks, the animal will demonstrate the progressive, fluctuating hearing loss and histologic evidence of ELH.Open in a separate windowClick here to view.^{(41M, flv)}     

Hidden hearing loss is associated with loss of ribbon synapses of cochlea inner hair cells

The present study aimed to observe the changes in the cochlea ribbon synapses after repeated exposure to moderate-to-high intensity noise. Guinea pigs received 95 dB SPL white noise exposure 4 h a day for consecutive 7 days (we regarded it a medium-term and moderate-intensity noise, or MTMI noise). Animals were divided into four groups: Control, 1DPN (1-day post noise), 1WPN (1-week post noise), and 1MPN (1-month post noise). Auditory function analysis by auditory brainstem response (ABR) and compound action potential (CAP) recordings, as well as ribbon synapse morphological analyses by immunohistochemistry (Ctbp2 and PSD95 staining) were performed 1 day, 1 week, and 1 month after noise exposure. After MTMI noise exposure, the amplitudes of ABR I and III waves were suppressed. The CAP threshold was elevated, and CAP amplitude was reduced in the 1DPN group. No apparent changes in hair cell shape, arrangement, or number were observed, but the number of ribbon synapse was reduced. The 1WPN and 1MPN groups showed that part of ABR and CAP changes recovered, as well as the synapse number. The defects in cochlea auditory function and synapse changes were observed mainly in the high-frequency region. Together, repeated exposure in MTMI noise can cause hidden hearing loss (HHL), which is partially reversible after leaving the noise environment; and MTMI noise-induced HHL is associated with inner hair cell ribbon synapses.     

Functional variants in NOS1 and NOS2A are not associated with progressive hearing loss in Ménière's disease in a European Caucasian population

Hearing loss in Ménière's disease (MD) is associated with loss of spiral ganglion neurons and hair cells. In a guinea pig model of endolymphatic hydrops, nitric oxide synthases (NOS) and oxidative stress mediate loss of spiral ganglion neurons. To test the hypothesis that functional variants of NOS1 and NOS2A are associated with MD, we genotyped three functional variants of NOS1 (rs41279104, rs2682826, and a cytosine-adenosine microsatellite repeat in exon 1f) and the CCTTT repeat in the promoter of NOS2A gene (rs3833912) in two independent MD sets (273 patients in total) and 550 controls. A third cohort of American patients was genotyped as replication cohort for the CCTTT repeat. Neither allele nor genotype frequencies of rs41279104 and rs2682826 were associated with MD, although longer alleles of the cytosine-adenosine microsatellite repeat were marginally significant (corrected p?=?0.05) in the Mediterranean cohort but not in a second Galicia cohort. Shorter numbers of the CCTTT repeat in NOS2A were significantly more frequent in Galicia controls (OR?=?0.37 [CI, 0.18-0.76], corrected p?=?0.04), but this finding could not be replicated in Mediterranean or American case-control populations. Meta-analysis did not support an association between CCTTT repeats and risk for MD. Severe hearing loss (>75?dB) was also not associated with any functional variants studied. Functional variants of NOS1 and NOS2A do not confer susceptibility for MD.     

Therapeutic effect of edaravone on inner ear barotrauma in the guinea pig

Inner ear barotrauma (IEB) that is caused by acute pressure changes can often lead to permanent severe sensorineural hearing loss (SNHL). However, the mechanism that causes IEB is still unknown. In the current study, we assessed the involvement of reactive oxygen species (ROS) in IEB and the therapeutic effect of 3-methyl 1-phenyl-2-pyrazolin-5-one (edaravone), which is a free radical scavenger. To create the IEB model, guinea pigs were subjected to quick pressure changes that resulted in acute SNHL. The animals were then divided into two groups, an edaravone-treated IEB group and a non-treated IEB group that only received normal saline. Immunohistochemical analyses for 8-hydroxy-2-deoxyguanosine (8-OHdG) and 4-hydroxy-2-nonenal (4-HNE) were performed to examine the amount of oxidative DNA damage and lipid peroxidation that occurred in guinea pig cochlea. To assess the curative efficacy of edaravone, auditory brainstem response (ABR) testing was performed to evaluate auditory function. Strong immunoreactivities against 8-OHdG and 4-HNE were observed in the inner ear tissues of the non-treated IEB group. Lesser amounts of immunoreactivity were observed in the same region of the edaravone-treated IEB group as compared to the non-treated IEB group. Furthermore, ABR measurement revealed that there was a faster improvement in the threshold shift for the edaravone-treated IEB group as compared to that of the non-treated IEB group. At the final 7-week time point, the threshold shift for the edaravone-treated IEB group was significantly smaller as compared to the non-treated IEB group. These results strongly suggest that ROS is produced in the cochlea in response to acute pressure changes and that ROS plays an important role in the pathophysiology of IEB. Furthermore, edaravone treatment had a therapeutic effect on IEB-induced acute SNHL and thus, edaravone might possibly be able to be used as a therapeutic treatment for IEB.     

Responses of prolactin and hair growth to selection for age at puberty in Angus cattle

A trial was carried out over a 7-year period (1999 to 2005 calf crops) to compare indicators of seasonality in Angus cattle, which were part of a long-term genetic selection experiment. Divergent selection was applied for early ('AGE-') or late ('AGE+') age at puberty (AP) in heifers, and selection lines differed over the 7-year period by 62 days (15% of the mean). The primary measures of seasonality studied in 629 heifer progeny (59 sire groups) were serum concentration of prolactin (PRL), and winter and summer hair growth. Serial samples were obtained for PRL from 11 to 18 months of age, and data were analysed with adjustment for cortisol concentration. Using restricted maximum likelihood procedures with an animal model, heritability estimates were: AP, 0.26 ± 0.03; log(e)PRL concentration, 0.23 ± 0.07; log(e)cortisol concentration, 0.22 ± 0.07; hair weight, 0.21 ± 0.04; and hair length, 0.09 ± 0.05. Corresponding repeatability estimates for the last four traits were 0.49 ± 0.03, 0.38 ± 0.03, 0.21 ± 0.04, and 0.64 ± 0.02, respectively. The genetic correlation between AP and log(e)PRL concentration was estimated at -0.29 ± 0.13 (P < 0.05). PRL concentration in the AGE- line after passing through puberty was 11 ± 5% lower than in the AGE+ line (P < 0.05). Line effects were not significant for hair weight or hair length. It was concluded that divergent selection for AP changed PRL concentration, which may partly reflect sensitivity to changing day length.     

窄带噪声暴露后豚鼠听阈偏移及毛细胞的损伤

为了探讨听觉损伤与毛细胞损伤的关系,本实验比较了噪声暴露后豚鼠皮层听阈及其与基底膜单位长度上毛细胞损伤率的关系。暴露声源中心频率1000Hz,为1/3倍频程的窄带噪声。强度为136dB作用1小时。108dB每天暴露1小时,5天/周连续1个月。结果表明,毛细胞损伤呈灶性,损伤部位与周围界线十分分明。毛细胞损伤在豚鼠间及左右耳间均存在相当程度的个体差异。136dB暴露,毛细胞损伤最重的部位在基底膜1.5转到2.5转之间,符合1000Hz声音在基底膜的最大振动范围。108dB的损伤部位局限在1.5转,其范围及程度明显轻于136dB。136dB造成的听阈偏移高于108dB,尤其在4、8 KHz高频听阈偏移最明显,但耳蜗底转毛细胞多无明显损伤。