Ultrasonic singing by the blue-throated hummingbird: a comparison between production and perception

Blue-throated hummingbirds produce elaborate songs extending into the ultrasonic frequency range, up to 30 kHz. Ultrasonic song elements include harmonics and extensions of audible notes, non-harmonic components of audible syllables, and sounds produced at frequencies above 20 kHz without corresponding hearing range sound. To determine whether ultrasonic song elements function in intraspecific communication, we tested the hearing range of male and female blue-throated hummingbirds. We measured auditory thresholds for tone pips ranging from 1 kHz to 50 kHz using auditory brainstem responses. Neither male nor female blue-throated hummingbirds appear to be able to hear above 7 kHz. No auditory brainstem responses could be detected between 8 and 50 kHz at 90 dB. This high-frequency cutoff is well within the range reported for other species of birds. These results suggest that high-frequency song elements are not used in intraspecific communication. We propose that the restricted hummingbird hearing range may exemplify a phylogenetic constraint.     

Low frequency hearing in cephalopods

Summary Classical conditioning was employed to test the sensitivity of cephalopods to vibrations between 1 and 100 Hz generated in a standing wave acoustic tube. The animals were trained to associate sound stimuli with a weak electric shock, and the recorded conditioned responses were changes in breathing and jetting activity. Five specimens of Sepia officinalis were tested, and all responded to these low frequency sounds. The relevant stimulus parameter was particle motion rather than sound pressure. The threshold values (measured as particle acceleration) decreased towards lower frequencies in the tested range, reaching values below 4 × 10^-3 m/s². The thresholds in the most sensitive range may have been masked by the considerable background noise at the experimental site (Naples). Two individuals of Octopus vulgaris and one Loligo vulgaris were also tested, and showed a similar sensitivity to low frequency sound.     

Lung mediated auditory contrast enhancement improves the Signal-to-noise ratio for communication in frogs

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Peripheral auditory processing in the bobtail lizard Tiliqua rugosa

Summary We have labelled single physiologically-characterized primary auditory neurones in the bobtail lizard and traced them to their innervation sites within the basilar papilla. The distribution of stained fibre terminals shows that low frequencies (up to a characteristic frequency, CF, of about 0.8 kHz) are processed in the smaller apical segment of the papilla and medium to high frequencies in the much longer basal segment. It is possible that the frequency ranges of these segments partly overlap in individual animals.The tonotopic organization of the basal segment is well described by an exponential relationship; the CF increases towards the basal end. Systematic, peripheral recordings from the auditory nerve very close to the papilla confirm this tonotopicity for the basal segment.The apical segment of the papilla shows an unusual tonotopic organization in that the CF appears to increase across the epithelium, from abneural to neural. A tonotopicity in this direction has not previously been demonstrated in vertebrates.All stained neurones branched within the basilar papilla to innervate, typically, between 4 and 14 hair cells. The branching patterns of fibres innervating in the apical and basal papillar segment, respectively, show characteristic differences. Apical fibres tend to innervate hair cells with the same morphological polarity and often branch extensively along the segment. Basal fibres, in contrast, typically innervate about equal numbers of hair cells of opposing polarity and are more restricted in their longitudinal branching.Abbreviation CF characteristic frequency     

Effects of delayed and extended antioxidant treatment on acute acoustic trauma

Abstract

Objective: Hair cell death caused by acute acoustic trauma (AAT) reaches a secondary maximum at 7–10 days after noise exposure due to a second oxidative stress. Therefore, this study tested the effects of a combination of hydroxylated alpha-phenyl-tert-butylnitrone (4-OHPBN), N-acetyl-L-cysteine (NAC) and acetyl-L-carnitine (ALCAR) on AAT when the duration of treatment was extended over the period of 7–10 days after noise exposure as well as when the initial treatment was delayed 24 to 48 h after noise exposure. Methods: Thirty chinchilla were exposed to a 105 dB octave-band noise centred at 4 kHz for 6 h and received the following treatments: (1) noise + saline (2–5) 4-OHPBN (20 mg/kg) + NAC (50 mg/kg) + ALCAR (20 mg/kg) intraperitoneally injected beginning 24 or 48 h after noise exposure twice daily for the next 2, 8 or 9 days. Auditory brainstem response (ABR) threshold shifts, outer hair cell (OHC) counts and organ of Corti immunohistochemistry were analyzed. Results: The combination administration decreased ABR threshold shifts, inhibited OHC loss and reduced 4-hydroxynonenal (4-HNE) immunostaining. Significant decreases in the threshold shifts and reduction in OHC loss were observed with a shorter delay before starting treatment (24 h) and longer duration (9 days) treatment. Conclusions: These results demonstrate that the administration of antioxidant drugs extended up to 10 days after noise exposure can effectively treat AAT in a chinchilla model. This may provide significant and potentially clinically important information about the effective therapeutic window for AAT treatment.     

Evaluación de los parámetros de hipoacusia laboral en trabajadores activos y su relación con los niveles de glucemia basal

IntroductionHearing loss due to noise is considered within the prevention plans of the most common occupational diseases. In addition to evaluation of working conditions, other personal factors increasing the risk of hypoacusis, such as diabetes, should be taken into account.ObjectivesTo explore hearing loss in the workplace and its relationship to impaired fasting baseline blood glucose levels.MethodsAn observational, cross-sectional study enrolling 1636 workers from service companies was conducted. Full audiometric evaluation was performed at different frequencies: high frequency (HF), early loss index (ELI), speech average loss (SAL), and monaural and binaural loss. Results were categorized by baseline blood glucose levels: G1 (< 100 mg/dl), G2 (100-125 mg/dl), and G3 (> 125 mg/dl).ResultsBased on both HF and ELI, 11% of workers had clear indication of deafness. Women with G3 levels showed significant differences in the results of HF and ELI indexes as compared to the G1 group (P = .038 and .046, respectively). A positive association was found between hearing loss and G3 blood glucose levels in HF (OR: .338; p = .002), ELI (OR: .407; p = .007), and the monaural test in the left ear (OR: 4.77 × 10-5; p = .006).ConclusionsDespite the methodological limitations of this study, there is evidence for an increased risk of high frequency hearing loss in workers with high baseline blood glucose levels.     

Establishment of sperm associated antigen 6 gene knockout mouse model and its mechanism of deafness

To investigate the effects of knocking out the Sperm associated antigen6 (Spag6) gene on the auditory system of mice, the heterozygous type Spag6 knockout mouse model built in the previous period was used for mating and breeding, and homozygous type Spag6 gene knockout mouse (Spag−/−), heterozygous type Spag6 gene knockout mouse (Spag+/−) and wild type mouse (Spag+/+) were obtained. PCR technology was used to verify mouse models with different genotypes. After verification, the hearing threshold responses of Spag+/+ and Spag−/− genotype mice were detected. The localization of Spag6 gene in the basal membrane of the cochlea of the inner ear was detected by immunofluorescence staining. The changes of middle ear tissues were observed by H.E. staining sections. The relative expression of Prestin gene and Pgrn gene in different age mice was detected by fluorescence quantitative PCR. The relative expression of Prestin gene was detected by western blot. The results showed that Spag−/− mice had hearing impairment compared with Spag+/+ mice. And Spag6 protein is distributed in different genotypes of mouse hair cells; Spag−/− mice showed otitis media. The expression of Prestin mRNA and protein in Spag−/− mice was significantly higher than that in Spag+/+ mice (P < 0.01). The expression of Pgrn gene in Spag+/+ mice was significantly higher than that in Spag−/− mice (P < 0.05). It indicates that the loss of Spag6 gene would lead to the decline of hearing sense in mice. It is likely that the Spag6 gene could affect hearing by regulating the expression of Prestin gene. And the absence of the Spag6 gene causes otitis media in mice. The results of this study can lay a theoretical foundation for the follow-up studies of Spag6 gene in deafness diseases.     

Pathogenic effects of a novel mutation (c.664_681del) in KCNQ4 channels associated with auditory pathology

Hearing loss is a common communication disorder caused by various environmental and genetic factors. Hereditary hearing loss is very heterogeneous, and most of such cases involve sensorineural defects in the auditory pathway. There are currently 57 known autosomal dominant non-syndromic hearing loss (DFNA) loci, and the causative genes have been identified at 22 of these loci. In the present study, we performed a genome-wide linkage analysis in a Korean family segregating autosomal dominant hearing loss. We observed linkage on chromosome 1p34, and at this locus, we detected a novel mutation consisting of an 18 nucleotide deletion in exon 4 of the KCNQ4 gene, which encodes a voltage-gated potassium channel. We carried out a functional in vitro study to analyze the effects of this mutation (c.664_681del) along with two previously described KCNQ4 mutations, p.W276S and p.G285C. Although the c.664_681del mutation is located in the intercellular loop and the two previously described mutations, p.W276S and p.G285C, are located in the pore region, all mutants inhibit normal channel function by a dominant negative effect. Our analysis indicates that the intercellular loop is as significant as the pore region as a potential site of pathogenic effects on KCNQ4 channel function.     

Coexistence of mitochondrial 12S rRNA C1494T and CO1/tRNA(Ser(UCN)) G7444A mutations in two Han Chinese pedigrees with aminoglycoside-induced and non-syndromic hearing loss

Mutations in mitochondrial DNA are one of the important causes of hearing loss. We report here the clinical, genetic, and molecular characterization of two Han Chinese pedigrees with maternally transmitted aminoglycoside-induced and nonsyndromic bilateral hearing loss. Clinical evaluation revealed the wide range of severity, age-at-onset, and audiometric configuration of hearing impairment in matrilineal relatives in these families. The penetrances of hearing loss in these pedigrees were 20% and 18%, when aminoglycoside-induced deafness was included. When the effect of aminoglycosides was excluded, the penetrances of hearing loss in these seven pedigrees were 10% and 15%. Sequence analysis of the complete mitochondrial genomes in these pedigrees showed the presence of the deafness-associated 12S rRNA C1494T and CO1/tRNA(Ser(UCN)) G7444A mutations. Their distinct sets of mtDNA polymorphism belonged to Eastern Asian haplogroup C4a1, while other previously identified six Chinese mitochondrial genomes harboring the C1494T mutation belong to haplogroups D5a2, D, R, and F1, respectively. This suggested that the C1494T or G7444A mutation occurred sporadically and multiplied through evolution of the mitochondrial DNA (mtDNA). The absence of functionally significant mutations in tRNA and rRNAs or secondary LHON mutations in their mtDNA suggest that these mtDNA haplogroup-specific variants may not play an important role in the phenotypic expression of the 12S rRNA C1494T and CO1/tRNA(Ser(UCN)) G7444A mutations in those Chinese families. However, aminoglycosides and other nuclear modifier genes play a modifying role in the phenotypic manifestation of the C1494T mutation in these Chinese families.