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 actionpotential threshold. In immature IHCs, we identified 9 known VGSC subtypes (Nav1.1a-1.9a), among which Nav1.7a was the most highly expressed subtype and the main contributor to Na ? currents in developing hair cells. Electrophysiological recordings of two cochlea-specific Nav1.7 variants (CbmNav1.7a and CbmNav1.7b) revealed a novel loss-of-function mutation (C934R) at the extracellular linker between segments 5 and 6 of domain II. In addition, post-transcriptional modification events, such as alternative splicing and RNA editing, amended the gating properties and kinetic features of CbmNav1.7a (C934). These results provide molecular and functional characteristics of VGSCs in mammalian IHCs and their contributions to spontaneous physiological activity during cochlear maturation.

The P2X7 receptor (P2X7R) plays an important role in inflammatory and neuropathic pain. Our recent study indicated that activation of P2X7R in microglial cells of spinal cord contributes to the inflammatory pain induced by BmK I, the major active compound from Buthus martensi Karsch (BmK). In the present study, we further investigated whether P2X7R in satellite glial cells (SGCs) of dorsal root ganglion (DRG) is involved in the BmK I-induced pain in rats. The results found that the expression of P2X7R in SGCs was increased in the ipsilateral side of L4-L5 DRGs after intraplantar injection of BmK I. Moreover, the expression of an inflammatory cytokine IL-1β was increased in DRG after BmK I injection. Systemic administration of an inhibitor of P2X7R (A-438079) significantly inhibited both spontaneous and evoked nociceptive behaviors induced by BmK I. These results suggest that the P2X7R in SGCs of DRG might contribute to pain induced by toxins that sensitize peripheral sensory nerves.

Cervical cancer is a common cancer in women. HPV16 E6 oncoprotein is a reliable biomarker for cervical cancer. Although there are other methods for detecting E6 oncoprotein, the electrochemical method...

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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. The power of raw local field potential oscillations and high-frequency β oscillation in the A1 cortex of NE rats were larger, whereas the power of high-frequency γ oscillation was smaller than that of control rats. In addition, the expression levels of five glutamate receptor (GluR) subunits in the A1 cortex of NE rats were decreased with laminar specificity. These results suggest that the altered neural excitability and decreased GluR expression may underlie the delay of functional maturation in the A1 cortex, and may have implications for the treatment of hearing impairment induced by environmental noise.