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All tetrapods (mammals, birds, reptiles, and amphibians) share the ability to breathe with their mouths closed due to the formation of choanae, which are openings that allow communication between the nasal and oral cavities. In most fishes, the nasal cavities serve a strictly olfactory function, possessing incurrent and excurrent nares that lie outside of the mouth and therefore, never communicate with the respiratory system. It is not until the evolution of tetrapods, in which the nasal cavities consistently open into the mouth, that they are used both for olfaction and for respiration. However, this developmental transition is poorly understood, with no consensus on the evolutionary origin of the choana in various groups despite decades of debate. Here, we use high-contrast 3D imaging in conjunction with histology and apoptotic cell analysis in non-mineralized embryonic tissues to study the formation of the choana in the axolotl (Ambystoma mexicanum), an aquatic salamander species. We show that the axolotl choana forms from an extension of the embryonic nasal sac, which pushes through intervening mesenchyme and connects with the palate epithelium of the oral cavity, eventually breaking through. This mechanism differs from caecilians, mammals and reptiles, where fusion across a bucconasal groove plays an active role in choana formation. Nevertheless, caecilians, mammals and axolotls converge on the development of a transient epithelial tissue that has to break down in order to develop a patent choana, adding another twist to the intriguing arguments on the evolutionary history of the choana.

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While task-dependent changes have been demonstrated in auditory cortex for a number of behavioral paradigms and mammalian species, less is known about how behavioral state can influence neural coding in the midbrain areas that provide auditory information to cortex. We measured single-unit activity in the inferior colliculus (IC) of common marmosets of both sexes while they performed a tone-in-noise detection task and during passive presentation of identical task stimuli. In contrast to our previous study in the ferret IC, task engagement had little effect on sound-evoked activity in central (lemniscal) IC of the marmoset. However, activity was significantly modulated in noncentral fields, where responses were selectively enhanced for the target tone relative to the distractor noise. This led to an increase in neural discriminability between target and distractors. The results confirm that task engagement can modulate sound coding in the auditory midbrain, and support a hypothesis that subcortical pathways can mediate highly trained auditory behaviors.SIGNIFICANCE STATEMENT While the cerebral cortex is widely viewed as playing an essential role in the learning and performance of complex auditory behaviors, relatively little attention has been paid to the role of brainstem and midbrain areas that process sound information before it reaches cortex. This study demonstrates that the auditory midbrain is also modulated during behavior. These modulations amplify task-relevant sensory information, a process that is traditionally attributed to cortex.

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Tinnitus and hyperacusis are life-disrupting perceptual abnormalities that are often preceded by acoustic overexposure. Animal models of overexposure have suggested a link between these phenomena and neural hyperactivity, i.e., elevated spontaneous rates (SRs) and sound-evoked responses. Prior work has focused on changes in central auditory responses, with less attention paid to the exact nature of the associated cochlear damage. The demonstration that acoustic overexposure can cause cochlear neuropathy without permanent threshold elevation suggests cochlear neuropathy per se may be a key elicitor of neural hyperactivity. We addressed this hypothesis by recording responses in the mouse inferior colliculus (IC) following a bilateral, neuropathic noise exposure. One to three weeks post-exposure, mean SRs were unchanged in mice recorded while awake, or under anesthesia. SRs were also unaffected by more intense, or unilateral exposures. These results suggest that neither neuropathy nor hair cell loss are sufficient to raise SRs in the IC, at least in 7-week-old mice, 1-3 weeks post exposure. However, it is not clear whether our mice had tinnitus. Tone-evoked rate-level functions at the CF were steeper following exposure, specifically in the region of maximal neuropathy. Furthermore, suppression driven by off-CF tones and by ipsilateral noise were reduced. Both changes were especially pronounced in neurons of awake mice. This neural hypersensitivity may manifest as behavioral hypersensitivity to sound - prior work reports that this same exposure causes elevated acoustic startle. Together, these results indicate that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis.

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Listeners with normal audiometric thresholds can still have suprathreshold deficits, for example, in the ability to discriminate sounds in complex acoustic scenes. One likely source of these deficits is cochlear neuropathy, a loss of auditory nerve (AN) fibers without hair cell damage, which can occur due to both aging and moderate acoustic overexposure. Since neuropathy can affect up to 50 % of AN fibers, its impact on suprathreshold hearing is likely profound, but progress is hindered by lack of a robust non-invasive test of neuropathy in humans. Reduction of suprathreshold auditory brainstem responses (ABRs) can be used to quantify neuropathy in inbred mice. However, ABR amplitudes are highly variable in humans, and thus more challenging to use. Since noise-induced neuropathy is selective for AN fibers with high thresholds, and because phase locking to temporal envelopes is particularly strong in these fibers, the envelope following response (EFR) might be a more robust measure. We compared EFRs to sinusoidally amplitude-modulated tones and ABRs to tone-pips in mice following a neuropathic noise exposure. EFR amplitude, EFR phase-locking value, and ABR amplitude were all reduced in noise-exposed mice. However, the changes in EFRs were more robust: the variance was smaller, thus inter-group differences were clearer. Optimum detection of neuropathy was achieved with high modulation frequencies and moderate levels. Analysis of group delays was used to confirm that the AN population was dominating the responses at these high modulation frequencies. Application of these principles in clinical testing can improve the differential diagnosis of sensorineural hearing loss.

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Many listeners with hearing thresholds within the clinically normal range nonetheless complain of difficulty hearing in everyday settings and understanding speech in noise. Converging evidence from human and animal studies points to one potential source of such difficulties: differences in the fidelity with which supra-threshold sound is encoded in the early portions of the auditory pathway. Measures of auditory subcortical steady-state responses (SSSRs) in humans and animals support the idea that the temporal precision of the early auditory representation can be poor even when hearing thresholds are normal. In humans with normal hearing thresholds (NHTs), paradigms that require listeners to make use of the detailed spectro-temporal structure of supra-threshold sound, such as selective attention and discrimination of frequency modulation (FM), reveal individual differences that correlate with subcortical temporal coding precision. Animal studies show that noise exposure and aging can cause a loss of a large percentage of auditory nerve fibers (ANFs) without any significant change in measured audiograms. Here, we argue that cochlear neuropathy may reduce encoding precision of supra-threshold sound, and that this manifests both behaviorally and in SSSRs in humans. Furthermore, recent studies suggest that noise-induced neuropathy may be selective for higher-threshold, lower-spontaneous-rate nerve fibers. Based on our hypothesis, we suggest some approaches that may yield particularly sensitive, objective measures of supra-threshold coding deficits that arise due to neuropathy. Finally, we comment on the potential clinical significance of these ideas and identify areas for future investigation.