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Neurod1 mimics Neurog1 with respect to shortening, disorganization and gene expression alteration in the cochlea [14].
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Accordingly, the Igf1−/− mouse shows poor growth rates, high mortality, profound sensorineural deafness and late postnatal morphological alterations in the cochlea [16] We have shown previously that the absence of IGF-I causes poor myelination and delayed maturation of auditory neurones that suffer apoptosis during the early postnatal mouse development P5-P20 [18], [18].
In addition, ischemia/reperfusion injury caused by an alteration of blood flow in the cochlea, glutamate excitotoxicity of auditory nerves caused by an excess release of glutamate in the inner hair cells (IHC) and calcium overload in the outer hair cells (OHC) in response to intense noise have been reported to have important roles in the pathological mechanism of NIHL.
These early changes in paraflocculus observed after two weeks may be evoked by an alteration in the direct input from the cochlea or in the indirect pathway described from the cortex as outlined below.
However, we could not detect any significant alteration in the expression of NeuroD1, Brn3a, ErbB2, or ErbB3 in the E14.5 cochleae (Fig. S8), in contrast to the reduction of neurotrophin receptors (Fig. 9B, C).
The fluid sends shudders through 16,000 tiny hair cells, also in the cochlea.
The improvement in the animals' hearing depended on the number of injected nerve cells that took hold in the cochlea.
In the cochlea, incoming signals are transformed into neuronal impulses.
Signal processing in the cochlea is non-linear.
At the outset of this work is the quest to understand signal processing in the cochlea.
CT can reveal pneumolabyrinth in the cochlea, the vestibule, or both.
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