Detection and differentiation of sensorineural hearing loss in mice using auditory steady-state responses and transient auditory brainstem responses

Pauli-Magnus, D.; Hoch, Gerhard; Strenzke, Nicola; Anderson, Samira; Jentsch, Thomas J.; Moser, Tobias

doi:10.1016/j.neuroscience.2007.08.010

Cited by 34 publications

(36 citation statements)

References 37 publications

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“…ABR signal to noise ratio was higher for click responses when compared to tones as is expected when comparing a broadband stimulus to pure tone. Tone-evoked ABR quality is comparable to previously published examples [46]. Although 64 and 80 kHz tones are not commonly used for ABR threshold analyses, they fall within the range of ultrasonic vocalizations produced by mice [16] and therefore probe an ethologically relevant frequency range.…”

Section: Results and Statistical Analysessupporting

confidence: 76%

Adult Plasticity in the Subcortical Auditory Pathway of the Maternal Mouse

et al. 2014

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Subcortical auditory nuclei were traditionally viewed as non-plastic in adulthood so that acoustic information could be stably conveyed to higher auditory areas. Studies in a variety of species, including humans, now suggest that prolonged acoustic training can drive long-lasting brainstem plasticity. The neurobiological mechanisms for such changes are not well understood in natural behavioral contexts due to a relative dearth of in vivo animal models in which to study this. Here, we demonstrate in a mouse model that a natural life experience with increased demands on the auditory system – motherhood – is associated with improved temporal processing in the subcortical auditory pathway. We measured the auditory brainstem response to test whether mothers and pup-naïve virgin mice differed in temporal responses to both broadband and tone stimuli, including ultrasonic frequencies found in mouse pup vocalizations. Mothers had shorter latencies for early ABR peaks, indicating plasticity in the auditory nerve and the cochlear nucleus. Shorter interpeak latency between waves IV and V also suggest plasticity in the inferior colliculus. Hormone manipulations revealed that these cannot be explained solely by estrogen levels experienced during pregnancy and parturition in mothers. In contrast, we found that pup-care experience, independent of pregnancy and parturition, contributes to shortening auditory brainstem response latencies. These results suggest that acoustic experience in the maternal context imparts plasticity on early auditory processing that lasts beyond pup weaning. In addition to establishing an animal model for exploring adult auditory brainstem plasticity in a neuroethological context, our results have broader implications for models of perceptual, behavioral and neural changes that arise during maternity, where subcortical sensorineural plasticity has not previously been considered.

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Section: Results and Statistical Analysessupporting

confidence: 76%

Adult Plasticity in the Subcortical Auditory Pathway of the Maternal Mouse

et al. 2014

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“…Experiments were performed as described in [46], complied with national animal care guidelines and were approved by the University of Goettingen Board for animal welfare and the animal welfare office of the state of Lower Saxony. In brief, animals were anaesthetized intraperitoneally with a combination of ketamine (125 mg/kg) and xylazin (2.5 mg/kg) and the core temperature was maintained constant at 37°C.…”

Section: Methodsmentioning

confidence: 99%

A Missense Mutation in a Highly Conserved Alternate Exon of Dynamin-1 Causes Epilepsy in Fitful Mice

et al. 2010

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Dynamin-1 (Dnm1) encodes a large multimeric GTPase necessary for activity-dependent membrane recycling in neurons, including synaptic vesicle endocytosis. Mice heterozygous for a novel spontaneous Dnm1 mutation—fitful—experience recurrent seizures, and homozygotes have more debilitating, often lethal seizures in addition to severe ataxia and neurosensory deficits. Fitful is a missense mutation in an exon that defines the DNM1a isoform, leaving intact the alternatively spliced exon that encodes DNM1b. The expression of the corresponding alternate transcripts is developmentally regulated, with DNM1b expression highest during early neuronal development and DNM1a expression increasing postnatally with synaptic maturation. Mutant DNM1a does not efficiently self-assemble into higher order complexes known to be necessary for proper dynamin function, and it also interferes with endocytic recycling in cell culture. In mice, the mutation results in defective synaptic transmission characterized by a slower recovery from depression after trains of stimulation. The DNM1a and DNM1b isoform pair is highly conserved in vertebrate evolution, whereas invertebrates have only one isoform. We speculate that the emergence of more specialized forms of DNM1 may be important in organisms with complex neuronal function.

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“…For example, electrocochleography results in similar find ings for patients with OPA1-associated auditory neuro pathy and OTOF-associated auditory synapt opathy 74,127 . Moreover, in animal models of auditory synaptopathy and neuropathy, the delayed and broadened compound action potentials can arise from either presynaptic 16,17,128 or post synaptic 21 defects. Assessing the extent of adap tation to pure tones, on the other hand, might facilitate differentiation between synaptopathy and neuropathy.…”

Section: Distinguishing Neuropathy and Synaptopathymentioning

confidence: 99%