Area:
Somatosensory, Auditory
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High-probability grants
According to our matching algorithm, Todd M. Mowery is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2013 — 2015 |
Mowery, Todd Michael |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Critical Periods of Recovery From Hearing Loss in the Developing Auditory Cortex
DESCRIPTION (provided by applicant): Developmental hearing loss (HL) can induce profound changes to auditory processing and cognitive processes, such as language acquisition. This is because the central nervous system is particularly vulnerable to disruptions of sensory activity during discrete intervals prior to adulthood. These intervals are often referre to as critical periods (CP). Consistent with basic research findings, early remediation of hearing loss in humans is highly correlated with recovery of normal function. This suggests that the critical period concept applies to human hearing loss. The core hypothesis of this proposal is that recovery from hearing loss-induced changes to cortical membrane and synaptic properties depends on the restoration of hearing prior to the closure of one or more critical periods. The key goals of this proposal are to determine the CPs during which mild hearing loss (i.e., bilateral earplugs), or the restoration of normal hearing (i.e., earplug removal) during development will influence cellular properties in auditory cortex. Both the onset of earplug insertion and the time of earplug removal will be varied as a function of postnatal age to explore the timing and termination of auditory CPs. Two key cellular properties that contribute to neuronal excitability will be assessed in the auditory cortex: (1) Membrane and firing properties, and (2) Inhibitory synaptic currents. There are two experimental Aims. Aim 1 asks whether there is more than one CP during which hearing loss affects cellular properties. To determine whether there are CPs for mild hearing loss, animals will be reared with bilateral earplugs and the age-of-onset for EP insertion will be varied. Whole-cell recordings will be obtained from layer 2/3 pyramidal neurons in thalamocortical brain slices from earplug-reared and age-matched unmanipulated animals. Current-clamp recordings will be used to measure membrane properties and voltage-clamp recordings will be used to measure spontaneous and evoked inhibitory synaptic currents. These measures will reveal whether there are multiple CPs during which specific cortical properties are sensitive to hearing loss. Aim 2 asks whether there is a critical period during which hearing restoration permits recovery of cellular properties. Therefore, animals will be reared with bilateral EPs and the age of EP removal will be varied throughout development. To evaluate the effects of earplug removal, whole cell recordings will be obtained in animals with restored hearing and age- matched controls. All data collection parameters and analytical approaches will be identical to Aim 1. The experiment will allow me to distinguish whether the critical period for EP insertion and removal occur within the same age window, or whether the critical periods for removal depend on the age of EP insertion. Together, these findings will reveal whether there are discrete critical periods for the maturation of cellular properties, and suggest whether there are optimal periods for remediation of developmental hearing loss.
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1 |
2015 — 2017 |
Mowery, Todd Michael |
R03Activity Code Description: To provide research support specifically limited in time and amount for studies in categorical program areas. Small grants provide flexibility for initiating studies which are generally for preliminary short-term projects and are non-renewable. |
The Effect of Developmental Hl On Cellular Properties in the Auditory Striatum
? DESCRIPTION (provided by applicant): Developmental hearing loss is associated with perceptual deficits and delayed language acquisition. Although perceptual sensory deficits are of primary importance, an emerging literature suggests that developmental HL also has an impact on cognitive processes. If so, then brain structures connected to auditory cortex may be altered by a period of deprivation. One brain region implicated in vocal learning, auditory related behavioral deficits, and language impairments is the striatum. Moreover, the projections between the auditory cortex and regions of the striatum receiving auditory inputs can drive behavioral responses. Given the fundamental role that the striatum plays during learning, developmental hearing loss may play a causative role in behavioral deficits. The core hypothesis of this proposal is that cellular properties in the striatum are persistently altered following developmental hearing loss that lead to behavioral deficits. Aim 1 will investigate whether developmental hearing loss induces cellular deficits in the striatum. Aim 2 will determine whether changes to cellular properties in the striatum are correlated with behavioral deficits. Together, this proposal will reveal whether cellular properties in the auditory-recipient striatum are vulnerable to transient HL during development, and offer an animal model on auditory-based learning deficits as seen in children with Otitis Media.
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1 |
2019 — 2020 |
Mowery, Todd Michael |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
The Impact of Transient Developmental Hl On Corticostriatal Eltp Expression During Auditory Learning.
PROJECT SUMMARY Auditory deprivation during the critical period of development can induce persistent changes along the entire auditory neuraxis, as well as, brain regions downstream of primary auditory cortex. One such brain region, the striatum, forms an excitatory circuit with the auditory cortex that drives decision-making. Recently, I have found that transient developmental HL leads to persistent changes in the excitatory synaptic strength, inhibitory synaptic strength, and cellular firing properties of gerbil auditory corticostriatal neurons. These changes involve receptors that mediate long-term potentiation. Thus the behavioral impairments that remain after recovery from developmental HL could in part be due to changes in the corticostriatal expression of excitatory long-term potentiation (eLTP) during task acquisition. The core hypothesis of this proposal is that auditory associative learning delay in HL subjects is caused by NMDA and GABA receptor mediated disruptions to eLTP expression along the auditory corticostriatal circuit. Aim one will assess how NMDA receptor and GABAA/B receptor function contributes to eLTP expression and auditory learning in the cortex and striatum. This will be accomplished by 1) carrying out whole-cell recording from corticostriatal brain slices in adult gerbils in the presence of NMDA or GABA receptor blockers during the induction of eLTP or 2) by infusing NMDA or GABA blockers directly into the cortex or striatum via micro cannula during auditory discrimination training. Aim two will assess how learning-induced changes to neural and synaptic properties in the cortex and striatum promote eLTP during task acquisition. This will be accomplished by 1) using in vitro whole-cell recordings from ACx L5 or striatum to measure the learning-induced changes to NMDA and GABA receptor function and how they alter the probability of eLTP expression during auditory discrimination learning or 2) by using in vivo electrophysiological recordings from ACx L5 or striatum to measure how changes to neural firing rates and patterns are correlated with increases in in vivo measures of eLTP during auditory discrimination learning. Aim three will ask how developmental HL-induced changes to the set point of synaptic strength or neural firing properties along the corticostriatal circuit affect eLTP expression during auditory learning. This will be accomplished by 1) using in vitro whole-cell recordings from ACx L5 or striatum of adult animals that experienced developmental HL to measure how the HL-induced changes to synaptic strength set points impact the learning-induced changes that drive eLTP expression during auditory discrimination learning or 2) by using in vivo electrophysiological recordings from ACx L5 or striatum of adult animals that experienced developmental HL to measure how HL-induced changes to neural firing properties impact the learning-induced changes that drive LTP during auditory discrimination learning. Together, this proposal will reveal how HL- induced changes to cellular and synaptic properties along the corticostriatal circuit interact with the learning-induced changes to cellular and synaptic properties that promote auditory learning.
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1 |