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Cochlear implants provide an auditory signal with which profoundly deaf users may monitor their own speech production. The vowel production of two adults and three children who used the Nucleus multiple-electrode cochlear implant was examined to assess the effect of altered auditory feedback. Productions of words were recorded under conditions where the talkers received auditory feedback (speech processor turned on) and where no auditory feedback was provided (speech processor turned off). Data were collected over 3 days at weekly intervals. First and second formant frequencies were measured and the data were analysed to assess significant differences between auditory feedback conditions, vowel context, and data collection points. Overall, the results varied across talkers, across the data collection days, and depended on the consonant environment of the vowel. However, two effects of auditory feedback were noted. First, there was a generalized shift in first formant frequencies between the processor on and processor off conditions across three of the five subjects, but the shift differed in direction for each subject. Second, for three of the five talkers, the two front vowels /epsilon/ and /i/ were more neutralised in the absence of auditory feedback. However, this effect was less pronounced than that noted by previous studies.
To receive information on the intracochlear magnitude and propagation properties of cochlear distortion products, the neuronal response of AVCN cells to distortion stimuli and the acoustical correlates in the ear canal (DPOAE) were measured for frequencies between 0.7 and 45.3 kHz. Comparison of the growth of neuronal response to a distortion stimulus and the neuronal rate-versus-level function for an externally applied pure tone of equal frequency allowed for an assessment of the intracochlear magnitude of the distortions. AVCN neurons with a characteristic frequency (CF) > 1.8 kHz started to respond to the intracochlear distortion stimulus, at primary levels for which the ear-canal level of the corresponding DPOAE was close to the pure-tone threshold of the units. This finding suggests that transmission of sound energy is comparable in the forward and reverse direction, and that mechanical distortions of the cochlea are fully encoded by neurons in the AVCN. For neurons with a CF < 1.8 kHz, the intracochlear magnitude of the distortion stimulus appeared to be about 15 to 30 dB higher than the corresponding DPOAE, at the threshold of neuronal response. This discrepancy between intracochlear magnitude of cochlear distortions and their acoustical expression may be explained by high-pass filter action of the middle ear during DPOAE re-emission from the cochlea. A contribution to the observed discrepancy of the type of distortion (cubic versus quadratic) used as stimulus, and possible differences in mechanical frequency processing between the apex and base of the gerbil cochlea, are also discussed. The delay of the neuronal response to an intracochlear distortion stimulus was on average 1.1 ms longer than the neuronal delay to an external pure tone of equal frequency and intensity, most likely stemming from the activation delay of the DPOAE generating mechanisms.
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Voltage-activated Ca(2+) currents have been studied in pyramidal cells isolated enzymatically from the dorsal cochlear nuclei of 6-11-day-old Wistar rats, using whole-cell voltage-clamp. From hyperpolarized membrane potentials, the neurones exhibited a T-type Ca(2+) current on depolarizations positive to -90 mV (the maximum occurred at about -40 mV). The magnitude of the T-current varied considerably from cell to cell (-56 to -852 pA) while its steady-state inactivation was consistent (E(50)=-88.2+/-1.7 mV, s=-6. 0+/-0.4 mV). The maximum of high-voltage activated (HVA) Ca(2+) currents was observed at about -15 mV. At a membrane potential of -10 mV the L-type Ca(2+) channel blocker nifedipine (10 microM) inhibited approximately 60% of the HVA current, the N-type channel inhibitor omega-Conotoxin GVIA (2 microM) reduced the current by 25% while the P/Q-type channel blocker omega-Agatoxin IVA (200 nM) blocked a further 10%. The presence of the N- and P/Q-type Ca(2+) channels was confirmed by immunochemical methods. The metabotropic glutamate receptor agonist (+/-)-1-aminocyclopentane-trans-1, 3-dicarboxylic acid (200 microM) depressed the HVA current in every cell studied (a block of approximately 7% on an average). The GABA(B) receptor agonist baclofen (100 microM) reversibly inhibited 25% of the HVA current. Simultaneous application of omega-Conotoxin GVIA and baclofen suggested that this inhibition could be attributed to the nearly complete blockade of the N-type channels. Possible physiological functions of the voltage-activated Ca(2+) currents reported in this work are discussed.
Recordings were made in vitro from cochlear nuclei of Gunn rats, a strain with a recessive mutation that predisposes rats to hyperbilirubinemia at birth. Delays between shocks to the auditory nerve and earliest synaptic responses of the cochlear nuclear neurons were on average longer in Gunn rats than in heterozygotes. Injections of sulfonamide further increased average synaptic delays in jaundiced rats. Responses to injected current in rats were like those in mice.
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The differences in path length of axons from the anteroventral cochlear nuclei (AVCN) to the medial superior olive (MSO) are thought to provide the anatomical substrate for the computation of interaural time differences (ITD). We made small injections of biotinylated dextran into the AVCN that produced intracellular-like filling of axons. This permitted three-dimensional reconstructions of individual axons and measurements of axonal length to individual terminals in MSO. Some axons that innervated the contralateral MSO had collaterals with lengths that were graded in the rostrocaudal direction with shorter collaterals innervating more rostral parts of MSO and longer collaterals innervating more caudal parts of MSO. These could innervate all or part of the length of the MSO. Other axons had restricted terminal fields comparable to the size of a single dendritic tree in the MSO. In the ipsilateral MSO, some axons had a reverse, but less steep, gradient in axonal length with greater axonal length associated with more rostral locations; others had restricted terminal fields. Thus, the computation of ITDs is based on gradients of axonal length in both the contralateral and ipsilateral MSO, and these gradients may account for a large part of the range of ITDs encoded by the MSO. Other factors may be involved in the computation of ITDs to compensate for differences between axons.
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The responses of cochlear nuclei single units in Vespertilionidae and Rhinolophidae were studied by means of ultrasound stimuli of different frequencies. Most neurons were found to have one or two complementary response areas with best frequencies equal to 1/2 and 1/3 of the highest one (which we regard as the basic best frequency). In Vespertilionidae which emit frequency-modulated signals some neurons have complementary areas with upper thresholds. The latency of responses do not correlate with the stimulus frequency. This suggests that there is no correlative reception of echosignals at this level of auditory system in bats.