Immunocytochemical and neurochemical evidence for age-related loss of GABA in the inferior colliculus: implications for neural presbycusis

Dm, Caspary; Raza, Ahmad; Armour, BA Lawhorn; Pippin, James A.; Sp, Arnerić

doi:10.1523/jneurosci.10-07-02363.1990

Cited by 224 publications

(114 citation statements)

References 45 publications

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“…Other investigations have been performed on age-related changes in the whole GABAergic system, such as the loss of GABA neurons [34], decreased levels of the enzyme needed to synthesize GABA [2], and some alterations in GABA A subunits and in the combination of the subunits [2,4]. Therefore, the present data support the current hypothesis by suggesting a reduction in GABA-mediated inhibition in the senescent brain.…”

Section: Discussionsupporting

confidence: 88%

Differential effects of aging on EEG after baclofen administration

Cui

2011

Sci. China Life Sci.

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Baclofen is a selective gamma-aminobutyric acid (GABA) type B agonist that may have important medicinal uses, such as in analgesics and drug addiction treatment. In addition, evidence is accumulating that suggests GABAergic-mediated neurotransmission is altered during aging. This study investigated whether baclofen administration (5 mg kg −1 ) induces differential effects on cortical electrical activity with age. Electroencephalograms (EEGs) were recorded from young (3-4 months) and aged (15-17 months) rats, and both the absolute and relative powers in five frequency bands (delta: 2-4 Hz; theta: 4-8 Hz; alpha: 8-12 Hz; beta: 12-20 Hz; gamma: 20-100 Hz) were analyzed. Before administration of baclofen, we found that the EEG relative power in the beta band was higher in the aged than that in the young rats. After administration of baclofen, there was a slower increase in the relative power in the delta band in the aged than that in the young rats. Moreover, there was no significant difference between the two age groups in absolute power in any frequency band. These findings indicate that baclofen treatment appears to differentially modify cortical EEG activity as a function of age. Our data further elucidate the relationship between GABA B receptor-mediated neurotransmission and aging.aging, baclofen, EEG, spectra power, rat Citation:

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Section: Discussionsupporting

confidence: 88%

Differential effects of aging on EEG after baclofen administration

Cui

2011

Sci. China Life Sci.

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“…GABA is one of the main inhibitory neurotransmitters that down-regulated with age in the auditory brainstem (Caspary et al, 1990(Caspary et al, , 1995Helfert et al, 1999). As we suggest a disturbance in the glutamate-related metabolic pathways, it may contribute to that excitatory/inhibitory neurotransmitters imbalance.…”

Section: Discussionmentioning

confidence: 71%

Glutamate-related gene expression changes with age in the mouse auditory midbrain

et al. 2007

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Glutamate is the main excitatory neurotransmitter in both the peripheral and central auditory systems. Changes of glutamate and glutamate-related genes with age may be an important factor in the pathogenesis of age-related hearing loss -presbycusis. In this study, changes in glutamate-related mRNA gene expression in the CBA mouse inferior colliculus with age and hearing loss were examined and correlations were sought between these changes and functional hearing measures, such as the auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAEs). Gene expression of 68 glutamate-related genes was investigated using both genechip microarray and real-time PCR (qPCR) molecular techniques for four different age/hearing loss CBA mouse subject groups. Two genes showed consistent differences between groups for both the genechip and qPCR. Pyrroline-5-carboxylate synthetase enzyme (Pycs) showed down-regulation with age and a highaffinity glutamate transporter (Slc1a3) showed up-regulation with age and hearing loss. Since Pycs plays a role in converting glutamate to proline, its deficiency in old age may lead to both glutamate increases and proline deficiencies in the auditory midbrain, playing a role in the subsequent inducement of glutamate toxicity and loss of proline neuroprotective effects. The up-regulation of Slc1a3 gene expression may reflect a cellular compensatory mechanism to protect against age-related glutamate or calcium excitoxicity.

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“…Central factors implicated in the age-related loss of temporal processing may be attributed in part to mechanisms that alter the excitability of central auditory neurons in response to reduced peripheral input, as has been shown in cases of conductive hearing loss Miko and Sanes 2009;Sanes and Bao 2009). This may result in changes such as a decrease in GABAergic function seen with age (Caspary et al 1990). Reduction in GABA would disrupt the balance between excitation and inhibition, which is thought to be essential in maintaining the precise temporal coding properties of neurons (LeBeau et al 1996;Wang et al 2000;LeBeau et al 2001;Caspary et al 2002;McAlpine and Palmer 2002;Wang et al 2002;Zhang and Kelly 2003), upsetting the normal relationships between auditory nerve activity and subsequent nuclei in the ascending auditory pathway.…”

Section: Introductionmentioning

confidence: 99%

Age-Related Changes in the Relationship Between Auditory Brainstem Responses and Envelope-Following Responses

Parthasarathy

Datta

Torres

et al. 2014

JARO

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Hearing thresholds and wave amplitudes measured using auditory brainstem responses (ABRs) to brief sounds are the predominantly used clinical measures to objectively assess auditory function. However, frequency-following responses (FFRs) to tonal carriers and to the modulation envelope (envelope-following responses or EFRs) to longer and spectro-temporally modulated stimuli are rapidly gaining prominence as a measure of complex sound processing in the brainstem and midbrain. In spite of numerous studies reporting changes in hearing thresholds, ABR wave amplitudes, and the FFRs and EFRs under neurodegenerative conditions, including aging, the relationships between these metrics are not clearly understood. In this study, the relationships between ABR thresholds, ABR wave amplitudes, and EFRs are explored in a rodent model of aging. ABRs to broadband click stimuli and EFRs to sinusoidally amplitude-modulated noise carriers were measured in young (3-6 months) and aged (22-25 months) Fischer-344 rats. ABR thresholds and amplitudes of the different waves as well as phase-locking amplitudes of EFRs were calculated. Age-related differences were observed in all these measures, primarily as increases in ABR thresholds and decreases in ABR wave amplitudes and EFR phaselocking capacity. There were no observed correlations between the ABR thresholds and the ABR wave amplitudes. Significant correlations between the EFR amplitudes and ABR wave amplitudes were observed across a range of modulation frequencies in the young. However, no such significant correlations were found in the aged. The aged click ABR amplitudes were found to be lower than would be predicted using a linear regression model of the young, suggesting altered gain mechanisms in the relationship between ABRs and FFRs with age. These results suggest that ABR thresholds, ABR wave amplitudes, and EFRs measure complementary aspects of overlapping neurophysiological processes and the relationships between these measurements changes asymmetrically with age. Hence, measuring all three metrics provides a more complete assessment of auditory function, especially under pathological conditions like aging.

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Immunocytochemical and neurochemical evidence for age-related loss of GABA in the inferior colliculus: implications for neural presbycusis

Cited by 224 publications

References 45 publications

Differential effects of aging on EEG after baclofen administration

Differential effects of aging on EEG after baclofen administration

Glutamate-related gene expression changes with age in the mouse auditory midbrain

Age-Related Changes in the Relationship Between Auditory Brainstem Responses and Envelope-Following Responses

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