Word Learning in Deaf Adults Who Use Cochlear Implants: The Role of Talker Variability and Attention to the Mouth.

OBJECTIVES: Although cochlear implants (CIs) facilitate spoken language acquisition, many CI listeners experience difficulty learning new words. Studies have shown that highly variable stimulus input and audiovisual cues improve speech perception in CI listeners. However, less is known whether these two factors improve perception in a word learning context. Furthermore, few studies have examined how CI listeners direct their gaze to efficiently capture visual information available on a talker's face. The purpose of this study was two-fold: (1) to examine whether talker variability could improve word learning in CI listeners and (2) to examine how CI listeners direct their gaze while viewing a talker speak. DESIGN: Eighteen adults with CIs and 10 adults with normal hearing (NH) learned eight novel word-object pairs spoken by a single talker or six different talkers (multiple talkers). The word learning task comprised of nonsense words following the phonotactic rules of English. Learning was probed using a novel talker in a two-alternative forced-choice eye gaze task. Learners' eye movements to the mouth and the target object (accuracy) were tracked over time. RESULTS: Both groups performed near ceiling during the test phase, regardless of whether they learned from the same talker or different talkers. However, compared to listeners with NH, CI listeners directed their gaze significantly more to the talker's mouth while learning the words. CONCLUSIONS: Unlike NH listeners who can successfully learn words without focusing on the talker's mouth, CI listeners tended to direct their gaze to the talker's mouth, which may facilitate learning. This finding is consistent with the hypothesis that CI listeners use a visual processing strategy that efficiently captures redundant audiovisual speech cues available at the mouth. Due to ceiling effects, however, it is unclear whether talker variability facilitated word learning for adult CI listeners, an issue that should be addressed in future work using more difficult listening conditions.

Early postnatal manganese exposure causes arousal dysregulation and lasting hypofunctioning of the prefrontal cortex catecholaminergic systems.

Studies have reported associations between environmental manganese (Mn) exposure and impaired cognition, attention, impulse control, and fine motor function in children. Our recent rodent studies established that elevated Mn exposure causes these impairments. Here, rats were exposed orally to 0, 25, or 50 mg Mn kg-1  day-1 during early postnatal life (PND 1-21) or lifelong to determine whether early life Mn exposure causes heightened behavioral reactivity in the open field, lasting changes in the catecholaminergic systems in the medial prefrontal cortex (mPFC), altered dendritic spine density, and whether lifelong exposure exacerbates these effects. We also assessed astrocyte reactivity (glial fibrillary acidic protein, GFAP), and astrocyte complement C3 and S100A10 protein levels as markers of A1 proinflammatory or A2 anti-inflammatory reactive astrocytes. Postnatal Mn exposure caused heightened behavioral reactivity during the first 5-10 min intervals of daily open field test sessions, consistent with impairments in arousal regulation. Mn exposure reduced the evoked release of norepinephrine (NE) and caused decreased protein levels of tyrosine hydroxylase (TH), dopamine (DA) and NE transporters, and DA D1 receptors, along with increased DA D2 receptors. Mn also caused a lasting increase in reactive astrocytes (GFAP) exhibiting increased A1 and A2 phenotypes, with a greater induction of the A1 proinflammatory phenotype. These results demonstrate that early life Mn exposure causes broad lasting hypofunctioning of the mPFC catecholaminergic systems, consistent with the impaired arousal regulation, attention, impulse control, and fine motor function reported in these animals, suggesting that mPFC catecholaminergic dysfunction may underlie similar impairments reported in Mn-exposed children.