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Antidepressants, while effective in treating depression and anxiety disorders, also induce deficits in sensory (particularly auditory) processing, which in turn may exacerbate psychiatric symptoms. How antidepressants cause auditory signature deficits remains largely unknown. Here, we found that fluoxetine-treated adult female rats were significantly less accurate when performing a tone-frequency discrimination task compared with age-matched control rats. Their cortical neurons also responded less selectively to sound frequencies. The degraded behavioral and cortical processing was accompanied by decreased cortical perineuronal nets, particularly those wrapped around parvalbumin-expressing inhibitory interneurons. Furthermore, fluoxetine induced critical period-like plasticity in their already mature auditory cortices; therefore, a brief rearing of these drug-treated rats under an enriched acoustic environment renormalized auditory processing degraded by fluoxetine. The altered cortical expression of perineuronal nets was also reversed as a result of enriched sound exposure. These findings suggest that the adverse effects of antidepressants on auditory processing, possibly because of a reduction in intracortical inhibition, can be substantially alleviated by simply pairing drug treatment with passive, enriched sound exposure. They have important implications for understanding the neurobiological basis of antidepressant effects on hearing and for designing novel pharmacological treatment strategies for psychiatric disorders. [ABSTRACT FROM AUTHOR]

An increasing number of studies have shown that cross-modal interaction can occur in early sensory cortices. Yet, how neurons in sensory cortices integrate multisensory cues in perceptual tasks and to what extent this influences behavior is largely unclear. To investigate, we examined visual modulation of auditory responses in the primary auditory cortex (A1) in a twoalternative forced-choice task. During the task, male rats were required to make a behavioral choice based on the pure tone frequency (low vs high) of the self-triggered stimulus to get a water reward. The result showed that the presence of a noninformative visual cue did not uniformly influence auditory response, with frequently enhancing just one of them. Closely correlated with behavioral choice, the visual cue mainly enhanced responsiveness to the auditory cue indicating a movement direction contralateral to A1 being recorded. Operating in this fashion provided A1 neurons a superior capability to discriminate sound during multisensory trials. Concomitantly, behavioral data and decoding analysis revealed that visual cue presence could speed the process of sound discrimination. We also observed this differential multisensory integration effect in well-trained rats when tested with passive stimulation and under anesthesia, albeit to a much lesser extent. We did not see this differentially integrative effect while recording in A1 in another similar group of rats performing a free-choice task. These data suggest that auditory cortex can engage in meaningful audiovisual processing, and perceptual learning can modify its multisensory integration mechanism to meet task requirements. [ABSTRACT FROM AUTHOR]

It has previously been shown that environmental enrichment can enhance structural plasticity in the brain and thereby improve cognitive and behavioral function. In this study, we reared developmentally noise-exposed rats in an acoustic-enriched environment for ~4 weeks to investigate whether or not enrichment could restore developmentally degraded behavioral and neuronal processing of sound frequency. We found that noise-exposed rats had significantly elevated sound frequency discrimination thresholds compared with agematched naive rats. Environmental acoustic enrichment nearly restored to normal the behavioral deficit resulting from early disrupted acoustic inputs. Signs of both degraded frequency selectivity of neurons as measured by the bandwidth of frequency tuning curves and decreased long-term potentiation of field potentials recorded in the primary auditory cortex of these noise-exposed rats also were reversed partially. The observed behavioral and physiological effects induced by enrichment were accompanied by recovery of cortical expressions of certain NMDA and GABAA receptor subunits and brain-derived neurotrophic factor. These studies in a rodent model show that environmental acoustic enrichment promotes recovery from early noise-induced auditory cortical dysfunction and indicate a therapeutic potential of this noninvasive approach for normalizing neurological function from pathologies that cause hearing and associated language impairments in older children and adults. [ABSTRACT FROM AUTHOR]

Although training-based auditory cortical plasticity in the adult brain has been previously demonstrated in multiparametric sound domains, neurochemical mechanisms responsible for this form of plasticity are not well understood. In this study, we trained adult rats to identify a target sound stimulus at a specific azimuth angle by using a reward-contingent auditory discrimination task. We found that auditory spatial discrimination training significantly enhanced representation of sound azimuths in the primary auditory cortex, as shown by sharper azimuth-selective curves and more evenly distributed best angles of cortical neurons. Training also facilitated longterm potentiation of field potentials in the primary auditory cortex induced by theta burst stimulation of the white matter. In parallel, there were significant alterations in expression levels of certain cortical GABAA and NMDA receptor subunits, resulting in a marked decrease in the level of GABAA relative to NMDA receptors. These changes in the expression profile of inhibitory and excitatory neurotransmitter receptor subunits might enhance synaptic transmission, thereby facilitating training-induced cortical plasticity in the spatial domain. [ABSTRACT FROM AUTHOR]