Neuroglial activation in the auditory cortex and medial geniculate body of salicylate-induced tinnitus rats.

Neuroglial activation has been recognized as a pathological hallmark of a variety of neurological diseases, yet the role of neuroglia in tinnitus hasn't been well established so far. To explore the potential roles of two types of glia cells (astrocyte and microglia) in the development of tinnitus, we examined markers associated with them in the primary auditory (A1) cortex and medial geniculate body (MGB) of rats with salicylate-induced tinnitus. The results demonstrated that acute and chronic administrations of salicylate could cause reversible tinnitus-like behavior in rats.

Aberrant expression of Nav1.6 in the cochlear nucleus correlates with salicylate-induced tinnitus in rats.

Hyperactivity in cochlear nucleus (CN) is one of the major neural correlates for tinnitus induction, yet the molecular factors that participate in the neuronal hyperexcitability remain unclear. The present study showed that acute and chronic administrations of salicylate were both capable of inducing reversible tinnitus in rats. The number of GAD 65/67-immunoreactive neurons in the AVCN and DCN was decreased, while the number of VGLUT 1/2-immunoreactive neurons in the AVCN and DCN was increased when rats were experiencing tinnitus, providing evidence for excitatory-inhibitory imbalance in CN is correlated with tinnitus.

Visual deprivation modifies glutamate receptor expression in visual and auditory centers.

Changes in the electrical activities of visual and auditory thalamic-cortical regions account for the cross-modal enhancement of auditory perception following visual deprivation, but the molecular regulatory factors mediating these changes remain elusive. In this study, we showed that the expression patterns of five glutamate receptor (GluR) subunits which involved in regulating the synaptic plasticity in mouse primary visual (V1) cortex and primary auditory (A1) cortex undergone elaborate modification with layer-specificity after visual deprivation using dark-exposure (DE). The expression levels of NR1 and NR2B were increased, and those of GluR1 and NR2B in the V1 cortex were decreased after DE.

Long-term exposure to moderate noise induces neural plasticity in the infant rat primary auditory cortex.

Previous studies have reported that rearing infant rat pups in continuous moderate-level noise delayed the formation of topographic representational order and the refinement of response selectivity in the primary auditory (A1) cortex. The present study further verified that exposure to long-term moderate-intensity white noise (70 dB sound pressure level) from postnatal day (P) 12 to P30 elevated the hearing thresholds of infant rats. Compared with age-matched control rats, noise exposure (NE) rats had elevated hearing thresholds ranging from low to high frequencies, accompanied by decreased amplitudes and increased latencies of the two initial auditory brainstem response waves.

Distribution and Functional Characteristics of Voltage-Gated Sodium Channels in Immature Cochlear Hair Cells.

Voltage-gated sodium channels (VGSCs) are transiently expressed in cochlear hair cells before hearing onset and play an indispensable role in shaping spontaneous activity. In this study, we showed that Na currents shaped the spontaneous action potentials in developing mouse inner hair cells (IHCs) by decreasing the time required for the membrane potential to reach the action-potential threshold. In immature IHCs, we identified 9 known VGSC subtypes (Nav1.