Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model.

Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model. Research Abstract Details 

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Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model. Abstract Text:

Thomas J Brozoski,T Joseph D Spires,Carol A Bauer,

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 gamma-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.

Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model. Publishing Authors By Initials

TJ Brozoski,TJ Spires,CA Bauer,

For similar organic chemicals: carboxylic acids: acids, acyclic: butyric acids: aminobutyric acids: gamma-aminobutyric acid: vigabatrin research abstracts see: organic chemicals: carboxylic acids: acids, acyclic: butyric acids: aminobutyric acids: gamma-aminobutyric acid: vigabatrin research

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Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of the Association for Research in Otolary

VOLUME: 8

Page Numbers: 105-18

Journal Abbreviation: J. Assoc. Res. Otolaryngol.

ISSN: 1525-3961

DAY: 13

MONTH: 01

YEAR: 2007

Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100892857

Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model. Keywords Mesh Terms:

KEYWORDS: Vigabatrin

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model. Information

Substance Name: 4-Aminobutyrate Transaminase

Registry Number: EC 2.6.1.19

Grant and Affiliation Information for Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model.

AFFILIATION: Division of Otolaryngology, Southern Illinois University School of Medicine, 801 N. Rutledge St., Rm. 3205, P. O. Box 19629, Springfield, IL 62794-9629, USA. tbrozoski@siumed.edu

Country: United States

AGENCY: United States NIDCD

GRANT: R01 DC4830-04

ACRONYM: DC

MEDLINETA: J Assoc Res Otolaryngol

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