Plastic Changes in Glycine and GABA Release and Uptake in Adult Brain Stem Auditory Nuclei after Unilateral Middle Ear Ossicle Removal and Cochlear Ablation

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

doi:10.1006/exnr.1998.6812

Cited by 161 publications

(132 citation statements)

References 126 publications

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“…This pathology may be relayed to the ICC through the indirect binaural projections of the VCN. Although a single unit analysis has not been applied to the binaural brainstem, local hyperactivity is implied by chronic changes in the expression of excitatory and inhibitory neurotransmitters (Potashner et al 1997;Suneja et al 1998).…”

Section: Role Of the Vcnmentioning

confidence: 99%

Effects of Unilateral Acoustic Trauma on Tinnitus-Related Spontaneous Activity in the Inferior Colliculus

Ropp

Tiedemann

Young

et al. 2014

JARO

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This study describes the long-term effects of soundinduced cochlear trauma on spontaneous discharge rates in the central nucleus of the inferior colliculus (ICC). As in previous studies, single-unit recordings in Sprague-Dawley rats revealed pervasive increases in spontaneous discharge rates. Based on differences in their sources of input, it was hypothesized that physiologically defined neural populations of the auditory midbrain would reveal the brainstem sources that dictate ICC hyperactivity. Abnormal spontaneous activity was restricted to target neurons of the ventral cochlear nucleus. Nearly identical patterns of hyperactivity were observed in the contralateral and ipsilateral ICC. The elevation in spontaneous activity extended to frequencies well below and above the region of maximum threshold shift. This lack of frequency organization suggests that ICC hyperactivity may be influenced by regions of the brainstem that are not tonotopically organized. Sound-induced hyperactivity is often observed in animals with behavioral signs of tinnitus. Prior to electrophysiological recording, rats were screened for tinnitus by measuring gap pre-pulse inhibition of the acoustic startle reflex (GPIASR). Rats with positive phenotypes did not exhibit unique patterns of ICC hyperactivity. This ambiguity raises concerns regarding animal behavioral models of tinnitus. If our screening procedures were valid, ICC hyperactivity is observed in animals without behavioral indications of the disorder. Alternatively, if the perception of tinnitus is strictly linked to ongoing ICC hyperactivity, our current behavioral approach failed to provide a reliable assessment of tinnitus state.

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Section: Role Of the Vcnmentioning

confidence: 99%

Effects of Unilateral Acoustic Trauma on Tinnitus-Related Spontaneous Activity in the Inferior Colliculus

Ropp

Tiedemann

Young

et al. 2014

JARO

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“…Unilateral damage to the peripheral auditory system induces bilateral changes in the anatomical and physiological characteristics of cochlear nucleus neurons Suneja et al 1998;Muly et al 2002Muly et al , 2004Sumner et al 2005;Rubio 2006). This plasticity may be induced by ossicular chain disruption, cochlea and auditory nerve ablation, or intense sound exposure.…”

Section: Functional Considerationsmentioning

confidence: 99%

Commissural Neurons in the Rat Ventral Cochlear Nucleus

Doucet

Lenihan

May

2009

JARO

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Commissural neurons connect the cochlear nucleus complexes of both ears. Previous studies have suggested that the neurons may be separated into two anatomical subtypes on the basis of percent apposition (PA); that is, the percentage of the soma apposed by synaptic terminals. The present study combined tract tracing with synaptic immunolabeling to compare the soma area, relative number, and location of Type I (low PA) and Type II (high PA) commissural neurons in the ventral cochlear nucleus (VCN) of rats. Confocal microscopic analysis revealed that 261 of 377 (69%) commissural neurons have mediumsized somata with Type I axosomatic innervation. The commissural neurons also showed distinct topographical distributions. The majority of Type I neurons were located in the small cell cap of the VCN, which serves as a nexus for regulatory pathways within the auditory brainstem. Most Type II neurons were found in the magnocellular core. This anatomical dichotomy should broaden current views on the function of the commissural pathway that stress the fast inhibitory interactions generated by Type II neurons. The more prevalent Type I neurons may underlie slow regulatory influences that enhance binaural processing or the recovery of function after injury.

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“…It has been hypothesized that partial deafferentation from various causes, such as acoustic trauma or age-related hearing loss, produces a loss of inhibitory tone in the auditory system. Loss of central inhibition would be expected to significantly alter auditory processing (Brozoski et al 2002;Caspary et al 1999;Suneja et al 1998a;Szczepaniak and Moller 1996;Willott and Lu 1982), which, in turn, could lead to inappropriate neuroplastic changes eventually expressed as a sensation of tinnitus. Because g-amino butyric acid (GABA) is a generally inhibitory neurotransmitter found in appreciable amounts at many levels of the central auditory pathway (Backoff et al 1997;Bauer et al 2000;Caspary et al 1995;Milbrandt et al 1996;Suneja et al 1998b), a corollary to the loss-of-inhibition and tinnitus hypothesis would be the down-regulation of GABA activity.…”

Section: Introductionmentioning

confidence: 99%

Vigabatrin, a GABA Transaminase Inhibitor, Reversibly Eliminates Tinnitus in an Animal Model

Brozoski

Spires

Bauer

2007

JARO

111

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Animal models have facilitated basic neuroscience research investigating the pathophysiology of tinnitus. It has been hypothesized that partial deafferentation produces a loss of tonic inhibition in the auditory system that may lead to inappropriate neuroplastic changes eventually expressed as tinnitus. The pathological down-regulation of g-amino butyric acid (GABA) provides a potential mechanism for this loss of inhibition. Using an animal model previously demonstrated to be sensitive to treatments that either induce or attenuate tinnitus, the present study examined the effect of the specific GABA agonist vigabatrin on chronic tinnitus. It was hypothesized that vigabatrin would decrease the evidence of tinnitus by restoring central inhibitory function through increased GABA availability. Vigabatrin has been demonstrated to elevate central GABA levels (Mattson et al. 1995). Tinnitus was induced in rats using a single 1-h unilateral exposure to band-limited noise, which preserved normal hearing in one ear. Psychophysical evidence of tinnitus was obtained using a free-operant conditioned-suppression method: Rats lever-pressed for food pellets and were trained to discriminate between the presence and absence of sound by punishing lever pressing with a mild foot shock (0.5 mA; 1 s) at the conclusion of randomly introduced silent periods (60 s) inserted into background low-level noise. Additional random insertion of pure tone and noise periods of variable intensity enabled the derivation of psychophysical functions that reflected the presence of tinnitus with features similar to 20-kHz tones. Vigabatrin was chronically administered via drinking water at 30 and 81 mg kg _ 1 day _ 1, with each dose level tested over 2 weeks, followed by a 0-mg washout test. Vigabatrin completely and reversibly eliminated the psychophysical evidence of tinnitus at both doses. Although vigabatrin has serious negative side effects that have prevented its clinical use in the USA, it is nevertheless a potentially useful tool in unraveling tinnitus pathophysiology.

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Plastic Changes in Glycine and GABA Release and Uptake in Adult Brain Stem Auditory Nuclei after Unilateral Middle Ear Ossicle Removal and Cochlear Ablation

Cited by 161 publications

References 126 publications

Effects of Unilateral Acoustic Trauma on Tinnitus-Related Spontaneous Activity in the Inferior Colliculus

Effects of Unilateral Acoustic Trauma on Tinnitus-Related Spontaneous Activity in the Inferior Colliculus

Commissural Neurons in the Rat Ventral Cochlear Nucleus

Vigabatrin, a GABA Transaminase Inhibitor, Reversibly Eliminates Tinnitus in an Animal Model

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