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in the HF half of the ICc. By 8 days SA recovered to normal levels in LF ICc. The HF half of the ICc sho- wed a decrement in SA, although less so than at earlier times. There was no further change in SA at 16 days (Supported by the Tinnitus Research Consortium and MRRC Center Grant HD02528).

Tinnitus and neural plasticity of the brain. Otol Neurotol. 2007 Feb;28(2):178-184. Bartels H, Staal MJ, Albers FW Department of Otorhinolaryngology, University Medical Center Groningen, Groningen, The Netherlands. h.bartels@kno.umcg.nl

Objective: To describe the current ideas about the manifestations of neural plasticity in generating tinni- tus. Data sources: Recently published source articles were identified using MEDLINE, PubMed, and Cochrane Library according to the key words mentioned below. Study selection: Review articles and controlled trials were particularly selected. Data extraction: Data were selected systematically, scaled on validity and comparability. Conclusion: An altered afferent input to the auditory pathway may be the initiator of a complex se- quence of events, finally resulting in the generation of tinnitus at the central level of the auditory nervous system. The effects of neural plasticity can generally be divided into early modifications and modifica- tions with a later onset. The unmasking of dormant synapses, diminishing of (surround) inhibition and initiation of generation of new connections through axonal sprouting are early manifestations of neural plasticity, resulting in lateral spread of neural activity and development of hyperexcitability regions in the central nervous system. The remodeling process of tonotopic receptive fields within auditory pathway structures (dorsal cochlear nucleus, inferior colliculus, and the auditory cortex) are late manifestations of neural plasticity. The modulation of tinnitus by stimulating somatosensory or visual systems in some people with tinnitus might be explained via the generation of tinnitus following the nonclassical pathway. The similarities between the pathophysiological processes of phantom pain sensations and tinnitus have stimulated the theory that chronic tinnitus is an auditory phantom perception.

Tinnitus behavior and hearing function correlate with the reciprocal expression patterns of BDNF and Arg3.1/arc in auditory neurons following acoustic trauma. Neuroscience. 2007 Jan 31. Tan J, Ruttiger L, Panford-Walsh R, Singer W, Schulze H, Kilian SB, Hadjab S, Zimmermann U, Kopschall I, Rohbock K, Knipper M University of Tubingen, Department of Otorhinolaryngology, Hearing Research CenterTubingen, Molecu- lar Neurobiology, Elfriede-Aulhorn-Strasse 5, 72076 Tubingen, Germany.

The molecular changes following sensory trauma and the subsequent response of the CNS are poor- ly understood. We focused on finding a molecular tool for monitoring the features of excitability which occur following acoustic trauma to the auditory system. Of particular interest are genes that alter their expression pattern during activity-induced changes in synaptic efficacy and plasticity. The expression of brain-derived neurotrophic factor (BDNF), the activity-dependent cytoskeletal protein (Arg3.1/arc), and the immediate early gene c-Fos were monitored in the peripheral and central auditory system hours and days following a traumatic acoustic stimulus that induced not only hearing loss but also phantom auditory perception (tinnitus), as shown in rodent animal behavior models. A reciprocal responsiveness of activity- dependent genes became evident between the periphery and the primary auditory cortex (AI): as c-Fos and BDNF exon IV expression was increased in spiral ganglion neurons, Arg3.1/arc and (later on) BDNF exon IV expression was reduced in AI. In line with studies indicating increased spontaneous spike activi- ty at the level of the inferior colliculus (IC), an increase in BDNF and GABA-positive neurons was seen in

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