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Far-field brainstem responses evoked by vestibular and auditory stimuli exhibit increases in interpeak latency as brain temperature is decreased.

The effect of decreasing brain temperature upon the transmission of neural signals along the brainstem auditory pathway has been well documented in cats and mice. The increase in the absolute and interpeak latencies of components of the brainstem auditory evoked response (BAER) has indicated that a progressive slowing occurs along the pathway as the signals ascend toward higher brainstem areas. Therefore to fully describe BAERs, both peak latencies and temperature are measured, especially in anesthetized preparations when brain temperature can be labile. In comparison to the numerous studies on the auditory system there are few studies that relate far-field responses evoked by angular acceleration to the vestibular system. Moreover the temperature dependence of such responses has apparently not been investigated. In this study we performed experiments designed to examine whether interpeak latencies of the BAER in rats depended upon temperature. This led to experiments designed to examine whether interpeak latencies of responses evoked by an angular acceleration show a dependence on temperature.

Acceleration↗

Fos-like immunoreactivity in central auditory neurons of the mouse.

Fos-like immunoreactivity was used to study sound-induced activation of neurons in the auditory brainstem. Immunoreactivity was assayed with a polyclonal antibody to Fos. In response to 6-kHz tone bursts, the pattern of staining was a band of immunoreactive neurons positioned at the tonotopically appropriate position within the cochlear nucleus and the inferior colliculus. The band was narrow at low sound pressure levels but wider along the tonotopic axis at higher sound levels. In response to noise bursts, the pattern was broader and often extended throughout the auditory nuclei. Often within this broad pattern were "sub-bands" of immunostained neurons, interspersed with bands of unstained neurons. With increasing sound pressure levels above 35-55 dB, the number of Fos-like immunoreactive neurons increased for the cochlear nucleus, superior olivary complex, and inferior colliculus. In the cochlear nucleus and inferior colliculus, the stained cells were small, and hence their activity would be difficult to sample in electrophysiological studies. In the medial nucleus of the trapezoid body, the stained neurons had larger somata and other characteristics of principal cells. Anesthesia with Nembutal or Avertin, but not with ketamine or urethane, decreased the number of Fos-like immunoreactive neurons in the cochlear nucleus. The different anesthetics produced more variable results in the inferior colliculus. In anesthetized, monaurally stimulated animals, the presence of staining in the contralateral cochlear nucleus indicates that some Fos-like immunoreactivity may be mediated by descending or commissural systems. These observations indicate that Fos assays are useful for studying the pattern of neuronal activation in the auditory system and may also be useful in studying the descending auditory pathways.

Acoustic Stimulation↗

Modulating calbindin and parvalbumin immunoreactivity in the cochlear nucleus by moderate noise exposure in mice. . A quantitative study on the dorsal and posteroventral cochlear nucleus.

The number of calbindin D-28k and parvalbumin immunoreactive (IR) neurons were characterized on sections from the cochlear nucleus, dorsal cochlear nucleus (DCN) and posteroventral cochlear nucleus (PVCN) using two-dimensional quantification. After noise exposure (6-12 kHz, 2 h, at either 80 dB SPL or 103 dB SPL), the number of calbindin and parvalbumin immunoreactive neurons increased in CBA/CBA mice. Quantitative analysis of calbindin-IR in the PVCN did not show a statistically significant difference between any of the groups, whereas statistically significant differences in calbindin-IR were found in the DCN for the 103 dB and 80 dB group compared to the control group, and 103 dB compared to the 80 dB group, respectively. A statistically significant increase in the number of parvalbumin-IR neurons in the PVCN and the DCN was evident in the 103 dB and 80 dB group compared to the control group, and in the 103 dB compared to the 80 dB group. The data indicate that increasing sound stimulation causes a graded increase in the expression of calcium-binding protein immunoreactivity in the DCN and PVCN neurons and neuropil. This increase of protein expression is due to increased positive immunoreactivity in 'silent' neurons. These findings implicate that these neurons have the possibility to react against trauma and display calbindin or parvalbumin as a rescue event. The ability to map sound-induced calcium-binding protein changes in auditory neurons may be useful in future studies designed for detecting early patterns of neurodegeneration and neuroprotection in the central auditory pathway.

Acoustic Stimulation↗

Morphometric comparison of the human corpus callosum in deaf and hearing subjects: an MRI study.

Auditory cortices are interconnected to each other by fibers passing through the corpus callosum (CC). In totally deaf persons no auditory impulses are conveyed to the auditory cortices, hence the auditory pathways become nonfunctional. It was reported that there has been cross-modal plasticity between auditory, visual, and somatosensory cortices. In this study, our aim was to make a comparison in the CC morphometry in hearing subjects and in a selected group in which the auditory system was deprived before the age of 2. 18 deaf and 18 hearing male, handedness matched volunteers, ages varying between 28 and 56 years old were examined. Audiometrical tests were applied to both groups and then T1-weighted midsagittal MR images were obtained. Certain dimensions and areas were measured on these images. There were no statistically significant difference between deaf and hearing subjects, either when dimensions and areas were analyzed by multivariate analysis of variance or when areas were analyzed by univariate analysis of variance. Absence of any significant morphometric difference in the CC of deaf subjects could be thought as an evidence of reflection of functional cortical plasticity.

Adult↗

Dose-dependent brainstem neuropathology following repeated arteether administration in rats.

Histopathological effects of the artemisinin antimalarial, beta-arteether, were evaluated in rats. Arteether (3.125-12.5 mg/kg/day, IM, in sesame oil) was administered for 7 consecutive days. Seven days following the last injection, histological evaluation of the brainstem was performed. Rats treated with 12.5 mg/kg showed significant neuropathology, including chromatolysis, in the nucleus trapezoideus and nucleus superior olive. To a lesser extent, neuropathology was present in the nucleus ruber. Mild neuropathology was also detected in other brainstem regions examined. Although no statistically significant neuropathology was found for the groups treated with 6.25 mg/kg/day and 3.125 mg/kg/day, substantial neuropathology was observed in a single rat in each of these treatment conditions. These results confirm and extend previous studies demonstrating brainstem neurotoxicity from artemisinin antimalarials. Furthermore, these results suggest that, in rats, brainstem auditory pathways may be particularly vulnerable. Early detection of arteether neuropathology may, therefore, require examination of auditory functions.

Animals↗

Timing and laminar profile of eye-position effects on auditory responses in primate auditory cortex.

We examined effects of eye position on auditory cortical responses in macaques. Laminar current-source density (CSD) and multiunit activity (MUA) profiles were sampled with linear array multielectrodes. Eye position significantly modulated auditory-evoked CSD amplitude in 24/29 penetrations (83%), across A1 and belt regions; 4/24 cases also showed significant MUA AM. Eye-position effects occurred mainly in the supragranular laminae and lagged the co-located auditory response by, on average, 38 ms. Effects in A1 and belt regions were indistinguishable in amplitude, laminar profile, and latency. The timing and laminar profile of the eye-position effects suggest that they are not combined with auditory signals at a subcortical stage of the lemniscal auditory pathways and simply "fed-forward" into cortex. Rather, these effects may be conveyed to auditory cortex by feedback projections from parietal or frontal cortices, or alternatively, they may be conveyed by nonclassical feedforward projections through auditory koniocellular (calbindin positive) neurons.

Acoustic Stimulation↗

The varieties of auditory neuropathy.

Auditory neuropathy (AN) was initially described as impairment of auditory neural function, with preserved cochlear hair cell function. In this report, 67 patients with audiological and neurophysiological criteria for hearing loss due to auditory neuropathy are described. Reviewing this large body of patients, AN appears to consist of a number of varieties, with different etiologies and sites affected. All varieties share a relatively spared receptor function, and an impaired neural response, with diminished ability to follow fast temporal changes in the stimulus, but different varieties in this general scheme can be distinguished. Analyses of the clinical features indicate that auditory neuropathies vary in several measures including age of onset, presence of peripheral neuropathy, etiology, and behavioral and physiological measures of auditory function. The sites affected along the peripheral auditory pathway may include dysfunction of the outer hair cells, the synapse between hair cell and auditory nerve, and the auditory nerve fibers, with myelin as well as axonal impairments contributing to the disorder.

Adolescent↗

Spect-studies of the brain with stimulation of the auditory cortex.

The radiopharmaceutical N-isopropyl-p-J-Amphetamin (IMP) permits a new approach in the study of cerebral perfusion and function. We advanced the hypothesis for an increased IMP-uptake on auditory cortex during stimulation by white noise. Auditory stimulation activates the auditory cortex. This is marked by an increased IMP-uptake. IMP-uptake by the auditory region on the left side during stimulation on the right ear is another evidence of the crossing of central auditory pathways to the contralateral side.

Acoustic Stimulation↗

Effects of visual and auditory stimuli on median nerve somatosensory evoked potentials in man.

To demonstrate electrophysiological evidence of neural connections of somatosensory with visual and auditory pathways, interactions of median nerve somatosensory evoked potentials (SEPs) with visual evoked potentials (VEPs) and auditory evoked potentials (AEPs) were analyzed in 12 healthy subjects. In Experiment I (SEP vs. VEP), three patterns of stimulation, namely, electric stimulation of left median nerve, binocular LED flash, and simultaneous electric and flash stimulation, were applied with random interstimulus intervals of 2-4 sec until more than 100 responses had been obtained and averaged for each pattern of stimulation. Simultaneous electric and visual responses were subtracted from arithmetical sums of SEPs and VEPs to show interactions between somatosensory and visual responses. In Experiment II (SEP vs. AEP), binaural short-duration tone bursis instead of LED flashes were used in the same manner as in Experiment I, and interactions between somatosensory and auditory responses were analyzed. Results indicated that the effects of both visual and auditory interaction on SEPs were significant around 120-130 msec of latency. In other words, cross-modal sensory interaction occurred in the late phase of sensory processing.

Acoustic Stimulation↗

Topographical distribution of reduced nicotinamide adenine dinucleotide phosphate-diaphorase in the brain of the Japanese quail.

The distribution of reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity was histochemically investigated in the Japanese quail brain. This enzyme is now considered responsible for the synthesis of nitric oxide, a novel neural messenger whose distribution has not been described in the avian brain until now. The histochemical technique provides a simple and reliable method for staining selected populations of neurons throughout the avian brain. In the telencephalon several regions showed heavily stained NADPH-diaphorase positive neurons and processes. In particular the paleostriatal-paraolfactory lobe complex showed the greatest presence of both positive cells and processes. Neurons and processes were also observed in several regions of the hyperstriatum as well as in the archistriatal nucleus taeniae. Some regions, such as the ectostriatum and the hippocampus, had no positive elements. In the diencephalon, the magnocellular hypothalamic system, which in mammals shows NADPH-diaphorase activity, did not show any particular accumulation of reaction product. On the contrary, retinorecipient areas, such as the visual suprachiasmatic nucleus and the lateral geniculate complex, displayed a composite structure of both positive neurons and processes. The brainstem revealed a large NADPH-diaphorase positive population extending through the tegmental nuclei to the locus coeruleus and subcoeruleus. A complex organization was also observed in the optic lobe, where fusiform elements were distributed within the stratum griseum and superficialis of the tectum. In the medulla, a dense terminal field was observed at the level of the nucleus of the solitary tract, whereas scattered neurons were located within the reticular nuclei. Although the staining of neurons and tracts was highly selective, the positive cells did not correspond to any single known neurotransmitter, neuropeptide, or neuroactive molecule system. Several sensory pathways were heavily stained for the NADPH-diaphorase, including part of the olfactory, visual, and auditory pathways. The findings of the present study reveal that the NADPH-diaphorase-containing systems in the avian brain are organized according to a pattern comparable, because of its complexity, to that observed in mammals. However, important interspecific differences suggest that this novel neural system might be involved in diverse tasks.

Animals↗

Auditory brainstem latencies in type I (insulin-dependent) diabetic patients.

INTRODUCTION: This study was undertaken to compare auditory brainstem response latencies in insulin-dependent diabetics, and to compare these findings with metabolic control, microangiopathy, neuropathy, and the duration of diabetes. METHODS: Auditory brainstem latencies were studied in 53 type I diabetic patients and 42 randomly selected nondiabetic control subjects, aged between 20 and 40 years. Three different stimulus repetition rates (10, 30, and 50 Hz) were used. All subjects had normal hearing ability. RESULTS: Wave V latencies were longer in diabetic patients when compared with those of control subjects at all repetition rates. At repetition rates of 10 and 50 Hz, diabetic patients had a prolonged I-V interwave latency, and at a repetition rate of 50 Hz, diabetics had a longer III-V interwave latency than control subjects. These findings indicate a central disturbance in the auditory pathway. Microvascular complications (retinopathy, nephropathy) and the duration of diabetes were associated with the prolongation of auditory brainstem latencies. In contrast, poor metabolic control (high fasting blood glucose and glycated hemoglobin A1c) at the time of the present study was only marginally associated with prolonged auditory brainstem latencies. The changes in auditory brainstem latencies associated with diabetic neuropathy (measured with five cardiac autonomic nervous function tests) appeared simultaneously with microvascular complications and in patients with diabetes of long duration, and thus a causative role of diabetic neuropathy in the pathogenesis of prolonged auditory brainstem latencies remains unsolved. CONCLUSION: Delayed auditory brainstem latencies in type I diabetic patients are probably caused by the long duration of diabetes and the microvascular complications associated with it.

Adult↗

Age-related synaptic changes in the central nucleus of the inferior colliculus of Fischer-344 rats.

The central nucleus of the inferior colliculus (ICc) is a major processing center for the ascending auditory pathways. Gamma-aminobutyric acid (GABA) and excitant amino acids (EAAs) are essential for coding many auditory tasks in the IC. Recently, a number of neurochemical and immunocytochemical studies have suggested an age-related decline in GABAergic inhibition in the ICc, and possibly excitant-amino-acid-mediated excitation as well. The objective of this study was to compare quantitatively changes in the synaptic organization of the ICc among three age groups (3, 19, and 28 months) of Fischer-344 rats. Immunogold electron microscopic methods were used to determine if there were age-related changes in the density, distribution, or morphology of GABA-immunoreactive (+) and GABA-immunonegative (-) synapses in the ICc. The data suggest similar losses of excitatory and inhibitory synapses in the ICc. There were significant reductions in the densities of GABA+ and GABA- synaptic terminals (approximately 30% and approximately 24%, respectively) and synapses (approximately 33% and approximately 26%, respectively) in the ICc of 28-month-old rats relative to 3-month-olds. The numeric values, which were adjusted to consider changes in volume of the IC with age, depict similar effects, although the effect magnitude for the adjusted values was reduced by approximately 9%. For both types of synapses, the decreases did not differ significantly from each other. The reductions in synaptic numbers appeared, to be related to a similar numeric decline in dendrites, in particular those with calibers of between 0.5 and 1.5 microm. The number and distribution of synaptic terminals on the remaining dendrites of GABA- neurons appeared not to undergo major age-related changes. GABA+ neurons, on the other hand, may have evolved patterns of synaptic and dendritic change during aging in which the distribution of synaptic terminals shifts to dendrites of larger caliber. In the 19-month group, the synaptic areas were elevated in terminals apposed to dendrites with calibers of 1.5 microm or less. However, this increase in synaptic size did not persist in the aged animals. No neuronal losses were detectable among the three age groups. Thus, the decrease in GABA and EAAs identified in the IC by previous studies may be attributable to synaptic and dendritic declines, rather than cell loss.

Aging↗

Speech-evoked brainstem frequency-following responses during verbal transformations due to word repetition.

Speech-evoked brainstem frequency-following responses (FFRs) were recorded to repeated presentations of the same stimulus word. Word repetition results in illusory verbal transformations (VTs) in which word perceptions can differ markedly from the actual stimulus. Previous behavioral studies support an explanation of VTs based on changes in arousal or attention. Horizontal and vertical dipole FFRs were recorded to assess responses with putative origins in the auditory nerve and central brainstem, respectively. FFRs were recorded from 18 subjects when they correctly heard the stimulus and when they reported VTs. Although horizontal and vertical dipole FFRs showed different frequency response patterns, dipoles did not differentiate between perceptual conditions. However, when subjects were divided into low- and high-VT groups (based on percentage of VT trials), a significant Condition x Group interaction resulted. This interaction showed the largest difference in FFR amplitudes during VT trials, with the low-VT group showing increased amplitudes, and the high-VT group showing decreased amplitudes, relative to trials in which the stimulus was correctly perceived. These results demonstrate measurable subject differences in the early processing of complex signals, due to possible effects of attention on the brainstem FFR. The present research shows that the FFR is useful in understanding human language as it is coded and processed in the brainstem auditory pathway.

Adolescent↗

Auditory cortical responses in patients with Bell's palsy.

We recorded auditory evoked magnetic responses with a whole-scalp 122-channel SQUID neuromagnetometer in 14 patients with Bell's palsy (9 with left-sided and 5 with right-sided) and in 10 controls. The stimuli were 50-ms 1-kHz tone bursts, delivered first to the left and then to the right ear at interstimulus intervals (ISIs) of 1, 2 and 4 s. In patients, the N100m, the 100-ms response originating in the auditory cortices peaked, on average, 8 ms earlier and the response strengths were, on average, 7 nAm stronger over the contralateral than ipsilateral hemisphere. The response latencies and strengths did not differ significantly from those of controls and there were no significant differences in response latencies and strengths between the stimulation of the affected and healthy side. On average, the response latencies and strengths increased as a function of ISI over both hemispheres both in patients and in controls. These findings suggest that Bell's palsy is an isolated peripheral neuropathy that does not affect the function of the auditory pathways.

Adult↗

Effects of click intensity and frequency on the brain-stem auditory evoked potentials in the common marmoset (Callithrix jacchus).

Brain-stem auditory evoked potentials (BAEPs) were recorded in 20 common marmosets (Callithrix jacchus) to investigate the effects of click frequency up to 99 kHz, in consideration of the higher hearing range of the marmoset, and intensity on wave forms and peak latencies. According to the results of BAEP recordings at frequencies of 4, 32, and 99 kHz, the number of components recorded was affected by the stimulus intensity and the clicks at an intensity of 80 dB peak equivalent sound pressure level (pe SPL) had the maximum number of clear components. Therefore, it was indicated that click stimulations at an intensity of 80 dB pe SPL over a broad range of frequencies appears to be useful for recording the maximum number of components in marmosets and may increase the information obtainable from BAEPs. BAEP latencies were prolonged as the stimulus intensity decreased from 100 to 50 dB pe SPL. The effects of stimulus frequency on the wave latencies and amplitudes in response to 80 dB pe SPL at frequencies between 0.5 and 99 kHz revealed various changes: the amplitude of wave I increased at 16 and 32 kHz, but that of waves III and V increased at 4-8 and 64-99 kHz. These increases in amplitudes of the waves may correlate with higher synchronous activity of the peripheral or central auditory pathways.

Acoustic Stimulation↗

Central auditory development in children with bilateral cochlear implants.

OBJECTIVE: To examine the time course of maturation of P1 latencies in infant sequential and simultaneous bilateral cochlear implant recipients. DESIGN: Retrospective case series. SETTING: Pediatric collaborative cochlear implant program. PATIENTS: Four children who received bilateral cochlear implants prior to age 2 years. INTERVENTION: Cortical auditory evoked potential was completed to determine the latency of the P1 response in 4 children with bilateral cochlear implants. MAIN OUTCOME MEASURES: Longitudinal development of the latency of the P1 cortical auditory evoked potential in children who received bilateral cochlear implants prior to age 2 years. RESULTS: In 2 patients who received sequential bilateral implants, P1 latencies recorded from the first implanted ear were within normal limits after 3 to 6 months of implant use. By comparison, P1 latencies from the second implanted ear reached normal limits as early as 1 month after implant use. In 2 patients who received simultaneous bilateral implants, P1 latencies from both ears were also within normal limits in a very short time frame (ie, by 1 month poststimulation). CONCLUSIONS: Our data suggest a high degree of plasticity of the central auditory pathways after early bilateral implantation. We find that P1 latencies provide a clinically useful biomarker of central auditory system development in children after cochlear implantation.

Auditory Cortex↗

Evidence of neuronal plasticity within the inferior colliculus after noise exposure: a study of evoked potentials in the rat.

Recent investigations have implicated that the central nervous system has a role in the changes that occur in auditory function following acoustic trauma caused by noise exposure. These investigations indicate that the inferior colliculus may be the primary anatomical location in the ascending auditory pathway where noise-induced neuronal plasticity occurs, thereby resulting in changes in the neuronal processing of auditory information. In the present investigation, we show that the amplitudes of all peaks in the click-evoked response from the external nucleus of the inferior colliculus decrease during a 30 min exposure to a tone (104 dB sound pressure level (SPL) at 4 kHz and 8 kHz). After tone exposure, the amplitudes of two of the peaks of the response from the external nucleus of the inferior colliculus that reflect the input from more caudal structures slowly returned to baseline levels, whereas the amplitudes of the two peaks reflecting neuronal activity in the inferior colliculus increased above baseline levels and remained at the increased levels for at least 90 min following exposure to the tone. We also show that exposure to a 4 kHz tone at 104 dB SPL causes changes in the neuronal processing of tonebursts in the form of changes in the temporal integration function for one of the peaks of the response from the external nucleus of the inferior colliculus that originates in the inferior colliculus. Before tone exposure the amplitude of this peak decreased with increasing stimulus duration, but after tone exposure the amplitude of this peak was independent of the duration of the toneburst stimulus. We interpret these changes as evidence that noise exposure (tone exposure) causes changes in the excitability of the inferior colliculus that are not seen in more caudal structures, and these changes are probably a result of a change in the balance between inhibition and excitation in the inferior colliculus.

Acoustic Stimulation↗

Developmental and genetic audiogenic seizure models: behavior and biological substrates.

Audiogenic seizure (AGS) models of developmental or genetic origin manifest characteristic indices of generalized seizures such as clonus or tonus in rodents. Studies of seizure-resistant strains in which AGS is induced by intense sound exposure during postnatal development provide models in which other neural abnormalities are not introduced along with AGS susceptibility. A critical feature of all AGS models is the reduction of neural activity in the auditory pathways from deafness during development. The initiation and propagation of AGS activity relies upon hyperexcitability in the auditory system, particularly the inferior colliculus (IC) where bilateral lesions abolish AGS. GABAergic and glutaminergic mechanisms play crucial roles in AGS, as in temporal lobe models of epilepsy, and participate in AGS modulatory and efferent systems including the superior colliculus, substantia nigra, basal ganglia and structures of the reticular formation. Catecholamine and indolamine systems also influence AGS severity. AGS models are useful for elucidating the underlying mechanisms for formation and expression of generalized epileptic behaviors, and evaluating the efficacy of modern treatment strategies such as anticonvulsant medication and neural grafting.

Acoustic Stimulation↗