Altered glycinergic synaptic activities in guinea pig brain stem auditory nuclei after unilateral cochlear ablation

Potashner, S.J.; Suneja, Sanoj K.; Benson, Christina G.

doi:10.1016/s0378-5955(00)00126-x

Cited by 76 publications

(81 citation statements)

References 71 publications

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“…Age-related hearing loss can be thought of as a slow peripheral deafferentation, and the present findings are consistent with a number of partial deafferentation models using acoustic trauma, disarticulation, and, to a lesser extent, cochlear destruction (Suneja et al, 1998a,b;Milbrandt et al, 2000;Potashner et al, 2000;Brozoski et al, 2002;Asako et al, 2005). Aged rodents exhibit a number of age-related peripheral auditory changes, including a sloping lowfrequency loss of outer-hair cells and a small loss of apical and basal inner-hair cells (for review, see Willott, 1991;Saitoh et al, 1994;Gratton et al, 1996Gratton et al, , 1997Spongr et al, 1997;Ingham et al, 1999; and auditory nerve fiber loss (Keithley et al, 1989(Keithley et al, , 1992Dazert et al, 1996;Schmiedt et al, 1996).…”

Section: Discussionsupporting

confidence: 90%

Age-Related Changes in the Inhibitory Response Properties of Dorsal Cochlear Nucleus Output Neurons: Role of Inhibitory Inputs

Caspary

Schatteman²,

Hughes³

2005

J. Neurosci.

156

114

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Age-related hearing loss frequently results in a loss in the ability to discriminate speech signals, especially in noise. This is attributable, in part, to a loss in temporal resolving power and ability to adjust dynamic range. Circuits in the adult dorsal cochlear nucleus (DCN) have been shown to preserve signal in background noise. Fusiform cells, major DCN output neurons, receive focused glycinergic inputs from tonotopically aligned vertical cells that also project to the ventral cochlear nucleus. Glycine-mediated inhibition onto fusiform cells results in decreased tone-evoked activity as intensity is increased at frequencies adjacent to characteristic frequency (CF). DCN output is thus shaped by glycinergic inhibition, which can be readily assessed in recordings from fusiform cells. Previous DCN studies suggest an age-related loss of markers for glycinergic neurotransmission. The present study postulated that response properties of aged fusiform cells would show a loss of inhibition, resembling conditions observed with glycine receptor blockade. The functional impact of aging was examined by comparing response properties from units meeting fusiform-cell criteria in young and aged rats. Fusiform cells in aged animals displayed significantly higher maximum discharge rates to CF tones than those recorded from young-adult animals. Fusiform cells of aged rats displayed significantly fewer nonmonotonic CF rate-level functions and an age-related change in temporal response properties. These findings are consistent with an age-related loss of glycinergic input, likely from vertical cells, and with findings from other sensory aging studies suggesting a selective age-related decrement in inhibitory amino acid neurotransmitter function.

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Section: Discussionsupporting

confidence: 90%

Age-Related Changes in the Inhibitory Response Properties of Dorsal Cochlear Nucleus Output Neurons: Role of Inhibitory Inputs

Caspary

Schatteman²,

Hughes³

2005

J. Neurosci.

156

114

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“…After AOE, inhibition-mediated gain increases were absent following MS and AN stimulations, and this could be explained by the down-regulation of IPSPs recorded in FCs observed in both AN and MS synaptic pathways. A loss of inhibition was also observed following unilateral cochlear ablation (58,59), and a decrease in glycine receptor expression in the DCN after AOE has been previously reported (60). In vivo studies have shown reduced spontaneous activity in the DCN a few days after acoustic overexposure (61).…”

Section: Discussionmentioning

confidence: 68%

Mechanisms contributing to central excitability changes during hearing loss

Pilati¹,

Ison

Barker³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Exposure to loud sound causes cochlear damage resulting in hearing loss and tinnitus. Tinnitus has been related to hyperactivity in the central auditory pathway occurring weeks after loud sound exposure. However, central excitability changes concomitant to hearing loss and preceding those periods of hyperactivity, remain poorly explored. Here we investigate mechanisms contributing to excitability changes in the dorsal cochlear nucleus (DCN) shortly after exposure to loud sound that produces hearing loss. We show that acoustic overexposure alters synaptic transmission originating from the auditory and the multisensory pathway within the DCN in different ways. A reduction in the number of myelinated auditory nerve fibers leads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitment. In contrast, a decreased membrane resistance of DCN granule cells (multisensory inputs) leads to a reduced maximal firing rate of DCN principal cells that is overcome when additional multisensory fibers are recruited. Furthermore, gain modulation by inhibitory synaptic transmission is disabled in both auditory and multisensory pathways. These cellular mechanisms that contribute to decreased cellular excitability in the central auditory pathway are likely to represent early neurobiological markers of hearing loss and may suggest interventions to delay or stop the development of hyperactivity that has been associated with tinnitus.auditory brainstem | fusiform cell | parallel fiber | deafness | whole-cell patch I t is well established that exposure to loud sound causes damage to the cochlea and results in an elevation of hearing thresholds (1) often accompanied by a reduction of auditory nerve (AN) firing rate (2-4). Although peripheral cellular mechanisms contributing to hearing loss have been thoroughly described (5-11), mechanisms in the central auditory system involved in the early stages of hearing loss following acoustic overexposure (AOE) are poorly understood. The dorsal cochlear nucleus (DCN) is one of the first relays within the central auditory pathway (12). Hyperactivity in the DCN has been reported weeks after AOE in vivo and in brain slices and has been correlated with tinnitus (13-15). Our recent study showed the presence of bursts in DCN fusiform cells (FCs) just a few days after AOE (16). Therefore, the aim of the current study was to investigate synaptic transmission at this early time point after AOE and determine whether changes in auditory or multisensory (MS) inputs to FCs might contribute to the altered excitability in the DCN. We postulate that changes following AOE could represent the earliest modifications of the central auditory pathway preceding the later development of DCN hyperactivity and tinnitus. DCN FCs integrate the acoustic information from AN fibers with MS signals transmitted via granule cell axons (parallel fibers) (17-19). DCN granule cells and their parallel fiber axons represent a site of integration of multimodal sensory in...

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“…Neurotransmission is no exception. Cochlear damage and middle ear ossicle removal induce both transient and persistent regulatory changes in transmitter release from glutamatergic, glycinergic, and GABAergic pathways in the mature auditory brainstem (Bledsoe et al, 1995;Potashner et al, 1997Potashner et al, , 2000Suneja et al, 1998). The circling mouse has recently been identified as an animal model for human deafness (Lee et al, 2001(Lee et al, , 2002Chung et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Glutamatergic Transmission Is Sustained at a Later Period of Development of Medial Nucleus of the Trapezoid Body–Lateral Superior Olive Synapses in Circling Mice

Hong¹,

Kim²,

Ahn³

2008

J. Neurosci.

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Synaptic transmission between the medial nucleus of the trapezoid body (MNTB) and the lateral superior olive (LSO) was investigated in circling mice, an animal model for inherited deafness, using the voltage-clamp technique. In postnatal day 9 (P9)ϳP11 homozygous (cir/cir) circling mice, perfusion with 10 M DL-APV and 10 M CNQX reduced the 10 min average of postsynaptic currents (PSCs) to 8.8 Ϯ 3.0% compared with controls (n ϭ 6). In heterozygous (؉/cir) mice in the same age range, the 10 min PSCs average was reduced to 87.5 Ϯ 3.7% compared with controls (n ϭ 7). In P0ϳP2 homozygous (cir/cir) and heterozygous (ϩ/cir) mice, the 10 min PSCs averages were 11.0 Ϯ 2.6% (n ϭ 9) and 84.1 Ϯ 4.6% (n ϭ 11), respectively. The effects of a glutamate antagonist mixture were almost the same in single fiber stimulation of P9ϳP11 mice, reducing mean PSCs to 5.2 Ϯ 3.1% (homozygous (cir/cir) mice, n ϭ 8) and 78.3 Ϯ 4.3% (heterozygous (ϩ/cir) mice, n ϭ 12). Immunohistochemical study revealed that glycine receptor (GlyR) immunoreactivity in heterozygous (ϩ/cir) mice was more prominent than in homozygous (cir/cir) mice, while immunoreactivities of NR1 and NR2A-type NMDAR of P16 homozygous (cir/cir) mice were more prominent than in heterozygous (ϩ/cir) mice of the same age. No significant difference was found in the immunoreactivity of NR2B-type NMDAR. These results indicate that glutamatergic transmission is sustained at a later period of developing MNTB-LSO synapses in homozygous (cir/cir) mice.

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Altered glycinergic synaptic activities in guinea pig brain stem auditory nuclei after unilateral cochlear ablation

Cited by 76 publications

References 71 publications

Age-Related Changes in the Inhibitory Response Properties of Dorsal Cochlear Nucleus Output Neurons: Role of Inhibitory Inputs

Age-Related Changes in the Inhibitory Response Properties of Dorsal Cochlear Nucleus Output Neurons: Role of Inhibitory Inputs

Mechanisms contributing to central excitability changes during hearing loss

Glutamatergic Transmission Is Sustained at a Later Period of Development of Medial Nucleus of the Trapezoid Body–Lateral Superior Olive Synapses in Circling Mice

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