Encoding the Timing of Inhibitory Inputs

Manis, Paul B.

doi:10.1152/jn.00910.2004

Cited by 23 publications

(27 citation statements)

References 55 publications

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“…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;.…”

Section: Discussionsupporting

confidence: 61%

“…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%

“…Inhibitory inputs onto fusiform cells can alter rapidly inactiviating K + currents which help determine the nature of the PSTH temporal response and can affect temporal precision over tens of milliseconds (Rhode and Smith, 1996;Manis, 1990;Hewitt and Meddis, 1995;Hancock and Voigt, 2002a;Kanold and Manis, 1999;Street and Manis, 2007). The degree of hyperpolarization existing just prior to excitation by an acoustic stimulus likely determines the relative deinactivation of rapidly inactivating K + currents (Manis, 1990;Hancock and Voigt, 2002a;Kanold and Manis, 2005;Street and Manis, 2007). We hypothesize that there is an age-related loss of, or small/mis-timed IPSCs, or loss of tonic inhibition impinging on the aged fusiform cell.…”

Section: Discussionmentioning

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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Section: Discussionsupporting

confidence: 61%

supporting

confidence: 62%

Section: Discussionmentioning

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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“…I A is activated by hyperpolarization and subsequently opposes any membrane depolarization, resulting in a delay to reach firing threshold. In cells expressing I A , the relationship between latency and membrane voltage has been shown to be monotonic, such that greater hyperpolarization causes longer delays to first spike (Shibata et al, 2000;Kanold and Manis, 2005). First-spike latency has been studied in many sensory systems in which the magnitude of a sensory input can be more effectively encoded by action potential timing than through changes in spike frequency (Thorpe et al, 1996;Heil, 2004;Johansson and Birznieks, 2004;VanRullen et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

A-Type and T-Type Currents Interact to Produce a Novel Spike Latency-Voltage Relationship in Cerebellar Stellate Cells

Molineux¹,

Fernandez²,

Mehaffey³

et al. 2005

J. Neurosci.

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The modification of first-spike latencies by low-threshold and inactivating K ϩ currents (I A ) have important implications in neuronal coding and synaptic integration. To date, cells in which first-spike latency characteristics have been analyzed have shown that increased hyperpolarization results in longer first-spike latencies, producing a monotonic relationship between first-spike latency and membrane voltage. Previous work has established that cerebellar stellate cells express members of the K v 4 potassium channel subfamily, which underlie I A in many central neurons. Spike timing in stellate cells could be particularly important to cerebellar output, because the discharge of even single spikes can significantly delay spike discharge in postsynaptic Purkinje cells. In the present work, we studied the first-spike latency characteristics of stellate cells. We show that first-spike latency is nonmonotonic, such that intermediate levels of prehyperpolarization produce the longest spike latencies, whereas greater hyperpolarization or depolarization reduces spike latency. Moreover, the range of first-spike latency values can be substantial in spanning 20 -128 ms with preceding membrane shifts of Ͻ10 mV. Using patch clamp and modeling, we illustrate that spike latency characteristics are the product of an interplay between I A and lowthreshold calcium current (I T ) that requires a steady-state difference in the inactivation parameters of the currents. Furthermore, we show that the unique first-spike latency characteristics of stellate cells have important implications for the integration of coincident IPSPs and EPSPs, such that inhibition can shift first-spike latency to differentially modulate the probability of firing.

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“…Therefore, these channels may play a role in synaptic plasticity, where activity-dependent signaling can alter the inherent excitability of target neurons. Changes in auditory nerve activity following deafness have been shown to induce changes in excitability and response properties in the cochlear nucleus (Francis and Manis, 2000;Kaltenbach and Afman, 2000;Kanold and Manis, 2005;Wang and Manis, 2005) and inferior colliculus (Bledsoe et al, 1995(Bledsoe et al, , 1997Mossop et al, 2000;Salvi et al, 2000;Syka and Rybalko, 2000;Vale and Sanes, 2002;Vale et al, 2004) (for reviews Moller, 2005;Syka, 2002). While the acoustic environment has been shown to influence auditory brain stem responses through modulation of voltage-gated potassium channels, this is achieved largely through phosphorylation rather than chronic alterations in gene expression (Chambard and Ashmore, 2005;Kaczmarek et al, 2005;Macica et al, 2003;Song et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Deafness associated changes in expression of two-pore domain potassium channels in the rat cochlear nucleus

et al. 2006

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Two-pore domain potassium channels ( ) play an important role in setting resting membrane potential by regulating background leakage of potassium ions, which in turn controls neuronal excitability. To determine whether these channels contribute to activity-dependent plasticity following deafness, we used quantitative real-time PCR to examine the expression of 10 subunits in the rat cochlear nucleus at 3 days, 3 weeks and 3 months after bilateral cochlear ablation. There was a large sustained decrease in the expression of TASK-5, a subunit that is predominantly expressed in auditory brain stem neurons, and in the TASK-1 subunit which is highly expressed in several types of cochlear nucleus neurons. TWIK-1 and THIK-2 also showed significant decreases in expression that were maintained across all time points. TWIK-2, TREK-1 and TREK-2 showed no significant change in expression at 3 days but showed large decreases at 3 weeks and 3 months following deafness. TRAAK and TASK-3 subunits showed significant decreases at 3 days and 3 weeks following deafness, but these differences were no longer significant at 3 months. Dramatic changes in expression of subunits suggest these channels may play a role in deafness-associated changes in the excitability of cochlear nucleus neurons.

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Encoding the Timing of Inhibitory Inputs

Cited by 23 publications

References 55 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

A-Type and T-Type Currents Interact to Produce a Novel Spike Latency-Voltage Relationship in Cerebellar Stellate Cells

Deafness associated changes in expression of two-pore domain potassium channels in the rat cochlear nucleus

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