γ-Aminobutyric acidergic and glycinergic inputs shape coding of amplitude modulation in the chinchilla cochlear nucleus

Backoff, Patricia M.; Palombi, Peggy Shadduck; Caspary, Donald M.

doi:10.1016/s0378-5955(99)00071-4

Cited by 49 publications

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“…At all temporal modulation depths, and at either age, buildup and pauser-buildup units have higher peak modulation sync functions than units showing widechopper temporal responses at all temporal modulation depths, and at either age. Thus the agerelated shift toward wide-chopper response types, a temporal response type with higher firing rates and a decreased ability to synchronize to a SAM envelop could explain the present findings and is consistent with a loss of glycinergic inhibition.Inhibitory circuitry may play a role in maintaining/enhancing synchronization to SAM tones (Frisina et al, 1994;Rhode and Greenberg, 1994;Zhao and Liang, 1995;Young, 1998;Backoff et al, 1999;Krishna and Semple, 2000;Hancock and Voigt, 2002b;Joris et al, 2004;Kanold and Manis, 2005;Street and Manis, 2007). The present findings from aged DCN output neurons resemble what is seen when inhibitory neurotransmission is blocked during temporal processing paradigms in CN and IC (Koch and Grothe, 1998;Backoff et al, 1999;.…”

supporting

confidence: 62%

“…Amplitude-modulation is an important temporal feature of sounds found in speech and other species-specific vocalizations. The envelope of sinusoidally amplitude modulated (SAM) sound is coded at all levels of the central auditory system (Joris et al, 2004;Ter-Mikaelian et al, 2007), where inhibitory circuits are thought to enhance temporal coding (Koch and Grothe 1998;Backoff et al, 1999;Krishna and Semple, 2000;Caspary et al, 2002;Ter-Mikaelian et al, 2007). Humans show age-related deficits in amplitude modulation depth discrimination (Takahashi and Bacon, 1992; LeighPaffenroth and Fowler, 2006) and numerous other temporally-challenging discrimination tasks including speech discrimination, gap detection and localization of sounds in space (Warren et al, 1978;Brown, 1984;Barsz et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…These cells appear to enhance coding of SAM tones with respect to auditory nerve fibers by preferentially locking to a restricted range of envelope frequencies (band-pass tMTFs) with maximal sensitivity at a particular (best) modulation frequency (BMF) (Moller, 1974(Moller, , 1976Kim et al, 1990; Langner, 1992;Frisina et al, 1994;Rhode and Greenberg, 1994; Liang, 1995, 1997;Joris et al, 2004). Application of the glycine receptor antagonist strychnine, onto DCN neurons increased discharge rate and reduced synchronization to the SAM envelope at low and near BMF frequencies, which in turn, resulted in a flatter less band-pass like tMTF (Backoff et al, 1999).In light of these neurophysiological and neurochemical studies (also see discussion) suggestive of an age-related decrease in glycinergic inhibition in DCN as well as studies suggesting a role for inhibition in shaping temporal response properties, the present study examined age-related functional changes in the response properties of putative DCN output/fusiform cells to SAM stimuli. Response properties of these putative fusiform cells to simple stimuli have been previously reported .…”

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confidence: 99%

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confidence: 99%

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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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confidence: 62%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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

2008

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“…Glycinergic synaptic inhibition in brain stem auditory pathways is an important component of acoustic information processing and, together with GABAergic inhibition, contributes to the regulation of neuronal excitation (Caspary et al, 1994;Faingold et al, 1991;Grothe and Sanes, 1994;Backoff et al, 1999;Davis and Young, 2000). Glycinergic inhibition, however, may become impaired after sensorineural hearing loss, which usually involves damage to the cochlea and degeneration of the cochlear nerve.…”

Section: Introductionmentioning

confidence: 99%

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation

2007

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Glycinergic synaptic inhibition is part of acoustic information processing in brain stem auditory pathways and contributes to the regulation of neuronal excitation. We found previously that unilateral cochlear ablation (UCA) in young adult guinea pigs decreased [ 3 H]strychnine binding activity in several brain stem auditory nuclei. This study determined if the UCA-induced deficit could be regulated by protein kinase C (PKC), protein kinase A (PKA) or Ca 2+ /calmodulin-dependent protein kinase II (CaMKII). The specific binding of [ 3 H]strychnine was measured in slices of the dorsal (DCN), posteroventral (PVCN) and anteroventral (AVCN) cochlear nucleus (CN), the lateral (LSO) and medial (MSO) superior olive, and the inferior colliculus (IC) 145 days after UCA. Tissues from age-matched unlesioned animals served as controls. UCA induced deficits in specific binding in the AVCN, PVCN and LSO on the ablated side and in the MSO bilaterally. These deficits were reversed by 3 μM phorbol 1,2-dibutyrate, a PKC activator, or 0.2 mM dibutyryl-cAMP, a PKA activator. However, 50 nM Ro31-8220, a PKC inhibitor, and 2 μM H-89, a PKA inhibitor, had no effect in unlesioned controls and after UCA. In contrast, 4 μM KN-93, a CaMKII inhibitor, relieved or reversed the UCA-induced binding deficits and elevated binding in the IC. These findings suggest a UCA-induced down regulation of glycine receptor synthesis may have occurred via reduced phosphorylation of proteins that control receptor synthesis; this effect was reversed by diminishing CaMKII activity or increasing PKC and PKA activity.

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Avian superior olivary nucleus provides divergent inhibitory input to parallel auditory pathways

et al. 2004

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The avian auditory brainstem displays parallel processing, a fundamental feature of vertebrate sensory systems. Nuclei specialized for temporal processing are largely separate from those processing other aspects of sound. One possible exception to this parallel organization is the inhibitory input provided by the superior olivary nucleus (SON) to nucleus angularis (NA), nucleus magnocellularis (NM), and nucleus laminaris (NL) and contralateral SON (SONc). We sought to determine whether single SON neurons project to multiple targets or separate neuronal populations project independently to individual target nuclei. We introduced two different fluorescent tracer molecules into pairs of target nuclei and quantified the extent to which retrogradely labeled SON neurons were double labeled. A large proportion of double-labeled SON somata were observed in all cases in which injections were made into any pair of ipsilateral targets (NA and NM, NA and NL, or NM and NL), suggesting that many individual SON neurons project to multiple targets. In contrast, when injections involved the SONc and any or all of the ipsilateral targets, double labeling was rare, suggesting that contralateral and ipsilateral targets are innervated by distinct populations of SON neurons arising largely from regionally segregated areas of SON. Therefore, at the earliest stages of auditory processing, there is interaction between pathways specialized to process temporal cues and those that process other acoustic features. We present a conceptual model that incorporates these results and suggest that SON circuitry, in part, functions to offset interaural intensity differences in interaural time difference processing.

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γ-Aminobutyric acidergic and glycinergic inputs shape coding of amplitude modulation in the chinchilla cochlear nucleus

Cited by 49 publications

References 47 publications

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

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

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation

Avian superior olivary nucleus provides divergent inhibitory input to parallel auditory pathways

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