Age-related changes in the response properties of cartwheel cells in rat dorsal cochlear nucleus

Caspary, Donald M.; Hughes, Larry F.; Schatteman, Tracy A.; Turner, Jeremy G.

doi:10.1016/j.heares.2006.03.005

Cited by 43 publications

(34 citation statements)

References 79 publications

(104 reference statements)

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“…The intrinsic excitability of fusiform cells (the major excitatory output from the DCN) is elevated bilaterally even after unilateral noise exposure (Brozoski et al, 2002). This activity change mirrors those seen in the response profiles of fusiform cells (Caspary et al, 2005) and glycinergic cartwheel cells (Caspary et al, 2006) during presbyacusis onset in rats. Although amplified responses may be derived from systemic inhibitory dysfunction (Middleton et al, 2011), the existence of a correlation between OHC disruption and DCN spontaneous discharge indicates that the onset of hyperactivity within the DCN is probably the result of a confluence of factors (Kaltenbach et al, 2002; Rachel et al, 2002).…”

Section: Neuronal Spontaneous and Evoked Response Properties Undergo supporting

confidence: 68%

Insult-induced adaptive plasticity of the auditory system

Gold

Bajo

2014

Front. Neurosci.

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The brain displays a remarkable capacity for both widespread and region-specific modifications in response to environmental challenges, with adaptive processes bringing about the reweighing of connections in neural networks putatively required for optimizing performance and behavior. As an avenue for investigation, studies centered around changes in the mammalian auditory system, extending from the brainstem to the cortex, have revealed a plethora of mechanisms that operate in the context of sensory disruption after insult, be it lesion-, noise trauma, drug-, or age-related. Of particular interest in recent work are those aspects of auditory processing which, after sensory disruption, change at multiple—if not all—levels of the auditory hierarchy. These include changes in excitatory, inhibitory and neuromodulatory networks, consistent with theories of homeostatic plasticity; functional alterations in gene expression and in protein levels; as well as broader network processing effects with cognitive and behavioral implications. Nevertheless, there abounds substantial debate regarding which of these processes may only be sequelae of the original insult, and which may, in fact, be maladaptively compelling further degradation of the organism's competence to cope with its disrupted sensory context. In this review, we aim to examine how the mammalian auditory system responds in the wake of particular insults, and to disambiguate how the changes that develop might underlie a correlated class of phantom disorders, including tinnitus and hyperacusis, which putatively are brought about through maladaptive neuroplastic disruptions to auditory networks governing the spatial and temporal processing of acoustic sensory information.

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Section: Neuronal Spontaneous and Evoked Response Properties Undergo supporting

confidence: 68%

Insult-induced adaptive plasticity of the auditory system

Gold

Bajo

2014

Front. Neurosci.

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“…Physiologic changes associated with aging observed in the present study and age-related preand postsynaptic glycinergic neurochemical changes described above are suggestive of a net loss of glycinergic inhibition in fusiform and cartwheel cell neurotransmission in aged DCN (Caspary et al, , 2006. Rodent aging studies describe decreased glycine immunostaining in aged C57 mouse DCN (Willott et al, 1997), while Banay-Schwartz et al (1989) found an age-related decrease in glycine levels in aged rat cochlear nucleus.…”

Section: Discussionsupporting

confidence: 65%

“…The present study found that aged putative DCN output neurons exhibited significantly decreased peak sync values, consistent with a decrease in glycinergic inhibition. Furthermore, the age-related shift toward more low-pass tMTFs with notches (LPN, DP and complex tMTFs) is expected with a flattening observed with age-related decreases in vector strength near BMF.Physiologic changes associated with aging observed in the present study and age-related preand postsynaptic glycinergic neurochemical changes described above are suggestive of a net loss of glycinergic inhibition in fusiform and cartwheel cell neurotransmission in aged DCN (Caspary et al, , 2006. Rodent aging studies describe decreased glycine immunostaining in aged C57 mouse DCN (Willott et al, 1997), while Banay-Schwartz et al (1989) found an age-related decrease in glycine levels in aged rat cochlear nucleus.…”

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confidence: 65%

Aged-related loss of temporal processing: Altered responses to amplitude modulated tones in rat dorsal cochlear nucleus

2008

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Loss of temporal processing is characteristic of age-related loss of speech understanding observed in the elderly. Inhibitory glycinergic circuits provide input onto dorsal cochlear nucleus (DCN) projection neurons which likely serve to modulate excitatory responses to time-varying complex acoustic signals. The present study sought to test the hypothesis that age-related loss of inhibition would compromise the ability of output neurons to encode sinusoidally amplitude modulated (SAM) tones. Extracellular recordings were obtained from young and aged FBN rat DCN putative fusiform cells. Stimuli were SAM tones at 3 modulation depths (100, 50, and 20%) at 30 dB HL with the carrier frequency set to the unit's characteristic frequency. Discharge rate and synchrony were calculated to describe SAM responses. There were significant age-related changes in the shape and peak vector strength [best modulation frequency (BMF)] of temporal modulation transfer functions (tMTFs), with no significant age-related changes in rate modulation transfer functions (rMTFs) at BMF. Young neurons exhibited band-pass tMTFs for most SAM conditions while aged fusiform cells exhibited significantly more low-pass or double-peaked tMTFs. There were significant differences in tMTFs between buildup, pauser-buildup, and wide-chopper temporal response types. Young and aged wide-choppers displayed significantly lower vector strength values than the other two temporal DCN response types. Age-related decreases in the number of pauser-buildup response types and increases in wide-chopper types with age reported previously, could account, in part, for the observed loss of temporal coding of the aged fusiform cell. Age-related changes in SAM coding were similar to changes observed with receptor blockade of glycinergic inhibition onto fusiform cells and consistent with previously observed age-related loss of endogenous glycine levels and changes in normal adult glycine receptor function. DCN changes in SAM coding could, in part, underpin temporal processing deficits observed in the elderly. KeywordsDorsal Cochlear Nucleus; Aging; Auditory; Glycine; Amplitude Modulation; Temporal Processing Presbycusis, age-related hearing loss, is a complex disorder that may result in a slow deterioration of peripheral auditory input to auditory regions of the brain (see Willott, 1991; Corresponding Author: Dr. Donald M. Caspary, Department of Pharmacology, Southern Illinois University School of Medicine, P.O. Box 19629, Springfield, IL 62794-9629. Phone: (217) 545-2195, Fax: (217) 545-0145, email: dcaspary@siumed.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal...

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“…Furthermore, decreased inhibitory neurotransmission and other age-related changes may also have an impact on subcortical auditory processing in the midbrain (Walton et al 1997; Caspary et al 2005; Caspary et al 2006). One of the functions of inhibitory neurotransmitters is to sharpen neural responses to rapidly varying acoustic stimuli (reviewed in Caspary et al 2008); therefore, a reduction in inhibitory neurotransmission may lead to a timing deficit specific to the changing formant transition region of the speech syllable.…”

Section: Discussionmentioning

confidence: 99%

Effects of Aging on the Encoding of Dynamic and Static Components of Speech

et al. 2015

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Objectives The authors investigated aging effects on the envelope of the frequency following response to dynamic and static components of speech. Older adults frequently experience problems understanding speech, despite having clinically normal hearing. Improving audibility with hearing aids provides variable benefit, as amplification cannot restore the temporal precision degraded by aging. Previous studies have demonstrated age-related delays in subcortical timing specific to the dynamic, transition region of the stimulus. However, it is unknown whether this delay is mainly due to a failure to encode rapid changes in the formant transition because of central temporal processing deficits or as a result of cochlear damage that reduces audibility for the high-frequency components of the speech syllable. To investigate the nature of this delay, the authors compared subcortical responses in younger and older adults with normal hearing to the speech syllables /da/ and /a/, hypothesizing that the delays in peak timing observed in older adults are mainly caused by temporal processing deficits in the central auditory system. Design The frequency following response was recorded to the speech syllables /da/ and /a/ from 15 younger and 15 older adults with normal hearing, normal IQ, and no history of neurological disorders. Both speech syllables were presented binaurally with alternating polarities at 80 dB SPL at a rate of 4.3 Hz through electromagnetically shielded insert earphones. A vertical montage of four Ag–AgCl electrodes (Cz, active, forehead ground, and earlobe references) was used. Results The responses of older adults were significantly delayed with respect to younger adults for the transition and onset regions of the /da/ syllable and for the onset of the /a/ syllable. However, in contrast with the younger adults who had earlier latencies for /da/ than for /a/ (as was expected given the high-frequency energy in the /da/ stop consonant burst), latencies in older adults were not significantly different between the responses to /da/ and /a/. An unexpected finding was noted in the amplitude and phase dissimilarities between the two groups in the later part of the steady-state region, rather than in the transition region. This amplitude reduction may indicate prolonged neural recovery or response decay associated with a loss of auditory nerve fibers. Conclusions These results suggest that older adults’ peak timing delays may arise from decreased synchronization to the onset of the stimulus due to reduced audibility, though the possible role of impaired central auditory processing cannot be ruled out. Conversely, a deterioration in temporal processing mechanisms in the auditory nerve, brainstem, or midbrain may be a factor in the sudden loss of synchronization in the later part of the steady-state response in older adults.

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Age-related changes in the response properties of cartwheel cells in rat dorsal cochlear nucleus

Cited by 43 publications

References 79 publications

Insult-induced adaptive plasticity of the auditory system

Insult-induced adaptive plasticity of the auditory system

Aged-related loss of temporal processing: Altered responses to amplitude modulated tones in rat dorsal cochlear nucleus

Effects of Aging on the Encoding of Dynamic and Static Components of Speech

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