Objectives: Functional near-infrared spectroscopy (fNIRS) is a brain imaging technique particularly suitable for hearing studies. However, the nature of fNIRS responses to auditory stimuli presented at different stimulus intensities is not well understood. In this study, we investigated whether fNIRS response amplitude was better predicted by stimulus properties (intensity) or individually perceived attributes (loudness). Design: Twenty-two young adults were included in this experimental study. Four different stimulus intensities of a broadband noise were used as stimuli. First, loudness estimates for each stimulus intensity were measured for each participant. Then, the 4 stimulation intensities were presented in counterbalanced order while recording hemoglobin saturation changes from cortical auditory brain areas. The fNIRS response was analyzed in a general linear model design, using 3 different regressors: a non-modulated, an intensity-modulated, and a loudness-modulated regressor. Results: Higher intensity stimuli resulted in higher amplitude fNIRS responses. The relationship between stimulus intensity and fNIRS response amplitude was better explained using a regressor based on individually estimated loudness estimates compared with a regressor modulated by stimulus intensity alone. Conclusions: Brain activation in response to different stimulus intensities is more reliant upon individual loudness sensation than physical stimulus properties. Therefore, in measurements using different auditory stimulus intensities or subjective hearing parameters, loudness estimates should be examined when interpreting results.
During development, regulation of the strength of synaptic transmission plays a central role in the formation of mammalian brain circuitries. In taiep rat, a neurological mutant with severe reactive astrogliosis and demyelination, we have described alterations in the synaptic transmission in central neurons, characterized by asynchronous excitatory postsynaptic currents ((ASYN)EPSCs), because of delayed neurotransmitter release. This hippocampal synaptic dysfunction has been described in juvenile mutants, concomitantly with the appearance of their main glial alterations. However, it is unknown whether this abnormal synaptic activity is correlated with some alterations of synaptic maturation during the postnatal development. Using intracellular electrophysiological recordings and immunohistochemistry assays, we studied the maturation of CA3-CA1 synapses in taiep rats. In taiep, the number of (ASYN)EPSCs evoked by conventional stimulation of Schaffer collaterals increases with age (P7-P30) and can be evoked by stimulation of single fiber. The amplitude and frequency of spontaneous EPSC (sEPSC) increased during the postnatal development in both control and taiep rats. However, in taiep, the increase of sEPSC frequency was significantly higher than in the control rats. The frequency of miniature EPSC (mEPSC) increased over the studied age range, without differences between taiep and control rats. In both control and taiep groups, the synaptophysin immunostaining (SYP-IR) in the stratum radiatum of CA1 region was significantly lower in the juvenile (P30) than in the neonatal (P10) rats, suggesting that synaptic pruning is normally occurring in taiep, even when SYP-IR was higher in taiep than control in both ages studied. These results suggest that, in taiep mutants, the asynchronic transmission is due to a dysfunction in the glutamate release mechanisms that progressively increases during development, which is not attributable to the existence of aberrant synaptic contacts. Synapse 63:502-509, 2009. (c) 2009 Wiley-Liss, Inc.
For the taiep rat, a neurological mutant with severe astrogliosis secondary to demyelination, we have described alterations in spinal cord synaptic transmission. Asynchronous responses result from phasic action potential-derived glutamate release in this mutant. To evaluate whether this anomalous transmission is also produced in other regions of the taiep CNS and whether its nature involves a presynaptic or postsynaptic disruption, we studied the CA3-CA1 hippocampal synapses. Excitatory postsynaptic currents (EPSC) evoked by stimulation of Schaffer collaterals were recorded from CA1 pyramidal cells on picrotoxin-treated slices. Initial fast and time-locked EPSCs were evoked by conventional stimulation in both control and taiep neurons, showing similar latency and amplitude values unimodally distributed. In a high percentage of taiep neurons (47%), the initial EPSC was frequently followed by additional asynchronous synaptic currents (EPSC(ASYN)) with latencies ranging from 10 to 300 msec. As with initial EPSCs, EPSC(ASYN) were action potential dependent, sensitive to tetrodotoxin, and blocked by D-2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2,3-dione. The occurrence probability of these events decayed monoexponentially as a function of poststimulus time. The elevation of extracellular Ca(2+) induced a reduction of amplitudes and a rate increase of EPSC(ASYN), in parallel with a reduction of paired pulse facilitation of initial EPSCs. The presynaptic fiber volley, extracellularly recorded, showed no significant differences between groups, with similar mean values of area and decay time. These findings in hippocampal circuitry suggest that, in taiep, the asynchronous evoked activity represents a rather generalized phenotype of the glutamatergic synapses and that EPSC(ASYN) seems to be determined by presynaptic alterations.
Background. Evidence-based information on genetic sensorineural hearing loss in Latin America is limited, hindering the advancement of related clinical practice and the development of relevant healthcare policies in the field. This study describes sociodemographic and clinical characteristics of a group of Chilean participants with congenital, childhood, progressive or late-onset sensorineural hearing loss of unknown etiology; all non-genetic causes of hearing loss were excluded. Methods. A quantitative study, with a non-experimental, observational, cross-sectional design and a descriptive scope. From 978 patients diagnosed with SNHL, 286 subjects fulfilled the inclusion criteria, and 138 patients accepted to participate. Results. The most frequent audiological-profile was symmetrical-bilateral-profound-SNHL with a sloping pattern. The median age at audiological diagnosis was 24.5 months (IQR:12-53) and at first-time Hearing-Assistive-Device-use (HAD-use) was 30 months (IQR:13-69). 71% of HAD were financed by public resources. Conclusion. The age at audiological diagnosis in SNHL of suspected genetic causes is still far from international standards. These results are valuable for public health research and policy development, not only for the Chilean population, but also for other Hispanic communities and other middle-high income countries.
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