We investigated the effect of pulse duration (PD) and interphase-gap (IPG) on the electrically-evoked auditory brain stem response (EABR) and viiith nerve compound action potential (ECAP) of deafened guinea pigs in order to test the hypothesis that the extent of change in these neural responses is affected by the histological status of the auditory nerve. Fifteen guinea pigs were deafened by co-administration of kanamycin and furosemide. Animals were acutely implanted with an 8-band electrode array at 1, 4 or 12 weeks following deafening. EABR and ECAP input/output functions were recorded in response to charge balanced biphasic current pulses. We determined the change in current required to equalize; (i) the EABR amplitude when the duration of the current pulse was doubled (104-208 micros/phase); and (ii) the EABR and ECAP amplitudes when the IPG was increased from 8 to 58 micros using a 104 micros/phase current pulse. Following the completion of each experiment the cochleae were examined quantitatively for spiral ganglion neuron survival. As expected, the current level required to evoke an EABR with equal amplitude was lower when the animal was stimulated with current pulses of 208 compared with 104 micros/phase. Moreover, the current level required to evoke EABR/ECAPs with equal amplitude was lower when current pulses had an IPG of 58 versus 8 micros. Importantly, there was a reduction in the magnitude of this effect with greater neural loss; the reduced efficacy of changing both PD and IPG on these electrically-evoked potentials was statistically correlated with neural survival. These results may provide a tool for investigating the contribution of auditory nerve survival to clinical performance among cochlear implant subjects.

Neural entrainment is the synchronization of neural activity to the frequency of repetitive external stimuli, which can be observed as an increase in the electroencephalogram (EEG) power spectrum at the driving frequency, -also known as the steady-state response. Although it has been systematically reported that the entrained EEG oscillation persists for approximately three cycles after stimulus offset, the neural mechanisms underpinning it remain unknown. Focusing on alpha oscillations, we adopt the dynamical excitation/inhibition framework, which suggests that phases of entrained EEG signals correspond to alternating excitatory/inhibitory states of the neural circuitry. We hypothesize that the duration of the persistence of entrainment is determined by the specific functional state of the entrained neural network at the time the stimulus ends. Steady-state visually evoked potentials (SSVEP) were elicited in 19 healthy volunteers at the participants' individual alpha peaks. Visual stimulation consisted of a sinusoidallyvarying light terminating at one of four phases: 0, π/2, π, and 3π/2. The persistence duration of the oscillatory activity was analyzed as a function of the terminating phase of the stimulus. Phases of the SSVEP at the stimulus termination were distributed within a constant range of values relative to the phase of the stimulus. Longer persistence durations were obtained when visual stimulation terminated towards the troughs of the alpha oscillations, while shorter persistence durations occurred when stimuli terminated near the peaks. Source localization analysis suggests that the persistence of entrainment reflects the functioning of fronto-occipital neuronal circuits, which might prime the sensory representation of incoming visual stimuli based on predictions about stimulus rhythmicity. Consequently, different states of the network at the end of the stimulation, corresponding to different states of intrinsic neuronal coupling, may determine the time windows over which coding of incoming sensory stimulation is modulated by the preceding oscillatory activity.

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Mutations in human connexin (Cx) genes have been related to diseases, which we termed connexinopathies. Such hereditary disorders include nonsyndromic or syndromic deafness (Cx26, Cx30), Charcot Marie Tooth disease (Cx32), occulodentodigital dysplasia and cardiopathies (Cx43), and cataracts (Cx46, Cx50). Despite the clinical phenotypes of connexinopathies have been well documented, their pathogenic molecular determinants remain elusive. The purpose of this work is to identify common/uncommon patterns in channels function among Cx mutations linked to human diseases. To this end, we compiled and discussed the effect of mutations associated to Cx26, Cx32, Cx43, and Cx50 over gap junction channels and hemichannels, highlighting the function of the structural channel domains in which mutations are located and their possible role affecting oligomerization, gating and perm/ selectivity processes.

Generation of the auditory steady state responses (ASSR) is commonly explained by the linear combination of random background noise activity and the stationary response. Based on this model, the decrease of amplitude that occurs over the sequential averaging of epochs of the raw data has been exclusively linked to the cancelation of noise. Nevertheless, this behavior might also reflect the non-stationary response of the ASSR generators. We tested this hypothesis by characterizing the ASSR time course in rats with different auditory maturational stages. ASSR were evoked by 8-kHz tones of different supra-threshold intensities, modulated in amplitude at 115 Hz. Results show that the ASSR amplitude habituated to the sustained stimulation and that dishabituation occurred when deviant stimuli were presented. ASSR habituation increased as animals became adults, suggesting that the ability to filter acoustic stimuli with no-relevant temporal information increased with age. Results are discussed in terms of the current model of the ASSR generation and analysis procedures. They might have implications for audiometric tests designed to assess hearing in subjects who cannot provide reliable results in the psychophysical trials.