Diversity and plasticity in amino acid receptor subunits in the rat auditory brain stem

Sato, Kazuo; Shiraishi, Shugo; Nakagawa, Hiroe; Kuriyama, Hiromichi; Altschuler, Richard A.

doi:10.1016/s0378-5955(00)00127-1

Cited by 46 publications

(35 citation statements)

References 56 publications

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“…Similar findings have been reported in animals deafened as adults, although in this case the reduction in the expression was transient [Sato et al, 2000]. In neonatally deafened animals, there is a reported increase in the expression of mRNAs encoding receptors to Á-aminobutyric acid, a major inhibitory neurotransmitter in this pathway .…”

Section: Cochlear Nucleussupporting

confidence: 87%

Deafness-Induced Changes in the Auditory Pathway: Implications for Cochlear Implants

Shepherd

Hardie²

2001

Audiol Neurotol

172

112

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A profound sensorineural hearing loss induces significant pathological and atrophic changes within the cochlea and central auditory pathway. We describe these deafness-induced morphological and functional changes following controlled lesions of the cochlea in experimental animals. Such changes are generally consistent with the limited number of reports describing deafness-induced changes observed in human material. The implications of these pathophysiological changes within the auditory pathway on cochlear implant function are discussed. Finally, the plastic response of the deafened auditory system to electrical stimulation of the auditory nerve is reviewed in light of the clinical implications for cochlear implant recipients.

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Section: Cochlear Nucleussupporting

confidence: 87%

Deafness-Induced Changes in the Auditory Pathway: Implications for Cochlear Implants

Shepherd

Hardie²

2001

Audiol Neurotol

172

112

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“…This would lead to a reduction in the Hebbian learning rules in fusiform cells (Doiron et al 2011;Zeng et al 2012). Similar to observations in other brain regions where changes in N-methyl-D-aspartate receptror (NMDAr) type and density have been associated with changes in long-term potentiation/long-term depression expression (Cho et al 2009;Peng et al 2010;Dalton et al 2012), a redistribution of the NMDAr-2B (Marianowski et al 2000;Sato et al 2000) at the synaptic terminals of the parallel fibers onto the fusiform and cartwheel cells may change the learning rule profiles in the DCN of the noise-exposed and tinnitus animals. Third, an important contribution to the plasticity of fusiform cell responses is provided by the degree of intrinsic neural excitability.…”

Section: Molecular Mechanisms Mediating Changes Following Noise Expossupporting

confidence: 61%

Stimulus-timing-dependent modifications of rate-level functions in animals with and without tinnitus

Stefanescu

Koehler

Shore

2015

Journal of Neurophysiology

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Stefanescu RA, Koehler SD, Shore SE. Stimulus-timing-dependent modifications of rate-level functions in animals with and without tinnitus. J Neurophysiol 113: 956 -970, 2015. First published November 21, 2014 doi:10.1152/jn.00457.2014.-Tinnitus has been associated with enhanced central gain manifested by increased spontaneous activity and sound-evoked firing rates of principal neurons at various stations of the auditory pathway. Yet, the mechanisms leading to these modifications are not well understood. In a recent in vivo study, we demonstrated that stimulus-timing-dependent bimodal plasticity mediates modifications of spontaneous and tone-evoked responses of fusiform cells in the dorsal cochlear nucleus (DCN) of the guinea pig. Fusiform cells from sham animals showed primarily Hebbian learning rules while noise-exposed animals showed primarily anti-Hebbian rules, with broadened profiles for the animals with behaviorally verified tinnitus (Koehler SD, Shore SE. J Neurosci 33: 19647-19656, 2013a). In the present study we show that well-timed bimodal stimulation induces alterations in the rate-level functions (RLFs) of fusiform cells. The RLF gains and maximum amplitudes show Hebbian modifications in sham and no-tinnitus animals but anti-Hebbian modifications in noise-exposed animals with evidence for tinnitus. These findings suggest that stimulus-timing bimodal plasticity produced by the DCN circuitry is a contributing mechanism to enhanced central gain associated with tinnitus. dorsal cochlear nucleus; multisensory integration; neural plasticity; rate-level functions; tinnitus TINNITUS, THE PATHOLOGICAL condition of phantom sound perception, has been often associated with enhanced central gain of the auditory pathway following an auditory insult. Increased spontaneous activity and tone-evoked firing rates have been reported in fusiform cells of the dorsal cochlear nucleus (DCN) (Brozoski et al. 2002;Kaltenbach et al. 2004;Dehmel et al. 2012b;Koehler and Shore 2013a) and in principal cells of the inferior colliculus (Bauer et al. 2008) and auditory cortex (Yang et al. 2007;Paul et al. 2009;Gu et al. 2010). Recent in vivo and in vitro studies of tinnitus animal models have suggested that specific synaptic plasticity mechanisms as well as changes in intrinsic excitability (Pilati et al. 2012a;Li et al. 2013) play an important role in mediating these changes.Fusiform cells in the DCN integrate auditory input relayed by the cochlear auditory nerve fibers (ANFs) and somatosensory input relayed by the granule cells parallel fibers (Shore et al. 2000;Zhou and Shore 2004;Shore 2005;Zhan and Ryugo 2007). Importantly, the parallel fiber synapses on fusiform and cartwheel cells of the DCN have been hypothesized to carry proprioceptive information, e.g., the position of the pinna relative to sound source location (Kanold and Young 2001) and to mediate suppression of internally generated body sounds, such as self-vocalization (Zhou and Shore 2004). In vitro studies investigating these synapses have demonstrated spiketiming-...

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“…3.3.1.7 NMDAR1: N-methyl-D-aspartate receptors (NMDAR) are involved in excitatory transmission in the mammalian brain and are crucial for brain development, learning, and memory (Sato et al 2000;Tsien et al 1996). NMDAR1 pre-mRNA has three alternative exons: 5, 21, and 22.…”

Section: Appmentioning

confidence: 99%

Misregulation of Alternative Splicing Causes Pathogenesis in Myotonic Dystrophy

Kuyumcu-Martinez

Cooper

2006

Alternative Splicing and Disease

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Myotonic dystrophy (DM), the most common form of adult onset muscular dystrophy, affects skeletal muscle, heart, and the central nervous system (CNS). Mortality results primarily from muscle wasting and cardiac arrhythmias. There are two forms of the disease: DM 1 and DM 2. DM 1, which constitutes 98% of cases, is caused by a CTG expansion in the 3′ untranslated region (UTR) of the DMPK gene. DM 2 is caused by a CCTG expansion in the first intron of the ZNF9 gene. RNA containing CUG-or CCUG-expanded repeats are transcribed but are retained in the nucleus in foci. Disease pathogenesis results primarily from a gain of function of the expanded RNAs, which alter developmentally regulated alternative splicing as well as pathways of muscle differentiation. The toxic RNA has been implicated in sequestration of splicing regulators and transcription factors thereby causing specific symptoms of the disease. Here we review the proposed mechanisms for the toxic effects of the expanded repeats and discuss the molecular mechanisms of splicing misregulation and disease pathogenesis.

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Diversity and plasticity in amino acid receptor subunits in the rat auditory brain stem

Cited by 46 publications

References 56 publications

Deafness-Induced Changes in the Auditory Pathway: Implications for Cochlear Implants

Deafness-Induced Changes in the Auditory Pathway: Implications for Cochlear Implants

Stimulus-timing-dependent modifications of rate-level functions in animals with and without tinnitus

Misregulation of Alternative Splicing Causes Pathogenesis in Myotonic Dystrophy

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