Frogs must have sharp hearing abilities during the warm summer months to successfully find mating partners. This study aims to understand how frog hair cell ribbon-type synapses preserve both sensitivity and temporal precision during temperature changes. Under room (ϳ24°C) and high (ϳ32°C) temperature, we performed in vitro patch-clamp recordings of hair cells and their afferent fibers in amphibian papillae of either male or female bullfrogs. Afferent fibers exhibited a wide heterogeneity in membrane input resistance (R in ) from 100 M⍀ to 1000 M⍀, which may contribute to variations in spike threshold and firing frequency. At higher temperatures, most fibers increased their frequency of spike firing due to an increase in spontaneous EPSC frequencies. Hair cell resting membrane potential (V rest ) remained surprisingly stable during temperature increases, because Ca 2ϩ influx and K ϩ outflux increased simultaneously. This increase in Ca 2ϩ current likely enhanced spontaneous EPSC frequencies. These larger "leak currents" at V rest also lowered R in and produced higher electrical resonant frequencies. Lowering R in will reduce the hair cells receptor potential and presumably moderate the systems sensitivity. Using membrane capacitance measurements, we suggest that hair cells can partially compensate for this reduced sensitivity by increasing exocytosis efficiency and the size of the readily releasable pool of synaptic vesicles. Furthermore, paired recordings of hair cells and their afferent fibers showed that synaptic delays shortened and multivesicular release becomes more synchronous at higher temperatures, which should improve temporal precision. Together, our results explain many previous in vivo observations on the temperature dependence of spikes in auditory nerves.

Expression of FosB gene in striatum is essential in addiction establishment. Activated glucocorticoid receptors (GRs) induce FosB gene expression in response to stressor. Therefore, elevation of FosB expression in striatum serves as one mechanism by which stress increases risk for addiction. In this study, adult male Sprague-Dawley rats were used to investigate whether chronic stress result in histone modifications at FosB gene promoter in striatum and how these histone modifications affect FosB expression and the establishment of addiction behavior after administration of drugs of abuse. Animals were randomly assigned to three groups: Electric foot shock (EFS) group received 7-day EFS to induce chronic stress; electric foot shock plus mifepristone (EFS + Mif) group were injected with mifepristone, a nonspecific GRs antagonist, before EFS; control group did not receive any EFS. All groups then received 2-day conditioned place preference (CPP) training with morphine (5 mg/kg body weight) to test vulnerability to drug addiction. Before and after morphine administration, FosB mRNA in striatum was quantified by real-time RT-PCR. Levels of histone H3/H4 acetylation and histone H3K4 dimethylation at FosB promoter in striatum after morphine administration were measured by using chromatin immunoprecipitation (ChIP) plus real-time PCR. EFS group had stronger place preference to morphine and had significantly higher level of FosB mRNA in striatum than the other two groups. H3K4 dimethylation was 2.6-fold higher in EFS group than control group, while no statistical difference in H3/H4 acetylation. Mifepristone administration before EFS decreased histone H3K4 dimethylation and FosB mRNA in striatum, and also diminished morphine-induced conditioned place preference. Altogether, increased level of H3K4 dimethylation at FosB promoter in striatum is partially dependent on the activation of GR and responsible for the elevated level of morphine-induced FosB mRNA in chronic stressed animals.