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1 nction and ribbon synapse regeneration after acoustic trauma.
2 ey role for ion homeostasis in resistance to acoustic trauma.
3 improves sound discrimination, and mitigates acoustic trauma.
4 enerate conditioning-induced protection from acoustic trauma.
5 s conditioned protection of the cochlea from acoustic trauma.
6 cochlea, and organ of Corti, all targets for acoustic trauma.
7 o accumulate in the murine cochlea following acoustic trauma.
8 y input and protection of the inner ear from acoustic trauma.
9  frequency tuning, and protects the ear from acoustic trauma.
10 erented map regions three or more days after acoustic trauma.
11 cell's baseline response properties prior to acoustic trauma.
12 nt stimuli, attention and protection against acoustic trauma.
13 tection against hearing loss following acute acoustic trauma.
14 to exhibit non-homeostatic excess gain after acoustic trauma.
15 the regulation of cochlear sensitivity after acoustic trauma.
16 posure to PCBs blocked hearing recovery from acoustic trauma.
17 ignaling after aminoglycoside ototoxicity or acoustic trauma.
18 ding the differential sensitivity of ANFs to acoustic trauma.
19                                          The acoustic trauma also reduced capillary density and incre
20                                  Second, the acoustic trauma altered dendritic morphology and decreas
21 imuli known to cause hair cell loss, such as acoustic trauma and aminoglycoside administration.
22  cochlear pericytes are markedly affected by acoustic trauma and display an abnormal morphology.
23 d tip links of hair cells are susceptible to acoustic trauma and ototoxic drugs.
24  are vulnerable to a variety of insults like acoustic trauma and ototoxic drugs.
25                          We exposed flies to acoustic trauma and quantified physiological and anatomi
26  million individuals, [2] often results from acoustic trauma and, [3] is very often exacerbated under
27 in cochlear gain control, protection against acoustic trauma, and attention.
28 ured cochlea during the first week following acoustic trauma, and further BMDC accumulation was seen
29 emporal precision was not degraded following acoustic trauma, and furthermore that sharpness of cochl
30 ed by others in the auditory nerve following acoustic trauma, and suggest that the map alterations ha
31  in the auditory nerve following less severe acoustic trauma, and thus would seem to have a periphera
32                                              Acoustic trauma (AT, loud sounds) slow AMPAR-EPSC decay
33                    Damaging levels of sound (acoustic trauma, AT) diminish peripheral synapses, but w
34 ed to resist cochlear damage associated with acoustic trauma by exposure to a variety of "conditionin
35                                 We find that acoustic trauma causes activation of PVM/Ms and physical
36                                              Acoustic trauma disrupts cochlear blood flow and damages
37                     Thus, Drosophila exhibit acoustic trauma effects resembling those found in verteb
38   Damage and regression of capillaries after acoustic trauma have long been observed, but the underly
39 itory nerve activity for several weeks after acoustic trauma; however, the underlying neural mechanis
40 s in the modulation of cochlear responses to acoustic trauma in rats.
41                             We simulated the acoustic trauma-induced tip link damage or stereociliary
42                        The primary effect of acoustic trauma is manifested as damage to the delicate
43 cochlear sensory cell degeneration following acoustic trauma is unknown.
44            This study explored the effect of acoustic trauma on cochlear pericytes.
45                                              Acoustic trauma, one of the leading causes of sensorineu
46 lls of the inner ear undergo apoptosis after acoustic trauma or aminoglycoside antibiotic treatment,
47 ccurring during hair cell regeneration after acoustic trauma or aminoglycoside treatment.
48                 Sensory hair cells die after acoustic trauma or ototoxic insults, but the signal tran
49  the cochlea in response to injury caused by acoustic trauma or ototoxicity, but the nature of the in
50 ry for repairing auditory circuits following acoustic trauma or promoting cochlear reinnervation duri
51                         Hair cells die after acoustic trauma, ototoxic drugs or aging diseases, leadi
52 ude surgical ablation of the organ of Corti, acoustic trauma, ototoxic drugs, and hereditary deafness
53 xpression is strongly upregulated days after acoustic trauma, potentially providing a sustained prote
54           The susceptibility of tip links to acoustic trauma raises questions as to whether these fra
55 icient in PLZF have hearing and responses to acoustic trauma similar to their wild type littermates b
56                    When birds are exposed to acoustic trauma, the normal pattern and number of nerve
57 VM/Ms and endothelial barrier breakdown from acoustic trauma to the mouse ear.
58 both these stimuli are present in vivo after acoustic trauma, TRPA1 activation after noise may affect
59          Excess cortical response gain after acoustic trauma was expressed heterogeneously among indi
60 r synergistic protection of the cochlea from acoustic trauma when given together with DFO and mannito
61 sceptible to glutamate excitotoxicity and to acoustic trauma, with potentially adverse consequences t