Recent neuroscience research suggests that tinnitus may reflect synaptic loss in the cochlea that does not express in the audiogram but leads to neural changes in auditory pathways that reduce sound level tolerance (SLT). Adolescents (N = 170) completed a questionnaire addressing their prior experience with tinnitus, potentially risky listening habits, and sensitivity to ordinary sounds, followed by psychoacoustic measurements in a sound booth. Among all adolescents 54.7% reported by questionnaire that they had previously experienced tinnitus, while 28.8% heard tinnitus in the booth. Psychoacoustic properties of tinnitus measured in the sound booth corresponded with those of chronic adult tinnitus sufferers. Neither hearing thresholds (≤15 dB HL to 16 kHz) nor otoacoustic emissions discriminated between adolescents reporting or not reporting tinnitus in the sound booth, but loudness discomfort levels (a psychoacoustic measure of SLT) did so, averaging 11.3 dB lower in adolescents experiencing tinnitus in the acoustic chamber. Although risky listening habits were near universal, the teenagers experiencing tinnitus and reduced SLT tended to be more protective of their hearing. Tinnitus and reduced SLT could be early indications of a vulnerability to hidden synaptic injury that is prevalent among adolescents and expressed following exposure to high level environmental sounds.Tinnitus (chronic ringing of the ears) reduces quality of life for millions worldwide. Although the majority of cases are diagnosed after the age of 50 years, persistent tinnitus can occur at any age including in childhood and adolescence 1 . Neuroscience research suggests that most cases of tinnitus are caused, not by pathological increased auditory nerve activity in the cochlea related to otological disease, but by neuroplastic changes that occur in central auditory pathways following deafferentation of those pathways by damage to the cochlear transduction mechanism (inner and outer hair cells and their stereocilia) or to auditory nerve fibers (ANFs) that convey sound information from ribbon synapses on inner hair cells to the brain [2][3][4][5] . Damage to these cochlear structures (sensorineural hearing loss) can increase thresholds for sound detection measured by the clinical audiogram, and accordingly, audiometric hearing loss putatively caused by noise exposure or the aging process is present in most tinnitus sufferers 6 . However, not all tinnitus patients have abnormal audiograms. Cochlear pathology in these cases may involve, not low-threshold ANFs that are tapped by the audiogram, but high-threshold ANFs that depolarize (fire) only to suprathreshold sounds. Studies in a mouse model of hearing loss found that ~45% of ribbon synapses on high-threshold ANFs were permanently lost following exposure to a level of sound similar to that of some discotheques, with no loss of ribbon synapses on low threshold ANFs or persisting structural damage to cochlear hair cells or their stereocilia [7][8][9][10] . Consequently, wave I of the auditory br...