Effects of noise exposure on development of tinnitus and hyperacusis: Prevalence rates 12 months after exposure in middle-aged rats.

Fischer Brown Norway (FBN) rats (n = 233) were unilaterally exposed to 12 different combinations of noise intensity, duration, and spectrum, while 46 rats served as sham-exposed controls. Rats were behaviorally tested for tinnitus and hyperacusis using gap-induced inhibition of the acoustic startle reflex (Gap) and prepulse inhibition (PPI) using 60-dB SPL before noise-exposure and at regular intervals for 12 mo. 12-mo after noise exposure the middle-aged rats were then tested again for tinnitus and hyperacusis before collecting Auditory Brainstem Response (ABR) thresholds.

Enhanced GABAA-Mediated Tonic Inhibition in Auditory Thalamus of Rats with Behavioral Evidence of Tinnitus.

Accumulating evidence suggests a role for inhibitory neurotransmitter dysfunction in the pathology of tinnitus. Opposing hypotheses proposed either a pathologic decrease or increase of GABAergic inhibition in medial geniculate body (MGB). In thalamus, GABA mediates fast synaptic inhibition via synaptic GABAA receptors (GABAARs) and persistent tonic inhibition via high-affinity extrasynaptic GABAARs.

Time course of tinnitus development following noise exposure in mice.

Gap-induced prepulse inhibition of acoustic startle (GPIAS) has been used in rats and mice to study the problem of tinnitus. The current study demonstrates that similar methods can be used to study the temporal development of tinnitus over time in middle-aged mice. Six-month-old mice on a mixed C57Bl6 × 129 background were anesthetized with isoflurane and exposed to unilateral noise (n = 15), or sham exposure for controls (n = 8), for 1 hr (16-kHz octave band signal, 116-dB SPL).

Normative data stratified for age, education, and gender on the Boston Naming Test.

Stratified normative data for age, education, and gender are provided for the 60-item Boston Naming Test (BNT) on 1026 older participants ages 50-95 years using overlapping age ranges. Tables are presented that convert BNT raw scores to scaled scores and percentiles. Mild dementia cases were eliminated using a comprehensive cognitive battery.

A cross-sectional study of the effects of age, education, and gender on the Boston Naming Test.

The effects of age, education, and gender on visual confrontation naming using the 60-item Boston Naming Test (BNT) were studied in 1111 "normal" elderly (ages 50-101) and 61 younger adults (ages 20-49). Significantly poorer mean BNT scores and increasing variability (measured in standard deviations) were found with successively older age groups and with lower educational levels even after stratification on the demographic variables. There was a non-significant trend for males to score slightly higher than females.

Prevention of noise- and drug-induced hearing loss with D-methionine.

A number of otoprotective agents are currently being investigated. Various types of agents have been found in animal studies to protect against hearing loss induced by cisplatin, carboplatin, aminoglycosides, or noise exposure. For over a decade we have been investigating D-methionine (D-met) as an otoprotective agent.

A longitudinal study of confrontation naming in the "normal" elderly.

The longitudinal effects of age on confrontation naming using the 60-item Boston Naming Test (BNT) were studied in 541 "normal" elderly (ages 50-99). For participants with at least 4 annual assessments (n = 238), 150 were followed for > or =6 years, 81 for > or =8 years, and 43 for > or =10 years. A small practice effect (0.

Glutathione ester but not glutathione protects against cisplatin-induced ototoxicity in a rat model.

Glutathione (GSH) provides an important antioxidant and detoxification pathway. We tested to determine if direct administration of GSH or GSH ester could reduce cisplatin- (CDDP) induced ototoxicity. We tested eight groups of five rats each: a control group, a group receiving 16 mg/kg ip CDDP infused over 30 minutes, and six groups receiving either GSH or GSH ester at 500, 1000, or 1500 mg/kg intraperitoneally 30 minutes prior to 16 mg/kg CDDP.