Biomedical subjects

G Loquet

Publications and source records attributed to G Loquet.

11 recordsLinked to original sources

PubMed2003

Effects of intensity of repetitive acoustic stimuli on neural adaptation in the ventral cochlear nucleus of the rat.

To study neural adaptation as a function of stimulus intensity, auditory near-field evoked potentials were recorded from the ventral cochlear nucleus in awake Long Evans rats. Responses to 250-ms trains of repetitive clicks (pulse rates ranging from 100 to 1000 pulses per second) were collected at stimulus intensities of 5, 10, 30, 50 and 70 dB SPL. The amplitude of the first negative (N1) component of the average evoked potentials to individual pulses in the train was measured by using a subtraction method. The N1 responses were normalized with respect to the highest cochlear nucleus potential observed in the train, and then plotted as a function of click position in the train. As expected, the general trend of the curves was an exponential decay reaching a plateau more or less rapidly as a function of both intensity and rate of stimulation. Fitting these curves with exponential decay equations revealed that the rapid time constant decreased for increasing stimulus intensities whereas the short-term time constant is relatively independent of intensity. The amount of adaptation (expressed as the ratio of the plateau to the first peak amplitude) was substantially less prominent at low intensities (5-10 dB SPL) and low rates (100-200 pulses per second) than at higher intensities and high rates. These results indicate that adaptation patterns obtained in the ventral cochlear nucleus by using near-field evoked potentials exhibit properties comparable to those already present at the level of the auditory nerve.

Acoustic Stimulation↗

PubMed2002

Neural adaptation to pulsatile acoustical stimulation in the cochlear nucleus of the rat.

This study, carried out in adult Long-Evans rats, was designed to investigate the adaptive properties of the cochlear nucleus to pulsatile acoustical stimuli. To achieve this purpose, near-field evoked potentials were picked up from the ventral cochlear nucleus in awake animals. Individual auditory thresholds were measured and responses to 250 ms trains of repetitive clicks with pulse rates ranging from 100 to 2000 pulses per second were collected. The amplitude of the first negative (N(1)) component of the evoked potentials to consecutive individual pulses in the train was measured by using a subtraction method. As expected, a rapid amplitude decrement of the responses in the train was obtained and a three phase adaptation was described. The decrease of individual N(1) component amplitude was fitted for each rate of stimulation with exponential decrease equations and time constants were calculated. Such an analysis allowed us to characterize three distinct adaptive processes which were discussed. The results were comparable to those obtained in previous studies in the auditory nerve and suggest that the adaptation recorded in the ventral cochlear nucleus by using near-field evoked potentials reflects the adaptive properties of auditory nerve fibers.

Acoustic Stimulation↗

PubMed2001

Styrene-induced hearing loss: a membrane insult.

Styrene is an aromatic solvent widely used as a precursor for polystyrene plastics in many factories which produce glass-reinforced plastic. This solvent has been shown to disrupt the auditory system in both humans and animals. In order to study the sequence of events which could explain the cochlear impairments, a time course experiment was carried out with 6-month-old rats. Male Long Evans rats were exposed to 1000 ppm styrene for 6 h/day, 5 days/week, for either 1, 2, 3, or 4 consecutive weeks. Auditory function was tested by recording the near field evoked potentials from the inferior colliculus, and histological analyses of the cochleae were performed with light and transmission electron microscopy. The electrophysiological results support a toxic mid-frequency process which keeps worsening even after the end of the exposure. The histological findings demonstrate that supporting cells are the first targets of the solvent. Then, the outer hair cells of the third row (OHC3) are disrupted, followed successively by OHC2 and OHC1 from the basal (20 kHz) to the upper turn (4 kHz) of the cochlea. Basically, the disorganization of the membranous structures could be the starting point for the cochlear injury induced by styrene. This paper presents a hypothesis that the accumulation of K+ in the spaces of Nuel underlies the toxic effects of styrene.

Animals↗

PubMed2000

Lack of growth-associated protein-43 reemergence or of growth-associated protein-43 mRNA modulation in deafferented vestibular nuclei during the first 6 weeks after unilateral inner ear lesion.

We investigated whether a unilateral inner ear lesion that destroyed the labyrinthine receptors, the cochlear receptors, and the spiral ganglion induced collateral sprouting in rat vestibular and auditory brainstem nuclei, using growth-associated protein-43 (GAP-43) as an indicator of synaptic remodeling. Both immunocytochemistry and in situ hybridization were performed to detect a potential modulation of GAP-43 and of its messenger RNA (mRNA) at different times after surgery. We failed to observe a reemergence of GAP-43 or a modulation of its mRNA in the deafferented vestibular nuclei at all survival times tested. In contrast, a substantial increase in the expression of GAP-43 was observed in the neuropil of the ipsilateral deafferented cochlear nuclei and in cell bodies of the ipsilateral superior olive. This increase was associated with an up- and downregulation of the mRNA coding for GAP-43 in the ipsilateral ventral cochlear nucleus and in the ipsilateral superior olive, respectively. These data indicate that synaptic remodeling, as assessed by GAP-43 expression, does not seem to occur in the deafferented vestibular complex during the first 6 weeks after labyrinthectomy, whereas it occurs within the first deafferented auditory relays at times as early as 4 days following spiral ganglion and cochlear receptors removal. We conclude that recovery of a normal resting discharge of the deafferented central vestibular neurons and consequently recovery of a normal resting posture and eye position may not depend on collateral sprouting of the remaining vestibular afferents. In contrast, we confirmed that a reactive synaptogenesis occurs in the brainstem auditory nuclei following cochlea and spiral ganglion removal. Its functional significance remains an open question.

Afferent Pathways↗

PubMed2000

Combined effects of exposure to styrene and ethanol on the auditory function in the rat.

In order to study the auditory effects of a metabolic interaction between ethanol and styrene, a first group of rats was gavaged once a day with ethanol (4 g/kg), a second group was exposed to 750 ppm styrene by inhalation, and a third group was exposed to both ethanol and styrene (5 days/week, 4 weeks). Auditory function was tested by recording brainstem (inferior colliculus) auditory evoked potentials, and cochlear hair cell loss was estimated by light microscopy. Cytochrome P450 2E1 and the main urinary styrene metabolites, namely mandelic, phenylglyoxylic and hippuric acids, were measured by high-performance liquid chromatography to check the effects of ethanol on styrene metabolism. In our experimental conditions, ethanol alone did not have any effect on auditory sensitivity, whereas styrene alone caused permanent threshold shifts and outer hair cell damage. Hearing and outer hair cell losses were larger after the exposure to both ethanol and styrene than those induced by styrene alone, indicating a clear potentiation of styrene ototoxicity by ethanol. As expected, metabolic data showed that ethanol alters styrene metabolism and can therefore be considered a modifying factor of styrene toxicokinetics.

Administration, Inhalation↗

PubMed2000

Combined effects of noise and styrene exposure on hearing function in the rat.

Combined exposure to both noise and aromatic solvents such as styrene is common in many industries. In order to study the combined effects of simultaneous exposure to both noise and styrene on hearing, male adult Long-Evans rats were exposed either to 750 ppm styrene alone, to a 97 dB SPL octave band of noise centered at 8 kHz, or to a combination of noise and styrene. The exposure duration was 6 h/day, 5 days/week, for 4 consecutive weeks. Auditory function was tested over a frequency range from 2 to 32 kHz by recording near field potentials from the inferior colliculus, whereas histopathological analyses of the cochleae were performed with conventional morphometric approaches. Whereas both noise and styrene each caused permanent threshold shifts, the mechanisms of cochlear damage were different. Noise-induced hearing loss was mainly related to injuries of the stereocilia, whereas styrene-induced hearing loss was related to outer hair cell losses. Following the combined exposure, the threshold elevations as well as the cell losses exceeded the summed loss caused by noise and by styrene alone in the range of 8-16 kHz. Therefore, these results suggest that the two ototoxicants can cause a permanent synergistic loss of auditory sensitivity.

Animals↗

PubMedDate not supplied

Cochlear pathology induced by styrene.

Hair cells, spiral fibers and spiral ganglion cells (SGCs) coming from cochleae of styrene-treated Long-Evans rats were counted in order to assess the extent and location of the cochlear injury after the solvent inhalation. If the hair cells, and more specifically the outer hair cells (OHCs), were undoubtedly the first targets of inhaled styrene, the histological results of the present study would seem to indicate that neurons of the spiral ganglion were also injured with increasing styrene doses. The degenerative process of SGCs and spiral fibers within the osseous lamina was predominant in the middle and mid-basal turn. The electrophysiological data, obtained by recording near-field potentials from the inferior colliculus, reflected the damages of the SGCs and fibers but were not consistent with the histopathological data of the organ of Corti. Because of the weak correlation between the styrene-induced injury at the level of the organ of Corti and that induced at the level of the spiral ganglion, it is likely that two different intoxication routes exist within the cochlea. Such an assumption is discussed in the present paper.

Animals↗

PubMedDate not supplied

Toluene ototoxicity in rats: assessment of the frequency of hearing deficit by electrocochleography.

To identify the frequency range most sensitive to toluene-induced auditory damage, the auditory function of adult Long-Evans rats exposed to 1750 ppm of toluene (6 h/day, 5 days/week, 4 weeks), was tested by recording auditory-evoked potentials directly from the round window of the cochlea. The present electrocochleographic findings do not support a specific mid- to high-frequency loss of auditory sensitivity. On the contrary, the electrophysiologic data, obtained for audiometric frequencies ranging from 2 to 32 kHz, showed a hearing deficit not only in the mid-frequency region (12-16 kHz), but also in the mid-low-frequency region (3-4 kHz). Actually, the effect of toluene was independent of the frequency in our experimental conditions. Histological analysis was consistent with electrophysiologic data because a broad loss of outer hair cells occurred in both mid- and mid-apical coil of the organ of Corti.

Animals↗

PubMedDate not supplied

Toluene and styrene intoxication route in the rat cochlea.

It is well established that organic solvents such as toluene and styrene are ototoxic in the rat; however, the intoxication route used to reach the organ of Corti is still questionable. The distribution of toluene and styrene in various tissues of Long-Evans rats (n = 2 x 8) was studied after inhalation of either 1750 ppm toluene or 1750 ppm styrene for 10 h (6 consecutive h + 4 h the following day). At the end of the solvent exposures, blood, brain, auditory nerves, the organ of Corti, cerebrospinal (CSF), and inner ear fluids (IEF) were sampled or removed to measure the rates of solvent uptake in each tissue by gas chromatography. Results indicate that CSF and IEF were free from detectable solvents, whereas the organ of Corti, the nerves, and the brain were contaminated. Therefore, both toluene- and styrene-induced hearing losses are caused by tissue intoxication rather than by fluid contamination. It is proposed that the outer sulcus is used as an intoxication route to reach the organ of Corti.

Administration, Inhalation↗

PubMedDate not supplied

Comparison of toluene-induced and styrene-induced hearing losses.

Toluene and styrene are industrial solvents that can severely damage the auditory function in adult rats. In the present study, toluene (1000 to 2000 ppm) and styrene doses (500 to 1500 ppm) were investigated according to the same schedule: 6 hours per day, 5 days per week, for 4 consecutive weeks. The auditory function of the animals was tested by recording evoked potentials from the inferior colliculus over a frequency range from 2 to 32 kHz, whereas pathological data were evaluated by conventional histologic techniques. The permanent threshold shifts (PTS) were obtained with a styrene dose 2.4 times lower than that of the toluene. The slope of the regression line (PTS/doses) was 2.1 steeper with styrene than that obtained with toluene in the same experimental conditions. The sequence of histopathological events along the organ of Corti, especially the orderliness and the location of the traumas, was similar for paired concentrations of styrene and toluene, which were respectively 650 ppm, 1500 ppm for the first match, and 850 ppm, 1750 ppm for the second one. Both electrophysiological and histological findings point out the higher ototoxic potency of the styrene compared to that of the toluene. Assumptions concerning the ototoxic mechanism are addressed in the present paper.

Acoustic Stimulation↗

PubMedDate not supplied

Combined effects of noise and styrene on hearing: comparison between active and sedentary rats.

In this study, two investigations were carried out with adult Long-Evans rats exposed to increasing concentrations of styrene. In the first experiment, the hearing of rats, which were forced to walk in a special wheel during the exposure, was compared to that of rats which were sleepy in their cage. The active rats were exposed to styrene concentrations ranging from 300 to 600 ppm, whereas the sedentary rats were exposed from 500 to 1000 ppm for 4 weeks, 5 days per week, 6 hours per day. In the second experiment, designed to evaluate the hearing risks at threshold limit values, active rats were exposed either to a noise having a Leq8h of 85 dB (equivalent level of a continuous noise for a typical 8-h workday), or to 400-ppm styrene or to a simultaneous exposure to noise and styrene. In both experiments, auditory function was tested by auditory-evoked potentials from the inferior colliculus and completed by morphological analyses of the organ of Corti. The results of the first experiment showed that the same amount of styrene-induced hearing loss can be obtained by using concentrations approximately 200 ppm lower in active rats than in sedentary rats. The second investigation showed that, in spite of the low-intensity noise and the low-concentration of styrene, there is a clear risk of potentiation of styrene-induced hearing loss by noise. These findings and exposure conditions were discussed and extrapolated with regard to the risk assessment for human beings. The authors propose to decrease the French threshold limit value of styrene for ensuring a high level of protection for human hearing.

Animals↗