Speech-evoked cognitive P300 potentials in cochlear implant recipients

The cognitive P300 evoked potential was elicited by speech stimuli in successful cochlear implant recipients, and the resulting P300 morphology was remarkably similar to that of normal-hearing individuals. The P300 was elicited by the synthesized speech pair/da/and/di/ presented using an oddball paradigm to nine "good" Nucleus cochlear implant users and nine age-matched normal-hearing subjects (34-81 yr old). There were no significant differences in P300 amplitude and latency between the two groups. Moreover, the N1 and P2 potentials occurred at similar latencies in the two groups, although the N1 amplitude was significantly smaller in the cochlear implant users. The P300 was absent in one "poor" cochlear implant user. The results suggest that the P300 may serve as a useful tool for evaluating the cognitive aspects of auditory processing in cochlear implant recipients, and that it may aid in assessing the success of cochlear implantation.     

Nitroprusside suppresses cochlear potentials and outer hair cell responses

Biochemical and pharmacological evidence supports a role for nitric oxide (NO) in the cochlea. In the present experiments, we tested sodium nitroprusside (SNP), an NO donor, applied by intracochlear perfusions on sound-evoked responses of the cochlea (CM, cochlear microphonic; SP, summating potential; EP, endocochlear potential; CAP, compound action potential) and in vitro on outer hair cell (OHC) voltage-induced length changes and current responses. In vivo application of SNP in increasing concentrations (10, 33, 100, 330 and 1000 microM) reduced all sound-evoked responses starting at about 300 microM. The responses continued to decline after a postdrug wash. At 1 mM SNP decreased EP slowly (approximately 80 min) whereas at 10 mM it reduced EP more rapidly (approximately 20 min). Ferricyanide (1 mM) and S-nitroso-N-acetylpenicillamine (SNAP; 1 mM) had no effect on sound-evoked cochlear potentials. Ferricyanide (1 mM and 10 mM) and ferrocyanide (10 mM) had no effect on EP. In vitro, SNP (10 mM) significantly reduced both OHC voltage-induced length changes and whole-cell outward currents. Results suggest that SNP, possibly acting by released NO, influences cochlear function through effects at the stria vascularis and at the OHCs.     

Evidence that inner hair cells are the major source of cochlear summating potentials

The role of the inner hair cells (IHCs) in generating the cochlear summating potentials (SP) was assessed by measuring SP, cochlear nerve action potentials (CAP), cochlear microphonics (CM) and 2f1-f2 distortion product otoacoustic emissions (DPOAEs) in 15 chinchillas with either acute chemical de-afferentation, accomplished by applying kainic acid to the round window, or surgical de-afferentation and basal IHC loss, which developed within two months after sectioning the auditory nerve. In the auditory nerve sectioned ears, type I ganglion cells disappeared whereas most, if not all, type II ganglion cells were still present. Histological analysis of surface preparations and sections through the modiolus verified the de-afferentation in both models and showed a large IHC loss at the base of the cochlea in the ears with the auditory nerve sectioned while other structures of the cochlea remained intact. Unoperated (left) ears of 9 animals served as controls. CM and DPOAEs were normal in all ears whereas the CAP was substantially depressed in de-afferented ears. Comparisons among the SP input-output functions suggest that (1) the IHCs are the major generator of SP recorded from the round window in chinchilla, in particular at low to moderate stimulus levels, (2) the SP recorded from the round window largely reflects the responses from hair cells at the base of the cochlea, and (3) kainic acid results in an increase of SP amplitude to high-level stimuli whereas the SP to low- to moderate-level stimuli remains in the normal range.     

Effects of K(+)-channel blockers on cochlear potentials in the guinea pig

The effects of different K+ channel blockers, 4-aminopyridine (4-AP), tetraethylammonium (TEA) and quinine, on the various cochlear potentials were observed by the means of perilymph infusion. Each of the three blockers depressed the compound action potential. However, they exerted quite different effects on other cochlear potentials, especially comparing 4-AP, a fast K(+)-channel blocker, with two other blockers. 4-AP induced a significant increase in the magnitude of summating potential, while TEA and quinine decreased it; 4-AP showed no effect on the general endocochlear potential (G-EP, the EP value recorded directly from the scala media, SM) and the negative EP component (N-EP), while TEA and Quinine increased G-EP and decreased the absolute value of N-EP. They also exerted different effects on the EP changes induced by exposure to intense noise. The results indicate the different roles of different K(+)-channels in the generation of cochlear potentials. The relationship of the two components of EP (positive and negative) and the G-EP was discussed.     

Effect of substrate-free vascular perfusion upon cochlear potentials and glycogen of the stria vascularis

The effect of vascular perfusion of the anterior inferior cerebellar artery with synthetic blood containing no metabolic substrates upon the endolymphatic potential (EP) and the cochlear microphonics (CM) was determined in the guinea pig. In substrate-free perfusion the potentials were maintained for an average of 84 min. Subsequently, the EP declined at an average rate of 1.4 mV/min until a new steady-state level was temporarily established when the potential had dropped to about 30 mV. The decline of the CM appeared to be accounted for largely by the decline of the EP. During substrate-free perfusion prior to the onset of the decline of the potentials, the level of strial glycogen remained unchanged; glycogen decreased significantly only after the potentials had started to decline. When substrate-free vascular perfusion was accompanied by simultaneous substrate-free perilymphatic perfusion, the potentials started to decline immediately. On the basis of these data, we conclude that strial glycogen plays no role in the prolonged maintenance of the EP during substrate-free perfusion; rather, the potential seems to be maintained by entry of glucose (and presumably other substrates) from perilymph into the stria vascularis.     

Glutamatergic and GABAergic agonists increase [Ca2+]i in avian cochlear nucleus neurons

Neurons of the avian cochlear nucleus, nucleus magnocellularis (NM), are stimulated by glutamate, released from the auditory nerve, and GABA, released from both interneurons surrounding NM and from cells located in the superior olivary nucleus. In this study, the Ca2+ indicator dye Fura-2 was used to measure Ca2+ responses in NM stimulated by glutamate- and GABA-receptor agonists using a chicken brainstem slice preparation. Glutamatergically stimulated Ca2+ responses were evoked by kainic acid (KA), alpha-amino-3-hydroxyl-5-methylisoxazole-4-propionic acid (AMPA), and N-methyl-D-aspartate (NMDA). KA- and AMPA-stimulated changes in [Ca2+]i were also produced in NM neurons stimulated in the presence of nifedipine, an L-type Ca2+ channel blocker, suggesting that KA- and AMPA-stimulated changes in [Ca2+]i were carried by Ca2(+)-permeable receptor channels. Significantly smaller changes in [Ca2+]i were produced by NMDA. When neurons were stimulated in an alkaline (pH 7.8) superfusate, NMDA responses were potentiated. KA- and AMPA-stimulated responses were not affected by pH. Several agents known to stimulate metabotropic receptors in other systems were tested on NM neurons bathed in a Ca2+ free-EGTA--buffered media, including L-cysteine sulfinic acid (L-CSA), trans-azetidine dicarboxylic acid (t-ADA), trans-aminocyclo-pentanedicarboxylic acid (t-ACPD), and homobromoibotenic acid (HBI). The only agent to reliably and dose-dependently increase [Ca2+]i was HBI, an analog of ibotenate. GABA also stimulated increases in [Ca2+]i in NM neurons. GABA-stimulated responses were reduced by agents that block voltage-operated channels and by agents that inhibit Ca2+ release from intracellular stores. Whereas GABA-A receptor agonist produced increases in [Ca2+]i GABA-B and GABA-C receptor agonists had no effect. There appear to be several ways for [Ca2+]i to increase in NM neurons. Presumably, each route represents a means by which Ca2+ can alter cellular processes.     

Effects of noise on inferior colliculus evoked potentials and cochlear anatomy in young and aged chinchillas

Site-specific modification of the chromosomal immunoglobulin locus by gene targeting is a powerful tool in studying the molecular requirements for immunoglobulin gene structure and function and in the production of engineered antibodies. Here, we describe a two step- integration then excision-gene targeting procedure for introducing planned genetic alterations into the chromosomal immunoglobulin locus. The efficiency of gene targeting with an enhancer-trap vector in which an enhancerless neo and HSV-tk gene were inserted into the vector backbone was compared to that of the corresponding enhancer-positive vector. Both insertion vectors also contained homology to the chromosomal immunoglobulin target locus along with the desired genetic alteration. The first step involved insertion of the transferred vector into the target locus by homologous recombination. An approximately 15-fold enrichment in the frequency of vector insertion was obtained with the enhancer-trap compared to the enhancer-positive vector. The majority of targeted cells (75%) contained a single copy of the vector integrated into the chromosomal immunoglobulin locus. The second step involved excision of the integrated vector by intrachromosomal homologous recombination between the duplicated region of homology that removed the integrated vector, neo and tk genes along with one copy of homologous DNA. Vector excision was very efficient generating G418S, FIAU(R) secondary recombinants at the high rate of approximately 10(-3)/cell generation. In the secondary recombinants, the overall structure of the chromosomal immunoglobulin locus was restored with the desired genetic alteration being present in an expected proportion of the cells.     

Transient changes in cochlear potentials and DPOAEs after low-frequency tones: the 'two-minute bounce' revisited

After exposure to a loud, non-traumatic low-frequency tone, auditory thresholds are elevated. Thresholds recover to normal in a non-monotonic manner, decreasing rapidly at first before increasing again, until they finally decrease monotonically towards normal. Although the transient elevation of thresholds after the initial improvement was originally called a 'bounce' by Hirsh and Ward (1952), Kemp (1986) suggests that the initial rapid recovery is the oddity: under some conditions a low-frequency tone can produce hypersensitivity in otoacoustic emissions, psychophysical thresholds, and perceived loudness (Kemp's 'bounce') without a later elevation of threshold (Hirsh and Ward's 'bounce'). Kemp also suggested that the transient hypersensitivity was caused by changes in the sensitivity of the active process within the cochlea. We have investigated the origin of this transient hypersensitivity (Kemp's bounce) in guinea pigs, recording cochlear potentials (CM, CAP, SP and EP) and otoacoustic emissions (DPOAEs at f2-f1, 2f1-f2, 2f2-2f1 and 3f1-2f2). Our results indicate that the bounce does not require neural activity, but is probably produced by non-neural cochlear mechanisms, possibly a transient decrease in the permeability of the organ of Corti which produces a small but significant change in standing current through outer hair cells. At least part of these changes, which are reduced as the stimulation frequency increases, and absent above 2 kHz, seem due to a small and transient movement of the cochlear partition towards scala tympani, probably due to a transient osmotic imbalance.     

Effects of endolymphatic and perilymphatic application of salicylate in the pigeon. I: Single fiber activity and cochlear potentials

The effects of salicylate on the mammalian cochlea function are well documented. However, there is a lack of reports on salicylate effects on the avian auditory periphery and it might well be that salicylate is not ototoxic at all in submammalian vertebrates. We therefore recorded single fiber activities, compound action potential (CAP) and endocochlear potential (EP) during application of salicylate (calculated final concentration of about 2-18 mmol/l) into the scala media of pigeons. We furthermore recorded CAP and EP during perilymphatic perfusion of salicylate (2-20 mmol/l). Salicylate applied into the scala media led to an elevation of tip threshold in single fibers ranging from 5 to 35 dB. The characteristic frequencies of the fibers were not changed. This effect on auditory nerve fibers was reflected in an elevation of CAP thresholds. The mean spontaneous discharge rate was either slightly increased or remained unchanged in the majority of fibers. Perilymphatic salicylate perfusion also led to an elevation of CAP thresholds that was reversible following subsequent perfusion with artificial perilymph. The EP remained unchanged in both application modes. The effects of salicylate were dose dependent and more pronounced in the mid- to high-frequency range. These results are consistent with an action of salicylate on the process (electrical or mechanical, or both) responsible for the sensitivity and frequency selectivity in the avian peripheral hearing organ.     

Biocompatibility of cochlear implants

Ceramic, titanium and platinum guarantee a perfect bio-compatibility for cochlear implants. Moreover the long term efficacy of the electrode nerve interface is obtained thanks to a limited electric current density. Failure risks of implanted electronic are decreased by use of carefully selected components.     

The cochlear nuclei of snakes

The cochlear nuclei of three burrowing snakes (Xenopeltis unicolor, Cylindrophis rufus, and Eryx johni) and three non-burrowing snakes (Epicrates cenchris, Natrix sipedon, and Pituophis catenifer) were studied. The posterior branch of the statoacoustic nerve and its posterior ganglion were destroyed and the degenerated nerve fibers and terminals traced to primary cochlear nuclei in 13 specimens of Pituophis catenifer. All these snake species possess three primary and one secondary cochlear nuclei. The primary cochlear nuclei consist of a small nucleus angularis located at the cerebello-medullary junction and a fairly large nucleus magnocellularis forming a dorsal cap over the cephalic end of the alar eminence. Nucleus magnocellularis may be subdivided into a medially placed group of rounder cells, nucleus magnocellularis medialis, and a laterally placed group of more ovate and paler-staining cells, nucleus magnocellularis lateralis. A small but well-defined secondary nucleus which showed no degenerated nerve terminals after nerve root section, nucleus laminaris, underlies the cephalic part of both nucleus magnocellularis medialis and nucleus magnocellularis lateralis. Larger and better-developed cochlear nuclei were found in burrowing species than in non-burrowing species of snakes. Of the three burrowing species studied, Xenopeltis showed the greatest development of cochlear nuclei; Eryx cochlear nuclei were not quite as large but were better differentiated than in Xenopeltis; and Cylindrophis cochlear nuclei were fairly large but not as well developed nor as well differentiated as in either Xenopeltis or Eryx. The cochlear nuclei of the three non-burrowing snakes, Epicrates, Natrix, and Pituophis, were not as large nor as well developed as those of the burrowing snakes. There is some, but not complete, correlation between cochlear development and papilla basilaris length and number of hair cells. Thus, Xenopeltis and Eryx, with well-developed cochlear nuclei, have relatively long papillae basilares; but the boid, Epicrates, with less well-developed cochlear nuclei, has a fairly well-developed papilla basilaris. Cylindrophis, a burrowing species, shows only a moderate degree of cochear nuclei and papilla basilaris development. The non-burrowers, Natrix and Pituophis, have both small cochlear nuclei and relatively short papillae basilares.     

Re-examination of the crowding hypothesis: Effects of age of onset.

The present study examined the crowding hypothesis in a cohort of epileptic patients whose left-hemisphere dysfunction occurred either before or aft 12 mo of age. The results reveal that the crowding effect depends not only on interhemispheric speech transfer but also on a lesion that occurs in the pre- or perinatal period. Right-hemisphere speech dominance alone does not provide a sufficient condition. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of efferent neurotransmitter acetylcholine and cochlear active substance ATP on cochlear outer hair cells

Toxoplasma antibody serological tests were carried out using the Dye test on sera of pregnant and postpartum Nigerian women to investigate whether there was any association between the levels of antibody titres and the occurrence of stillbirths and congenital malformations. There was a high prevalence of toxoplasma antibodies in the sera of both pregnant and postpartum women. The prevalence rates for the pregnant women ranged from 72.5% to 88.8% with an overall rate of 75.4%; whilst for the postpartum women, the prevalence rates ranged from 75.0% to 94.4% with an overall rate of 80.5%. The toxoplasma antibody titres of the sera from the live-born babies as well as stillbirths and congenitally malformed babies ranged from 1:16 to 1:1024. The exact role played by toxoplasma in the occurrence of stillbirths and congenital malformation in our area of study is, however, not clear. For future research, it is suggested that larger samples be studied in order to enhance the validity of the findings of the present study.     

Neural control of cochlear blood flow

Effects of intraarterial and intravenous injections of autonomic nervous system agents on cochlear blood flow were studied in order to investigate the neural control of the inner ear vessels. Blood flow changes in the inner ear of the guinea pig were measured with an electrical impedance plethysmograph. Rather weak control of the vertebrobasilar and labyrinthine arteries by the sympathetic nervous system of the alpha-receptor type did appear to exist. Beta-receptors of the sympathetic nerve appeared to be non-existent in the cochlear vessels, and parasympathetic modulation was not evident.     

In vitro studies of cochlear excitation

Cells in tissues coordinate their activity by sharing ions, second messengers, and small metabolites through clusters of intercellular channels called gap junctions. The thyroid hormones 3,3',5-triiodo-L-thyronine (T3) and L-thyroxine (T4) are capable of modulating gap junctional communication (GJC) as are 1,25-dihydroxyvitamin D3, retinoic acid, and other nuclear receptor ligands. T3 and T4 were found to stimulate GJC in WB-F344 rat liver epithelial cells dose-dependently at concentrations between 1 nM and 0.1 microM, assayed by the dye transfer method using Lucifer Yellow CH. The stimulation of cell-cell communication was preceded by an increase in connexin43 mRNA levels and was accompanied by an accumulation of connexin43 protein measurable 2 days after incubation with these compounds. These observations establish a novel role of thyroid hormones in the regulation of gap junctional intercellular communication via connexin43 gene expression.     

Stapedectomy in profound cochlear loss

Stapedectomy can be used in certain patients with profound sensorineural hearing loss and stapes fixation to improve hearing to a level at which a hearing aid may be effective. This study reviews the outcomes of 11 patients with profound cochlear loss secondary to otosclerosis who underwent stapes surgery performed by the senior author (M.E.G.) over a 25-year period. Postoperative hearing aid usage was effective in 9 of 11 patients. Preoperatively, these patients derived no benefits from hearing aids. Stapedectomy may be of immense value in patients with the proper history and profound cochlear loss.