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We review several neural models of tinnitus and discuss published findings from simulations using these models.
In animal models of tinnitus pathological neuronal activity has been demonstrated.
Animal models of tinnitus (e.g., noise or drug induced) produce increases in spontaneous neuronal activity, which are likely downstream consequences of changes in calcium and calcium channel-dependent neurotransmitter release.
To determine whether these temporal differences in hearing loss would differentially affect tinnitus percepts we recorded pASR and gASR across both animal models of tinnitus and normal hearing controls.
Few studies have examined NO-related mechanisms in animal models of tinnitus.
Animal models of tinnitus allow us to study the relationship between changes in neural activity and the tinnitus percept.
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In this study, the effect of DBS in the inferior colliculi is investigated in an animal model of tinnitus.
In contrast, the TRI algorithm promotes a medical model of tinnitus management.
Mouse model of tinnitus allows for behavioral separation of noise-exposed mice with either vulnerability or resilience to tinnitus.
(2006) examined the distribution of nNOS in the CN of rats using a salicylate-induced behavioural model of tinnitus.
To study the neural mechanisms underlying resilience to noise-induced tinnitus, we employed an animal model of tinnitus that permits behavioral separation of tinnitus from non-tinnitus mice.
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