Tuning shifts of the auditory system by corticocortical and corticofugal projections and conditioning

Suga, Nobuo

doi:10.1016/j.neubiorev.2011.11.006

Cited by 74 publications

(87 citation statements)

References 147 publications

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“…However, associative learning has now been shown to induce sophisticated stimulus-specific neuroplasticity in the mammalian auditory, visual, olfactory, somatosensory, and gustatory systems, which are only indirectly related to behavior. These effects have been observed not only in secondary sensory "association" cortices (Sacco and Sacchetti 2010) but also in primary sensory cortices (Morris et al 1998;Ohl and Scheich 2005;Polley et al 2007;Li et al 2008;Chen et al 2011;Gdalyahu et al 2012;Suga 2012;Weinberger 2015), subcortical sensory structures (Edeline andWeinberger 1991a,b, 1992;Cruikshank et al 1992;Kay and Laurent 1999;Gao and Suga 2000;Doucette et al 2011;Fletcher 2012), and even primary sensory neurons (Jones et al 2008;Kass et al 2013d;Dias and Ressler 2014).…”

Section: Instances Of Associative Learning-induced Sensory Plasticitymentioning

confidence: 99%

Associative learning and sensory neuroplasticity: how does it happen and what is it good for?

McGann

2015

Learn. Mem.

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Historically, the body's sensory systems have been presumed to provide the brain with raw information about the external environment, which the brain must interpret to select a behavioral response. Consequently, studies of the neurobiology of learning and memory have focused on circuitry that interfaces between sensory inputs and behavioral outputs, such as the amygdala and cerebellum. However, evidence is accumulating that some forms of learning can in fact drive stimulus-specific changes very early in sensory systems, including not only primary sensory cortices but also precortical structures and even the peripheral sensory organs themselves. This review synthesizes evidence across sensory modalities to report emerging themes, including the systems' flexibility to emphasize different aspects of a sensory stimulus depending on its predictive features and ability of different forms of learning to produce similar plasticity in sensory structures. Potential functions of this learning-induced neuroplasticity are discussed in relation to the challenges faced by sensory systems in changing environments, and evidence for absolute changes in sensory ability is considered. We also emphasize that this plasticity may serve important nonsensory functions, including balancing metabolic load, regulating attentional focus, and facilitating downstream neuroplasticity.

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Section: Instances Of Associative Learning-induced Sensory Plasticitymentioning

confidence: 99%

Associative learning and sensory neuroplasticity: how does it happen and what is it good for?

McGann

2015

Learn. Mem.

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“…The most likely pathway for these changes is, however, AI to the MGBv for excitation and AI to the MGBm through the TRN for inhibition, as reported by He et al (2002) and Zhang et al (2008). Since AI stimulation evokes the BF shifts of subthalamic auditory neurons (Suga 2012 for review), the BF shifts of MGBv neurons must be partly due to those subthalamic BF shifts.…”

Section: Sharpness Of the Frequency-tuning Curves Of Mgbm Neuronsmentioning

confidence: 99%

“…Tone-burst stimulation associated with electric stimulation of the basal nucleus evokes the BF shifts of MGBv neurons through AI (Zhang and Yan 2008). Focal electric stimulation of AI evokes BF shifts in not only AI and MGBv, but also subthalamic auditory nuclei (Suga 2012 for review). These BF shifts occur in a specific relation to the BF of the stimulated neurons or the frequency of the conditioning tone.…”

Section: Sharpness Of the Frequency-tuning Curves Of Mgbm Neuronsmentioning

confidence: 99%

Modulation of thalamic auditory neurons by the primary auditory cortex

Tang

Yang

Suga

2012

Journal of Neurophysiology

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Tang J, Yang W, Suga N. Modulation of thalamic auditory neurons by the primary auditory cortex. J Neurophysiol 108: [935][936][937][938][939][940][941][942] 2012. First published May 2, 2012; doi:10.1152/jn.00251.2012.-The central auditory system consists of the lemniscal and nonlemniscal pathways or systems, which are anatomically and physiologically different from each other. In the thalamus, the ventral division of the medial geniculate body (MGBv) belongs to the lemniscal system, whereas its medial (MGBm) and dorsal (MGBd) divisions belong to the nonlemniscal system. Lemniscal neurons are sharply frequency-tuned and provide highly frequencyspecific information to the primary auditory cortex (AI), whereas nonlemniscal neurons are generally broadly frequency-tuned and project widely to cortical auditory areas including AI. These two systems are presumably different not only in auditory signal processing, but also in eliciting cortical plastic changes. Electric stimulation of narrowly frequency-tuned MGBv neurons evokes the shift of the frequency-tuning curves of AI neurons toward the tuning curves of the stimulated MGBv neurons (tone-specific plasticity). In contrast, electric stimulation of broadly frequency-tuned MGBm neurons augments the auditory responses of AI neurons and broadens their frequency-tuning curves (nonspecific plasticity). In our current studies, we found that electric stimulation of AI evoked tone-specific plastic changes of the MGBv neurons, whereas it degraded the frequency tuning of MGBm neurons by inhibiting their auditory responses. AI apparently modulates the lemniscal and nonlemniscal thalamic neurons in quite different ways. High MGBm activity presumably makes AI neurons less favorable for fine auditory signal processing, whereas high MGBv activity makes AI neurons more suitable for fine processing of specific auditory signals and reduces MGBm activity. corticofugal modulation; frequency tuning; medial geniculate body; nonspecific plasticity; tone-specific plasticity THE CENTRAL AUDITORY SYSTEM of mammals consists of the lemniscal and nonlemniscal systems. In the thalamus, the lemniscal system is composed of the ventral division of the medial geniculate body (MGBv) that projects to the primary auditory cortex (AI) and anterior auditory field (AAF). The nonlemniscal system is composed of the medial (MGBm) and dorsal (MGBd) divisions of the MGB and the posterior intralaminar nucleus. The MGBd projects to the cortical auditory areas surrounding AI, whereas the MGBm projects to all auditory areas including AI (Imig and Morel 1983 for review; Andersen et al. 1980; Winer et al. 1977). The cortical auditory areas project back to the subcortical auditory nuclei: AI and AAF project back to the MGBv; AII to MGBd; and all auditory areas, including AI, to MGBm (Andersen et al. 1980;Rouiller 1997 In general, the MGBv is tonotopically organized by sharply frequency-tuned neurons, whereas the MGBm and MGBd are poorly tonotopically organized by broadly frequency-tuned neurons. The MGBm is polysenso...

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“…These structures generate multiple feedback loops that extract meaning from afferent stimulation through modulation 14,15 . Cortical stimulation affects the tuning curves of subcortical structures causing specific regions in the subcortical system to become robustly tuned to higher levels of activity [16][17][18] .…”

Section: Introductionmentioning

confidence: 99%

Detailed Analysis of High Frequency Auditory Brainstem Response in Patients with Tinnitus: A Preliminary Study

Pinkl

Wilson

Billingsly

et al. 2017

The International Tinnitus Journal

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Increased spontaneous activity and aberrant neural synchrony is thought to be the underlying cause of tinnitus. The perceived pitch of tinnitus may be dictated by frequency specific neural fibers of the subcortical pathway, or the projection of altered cortical activity by-way-of tonotopic reorganizations. Subcortical neural activity in relation to tinnitus was characterized using ABR measurements. In the present study, 11 patients (21 ears) with constant tonal tinnitus underwent a two-part experiment. Experiment 1 involved click ABR measurements and included two experimental groups: tinnitus with normal hearing from 2000-4000 Hz (GI) and tinnitus with hearing loss within the range of 2000-4000 Hz (GII). Experiment 2 utilized tone burst ABRs matched to each participant's perceived tinnitus pitch and included two experimental groups: tinnitus with normal hearing at the tinnitus pitch (GIa) and tinnitus with hearing loss at the tinnitus pitch (GIIa). These groups were compared to a control group (GIII) of ten monaurally tested (10 ears) participants with normal hearing thresholds at 250-20000 Hz and no tinnitus. Click ABR results indicate significantly prolonged V-III IPLs for GI and GII and a significantly extended absolute V latency for GII only. Tone burst ABRs matched to tinnitus pitch revealed significantly prolonged absolute latencies and IPLs at three of the seven frequencies for GIIa. ABR threshold seeking was completed and revealed negative eHL values for two of the four different stimuli for GI and GIa and four of the eight stimuli for GII and GIIa. Click ABRs results are suggestive of upper brainstem abnormalities for both groups. While GI demonstrated prolonged V-III IPLs, no significant differences were found for GIa. This suggests that there is no frequency specific subcortical characteristic associated with tinnitus with normal hearing. Frequency specific properties for subcortical activity could not be characterized due to varying results of GIIa.

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Tuning shifts of the auditory system by corticocortical and corticofugal projections and conditioning

Cited by 74 publications

References 147 publications

Associative learning and sensory neuroplasticity: how does it happen and what is it good for?

Associative learning and sensory neuroplasticity: how does it happen and what is it good for?

Modulation of thalamic auditory neurons by the primary auditory cortex

Detailed Analysis of High Frequency Auditory Brainstem Response in Patients with Tinnitus: A Preliminary Study

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