Projections from auditory cortex contact cells in the cochlear nucleus that project to the inferior colliculus

Schofield, Brett R.; Coomes, Diana L.

doi:10.1016/j.heares.2005.03.005

Cited by 32 publications

(26 citation statements)

References 35 publications

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“…A change in the balance between LTP and LTD may explain the decreased responsiveness of ACx in sound-deprived mice (21) and the decline of electrically evoked responses observed in congenitally deaf cats (45). L5 synaptic plasticity may have a significant impact on subthalamic processing because of the massive descending projection from ACx (28,(46)(47)(48)(49)(50). Furthermore, the specific complement of cortical plasticity mechanisms may support the functional takeover of ACx by other sensory modalities.…”

Section: Discussionmentioning

confidence: 99%

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Kotak

Breithaupt

Sanes³

2007

Proc. Natl. Acad. Sci. U.S.A.

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Severe hearing loss during early development is associated with deficits in speech and language acquisition. Although functional studies have shown a deafness-induced alteration of synaptic strength, it is not known whether long-term synaptic plasticity depends on auditory experience. In this study, sensorineural hearing loss (SNHL) was induced surgically in developing gerbils at postnatal day 10, and excitatory synaptic plasticity was examined subsequently in a brain slice preparation that preserves the thalamorecipient auditory cortex. Extracellular stimuli were applied at layer 6 (L6), whereas evoked excitatory synaptic potentials (EPSPs) were recorded from L5 neurons by using a whole-cell current clamp configuration. In control neurons, the conditioning stimulation of L6 significantly altered EPSP amplitude for at least 1 h. Approximately half of neurons displayed long-term potentiation (LTP), whereas the other half displayed long-term depression (LTD). In contrast, SNHL neurons displayed only LTD after the conditioning stimulation of L6. Finally, the vast majority of neurons recorded from control prehearing animals (postnatal days 9 -11) displayed LTD after L6 stimulation. Thus, normal auditory experience may be essential for the maturation of synaptic plasticity mechanisms.deafness ͉ long-term depression S evere hearing loss is known to affect auditory processing in humans. This loss includes impairments of signal detection in noise or in a multiple source environment, and disruption of intensity discrimination, frequency discrimination, and temporal resolution (1-4). Even transient bouts of conductive hearing loss can disrupt auditory processing, and months or years may be required for normal perception to resolve (5, 6). Because severe hearing loss during development is implicated in the deficient acquisition of auditory perceptual skills and language, which presumably require learning, we have examined whether synaptic plasticity is also affected.At a structural level, hearing impairments can lead to neuron death or atrophy and alter process outgrowth (7). Furthermore, direct examination of neuron function in brain slice preparations from deaf animals has revealed significant physiological changes to intrinsic and synaptic properties. In both the inferior colliculus and auditory cortex (ACx), early sensorineural hearing loss (SNHL) alters the balance of excitatory and inhibitory synaptic strength (8-10). A similar disruption in synaptic physiology and certain intrinsic properties also occurs in the auditory brainstem of the congenitally deaf mutant mouse (11,12).Both long-term potentiation (LTP) and depression (LTD) have been characterized in a series of studies on the rat ACx (13-18). For example, an NMDA receptor-mediated LTP in the ACx can be induced by stimulation of afferents innervating the ACx via the white matter (13), whereas thalamo-and corticocortical synapse activation can induce LTD (16). These cellular mechanisms may serve as a substrate for use-dependent alteration of coding properties in...

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Section: Discussionmentioning

confidence: 99%

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Kotak

Breithaupt

Sanes³

2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Interactions between top-down modulatory systems and the MOC efferent system are particularly intriguing, yet poorly understood, perhaps because of the frequent use of anesthesia in animal studies. A small percentage of deep layer cortical projection neurons directly target MOC neurons in the ventral nucleus of the trapezoid body (Coomes and Schofield 2004; Feliciano and Potashner 1995), but the more prominent routes from the auditory cortex to the MOC neurons are mediated by polysynaptic projections via the inferior colliculus (Doucet et al 2003;Thompson and Thompson 1993;Vetter et al 1993) or cochlear nucleus (Schofield and Coomes 2005). Direct electrical stimulation of the auditory cortex in awake bats can modulate the cochlear microphonic in a frequencyspecific fashion, suggesting that the anatomical links between the corticofugal and olivocochlear control systems have a functional counterpart as well (Suga et al 2002).…”

Section: The Olivocochlear Reflex Pathway and Its Top-down Modulationmentioning

confidence: 99%

Sound-Evoked Olivocochlear Activation in Unanesthetized Mice

Chambers

Hancock

Maison

et al. 2011

JARO

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Genetic tools available for the mouse make it a powerful model to study the modulation of cochlear function by descending control systems. Suppression of distortion product otoacoustic emission (DPOAE) amplitude by contralateral acoustic stimulation (CAS) provides a robust tool for noninvasively monitoring the strength of descending modulation, yet investigations in mice have been performed infrequently and only under anesthesia, a condition likely to reduce olivocochlear activation. Here, we characterize the contralateral olivocochlear reflex in the alert, unanesthetized mouse. Head-fixed mice were restrained between two closed acoustic systems, while an artifact rejection protocol minimized contamination from self-generated sounds and movements. In mice anesthetized with pentobarbital, ketamine or urethane, CAS at 80 dB SPL evoked, on average, a G1-dB change in DPOAE amplitude. In contrast, the mean CASinduced DPOAE suppression in unanesthetized mice was nearly 8 dB. Experiments in mice with targeted deletion of the α9 subunit of the nicotinic acetylcholine receptor confirmed the contribution of the medial olivocochlear efferents to this phenomenon. These findings demonstrate the utility of the CAS assay in the unanesthetized mouse and highlight the adverse effects of anesthesia when probing the functional status of descending control pathways within the auditory system.

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“…We have provided evidence that cortical projections to the cochlear nucleus contact cells that project to the inferior colliculus (IC) (Schofield and Coomes, 2005b). Cortical projections to the superior olivary complex (SOC) may also participate in loops.…”

Section: Introductionmentioning

confidence: 99%

Projections from auditory cortex contact ascending pathways that originate in the superior olive and inferior colliculus

Peterson

Schofield

2007

Hearing Research

Self Cite

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The superior olivary complex (SOC) and inferior colliculus (IC) are targets of cortical projections as well as sources of major ascending auditory pathways. This study examines whether the cortical projections contact cells in the SOC or IC that project to higher levels. First, we placed an anterograde tracer into the auditory cortex to label cortico-olivary axons and a retrograde tracer into the IC to label olivocollicular cells in guinea pigs. Cortical axons contacted many labeled cells in the ipsilateral SOC and fewer labeled cells in the contralateral SOC. Contacted cells projected to the ipsilateral or contralateral IC.In a second experiment, we labeled corticocollicular axons with an anterograde tracer and injected retrograde tracers into the medial geniculate (MG) to label colliculogeniculate cells. In the IC ipsilateral to the cortical injection, many cortical axons contacted colliculogeniculate cells in the dorsal cortex and external cortex of the IC. The contacted cells projected to the ipsilateral MG or, less often, to the contralateral MG.The results indicate that cortical projections are likely to contact cells in the SOC and IC that project to higher centers. This suggests that auditory cortex can modulate the ascending auditory pathways at multiple levels of the brainstem.

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Projections from auditory cortex contact cells in the cochlear nucleus that project to the inferior colliculus

Cited by 32 publications

References 35 publications

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Sound-Evoked Olivocochlear Activation in Unanesthetized Mice

Projections from auditory cortex contact ascending pathways that originate in the superior olive and inferior colliculus

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