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PubMedDate not supplied

Auditory brain-stem evoked potentials in cat after kainic acid induced neuronal loss. II. Cochlear nucleus.

Auditory brain-stem potentials (ABRs) were studied in cats for up to 6 weeks after kainic acid had been injected unilaterally into the cochlear nucleus (CN) producing extensive neuronal destruction. The ABR components were labeled by the polarity at the vertex (P, for positive) and their order of appearance (the arabic numerals 1, 2, etc.). Component P1 can be further subdivided into 2 subcomponents, P1a and P1b. The assumed correspondence between the ABR components in cat and man is indicated by providing human Roman numeral designations in parentheses following the feline notation, e.g., P2 (III). To stimulation of the ear ipsilateral to the injection, the ABR changes consisted of a loss of components P2 (III) and P3 (IV), and an attenuation and prolongation of latency of components P4 (V) and P5 (VI). The sustained potential shift from which the components arose was not affected. Wave P1a (I) was also slightly but significantly attenuated compatible with changes of excitability of nerve VIII in the cochlea secondary to cochlear nucleus destruction. Unexpectedly, to stimulation of the ear contralateral to the injection side, waves P2 (III), P3 (IV), and P4 (V) were also attenuated and delayed in latency but to a lesser degree than to stimulation of the ear ipsilateral to the injection. Changes in binaural interaction of the ABR following cochlear nucleus lesions were similar to those produced in normal animals by introducing a temporal delay of the input to one ear. The results of the present set of studies using kainic acid to induce neuronal loss in auditory pathway when combined with prior lesion and recording experiments suggest that each of the components of the ABR requires the integrity of an anatomically diffuse system comprising a set of neurons, their axons, and the neurons on which they terminate. Disruption of any portion of the system will alter the amplitude and/or the latency of that component.

Animals↗
PubMed2001

A physiologically based model of discharge pattern regulation by transient K+ currents in cochlear nucleus pyramidal cells.

Pyramidal cells in the dorsal cochlear nucleus (DCN) show three characteristic discharge patterns in response tones: pauser, buildup, and regular firing. Experimental evidence suggests that a rapidly inactivating K+ current (I(KIF)) plays a critical role in generating these discharge patterns. To explore the role of I(KIF), we used a computational model based on the biophysical data. The model replicated the dependence of the discharge pattern on the magnitude and duration of hyperpolarizing prepulses, and I(KIF) was necessary to convey this dependence. Phase-plane and perturbation analyses show that responses to depolarization are critically controlled by the amount of inactivation of I(KIF). Experimentally, half-inactivation voltage and kinetics of I(KIF) show wide variability. Varying these parameters in the model revealed that half-inactivation voltage, and activation and inactivation rates, controls the voltage and time dependence of the model cell discharge. This suggests that pyramidal cells can adjust their sensitivity to different temporal patterns of inhibition and excitation by modulating the kinetics of I(KIF). Overall, I(KIF) is a critical conductance controlling the excitability of DCN pyramidal cells.

Action Potentials↗
PubMed1998

Spatiotemporal tuning of low-frequency cells in the anteroventral cochlear nucleus.

Low-frequency cells in the anteroventral cochlear nucleus (AVCN) can be sensitive to changes in the spatiotemporal pattern of discharges across their auditory nerve (AN) inputs (). This sensitivity suggests that these cells may be tuned to particular spatiotemporal patterns, or features, in the discharge patterns of populations of AN fibers. To evaluate and characterize this sensitivity, we developed a technique whereby the physiological responses of AVCN cells to wide-band noise were analyzed using the simulated response of a population of AN fibers to the same noise stimulus. By averaging the simulated two-dimensional spatiotemporal pattern of AN activity that preceded each AVCN discharge, it was possible to derive a two-dimensional reverse-correlation function that characterized the spatiotemporal tuning of each AVCN cell. The derived spatiotemporal tuning pattern represented a feature in the AN population response that was most likely to precede discharges of the AVCN cell. To test the spatiotemporal tuning characterizations, we used these patterns to predict the responses of cells to noise stimuli statistically independent from the stimuli used to characterize the cells. This technique provides a general tool for the study of any neural system that involves the analysis of spatiotemporal input patterns.

Acoustic Stimulation↗
PubMed2005

Expression of reelin in the dorsal cochlear nucleus of the mouse.

The cytoarchitecture of dorsal cochlear nucleus (DCN), characterized by a distinct laminar structure similar to the cerebellar cortex of the normal mouse, is known to be disrupted in the Reelin-deficient mouse, reeler. Here, we have reexamined both the cytoarchitecture and myeloarchitecture of this nucleus and described expression pattern of Reelin protein during perinatal periods. Reelin-immunopositive granule cells were firstly recognized in the external granular layer of the DCN at embryological day 16 (E16). Next, we examined the cytoarchitecture of the DCN of the normal and reeler mice with Ca2+/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha) immunostaining. CaMKIIalpha-immunoreactive cartwheel cells were laminarly distributed in the layer II of the normal DCN, but scattered throughout the reeler DCN. Injection of retrograde tracer, Fluoro-Gold (FG) into the inferior colliculus of the reeler mouse resulted in that retrogradely labeled neurons in the DCN were radially scattered instead of being confined to a single layer as seen in the normal mouse. To examine whether CaMKIIalpha-immunopositive cartwheel cells are neurons projecting to the inferior colliculus or not, double labeling with CaMKIIalpha immunohistochemistry and retrograde labeling with an injection of FG into the inferior colliculus were made, which revealed that CaMKIIalpha-immunoreactive cartwheel cells do not send axons to the inferior colliculus. The present findings imply that Reelin may have some roles in the formation of laminar structures of the DCN.

Animals↗
PubMed2006

Endogenous mGluR activity suppresses GABAergic transmission in avian cochlear nucleus magnocellularis neurons.

GABAergic transmission in the avian cochlear nucleus magnocellularis (NM) of the chick is subject to modulation by gamma-aminobutyric acid type B (GABA(B)) autoreceptors. Here, I investigated modulation of GABAergic transmission in NM by metabotropic glutamate receptors (mGluRs) with whole cell recordings in brain slice preparations. I found that tACPD, a nonspecific mGluR agonist, exerted dose-dependent suppression on evoked inhibitory postsynaptic currents (eIPSCs) in NM neurons. At concentrations of 100 or 200 microM, tACPD increased the failure rate of GABAergic transmission. Agonists for group I (3,5-DHPG, 200 microM), group II (DCG-IV, 2 microM), and group III (L-AP4, 10 microM) mGluRs produced a significant reduction in the amplitude of eIPSCs and a significant increase in failure rate, indicating the involvement of multiple mGluRs in this modulation. The frequency, but not the amplitude, of miniature IPSCs (mIPSCs) was decreased significantly by 3,5-DHPG or DCG-IV. Neither frequency nor amplitude of mIPSCs was affected by L-AP4. mGluR antagonists LY341495 (20 microM) plus CPPG (10 microM) significantly increased the amplitude of eIPSCs, indicating that endogenous mGluR activity suppresses GABA release to NM neurons. Furthermore, blockage of mGluRs increased GABA-evoked discharges recorded under physiological Cl(-) concentrations, whereas tACPD (100 microM) eliminated them. The results indicate that mGluRs play important roles in achieving balanced excitation and inhibition in NM and preserving fidelity of temporal information encoded by NM neurons.

2-Amino-5-phosphonovalerate↗
PubMed1999

Transient potassium currents regulate the discharge patterns of dorsal cochlear nucleus pyramidal cells.

Pyramidal cells in the dorsal cochlear nucleus (DCN) show three distinct temporal discharge patterns in response to sound: "pauser," "buildup," and "chopper." Similar discharge patterns are seen in vitro and depend on the voltage from which the cell is depolarized. It has been proposed that an inactivating A-type K+ current (IKI) might play a critical role in generating the three different patterns. In this study we examined the characteristics of transient currents in DCN pyramidal cells to evaluate this hypothesis. Morphologically identified pyramidal cells in rat brain slices (P11-P17) exhibited the three voltage-dependent discharge patterns. Two inactivating currents were present in outside-out patches from pyramidal cells: a rapidly inactivating (IKIF, tau approximately 11 msec) current insensitive to block by tetraethylammonium (TEA) and variably blocked by 4-aminopyridine (4-AP) with half-inactivation near -85 mV, and a slowly inactivating TEA- and 4-AP-sensitive current (IKIS, tau approximately 145 msec) with half-inactivation near -35 mV. Recovery from inactivation at 34 degrees C was described by a single exponential with a time constant of 10-30 msec, similar to the rate at which first spike latency increases with the duration of a hyperpolarizing prepulse. Acutely isolated cells also possessed a rapidly activating (<1 msec at 22 degrees C) transient current that activated near -45 mV and showed half-inactivation near -80 mV. A model demonstrated that the deinactivation of IKIF was correlated with the discharge patterns. Overall, the properties of the fast inactivating K+ current were consistent with their proposed role in shaping the discharge pattern of DCN pyramidal cells.

4-Aminopyridine↗
PubMed2005

Temporal representation of the delay of iterated rippled noise in the dorsal cochlear nucleus.

It has been suggested that the dorsal cochlear nucleus (DCN) is involved in the temporal representation of both envelope periodicity and pitch. This hypothesis is tested using iterated rippled noise (IRN), which is generated by a cascade of delay and add [IRN(+)] or delay and subtract [IRN(-)] operations. The autocorrelation functions (ACFs) of the waveform and the envelope of IRN(+) have a first peak at the delay, which corresponds to the perceived pitch of the IRN. With the same delay, the pitch of IRN(-) is generally an octave lower than for IRN(+). This is reflected in a first peak at twice the delay in the ACF of the waveform for IRN(-). In contrast, for identical delays, the ACF of the envelope for both IRN(-) and IRN(+) is the same. Thus the use of IRN allows the distinction between envelope- or fine-structure sensitivity. Recordings were made from 135 single units (BFs <5 kHz) in the DCN of the anesthetized guinea pig using IRN with delays ranging from 1 to 32 ms. In our sample 42% were sensitive to the periodicity of IRN(+) and were tuned to a particular delay in their first-order interspike interval histograms (ISIHs). This tuning was highly correlated with their response to white noise. Most units with best frequencies (BFs) <500 Hz show a different all-order ISIH for IRN(+) and IRN(-), which corresponds to the perceived pitch difference, whereas units with higher BFs show a similar response to IRN(+) and IRN(-). The results indicate that low-frequency units (BF <500 Hz) in the DCN may be involved in the representation of the waveform fine structure, although units with BFs >500 Hz are able to encode only the envelope periodicity of broadband IRN in their temporal discharge characteristics.

Acoustic Stimulation↗
PubMed1988

Synaptic connections in the dorsal cochlear nucleus of mice, in vitro.

1. Intracellular recordings were made from the dorsal cochlear nucleus (DCN) in slices that contained the root of the auditory nerve and parts of the dorsal and ventral cochlear nuclei. Probably the largest and most common cells were impaled. 2. Weak shocks to the nerve usually evoked an excitatory postsynaptic potential (EPSP) that lasted about 90 ms and whose latency was often less than 1.2 ms, indicating monosynaptic input. 3. Stronger shocks elicited a larger EPSP and a later train of inhibitory postsynaptic potentials (IPSPs). Increasing the stimulus voltage shortened the latency of the train of IPSPs and increased its efficacy so that at large stimulus strengths inhibition dominated the synaptic response. 4. To determine whether any of the neuronal circuitry which generated the synaptic responses involved the ventral cochlear nucleus, recordings were made from slices containing only the dorsal nucleus. Synaptic responses to stimulation of the pial surface of the isolated DCN resembled those driven from the nerve root. That is, weak shocks evoked long-lasting, monosynaptic EPSPs and stronger stimuli elicited a larger EPSP followed by trains of IPSPs. The DCN, therefore, contains intrinsic inhibitory interneurones. 5. The parallel fibres of the DCN course superficially, near the stimulating electrodes, whereas the axons of the auditory nerve terminate in deeper areas. Thus, the monosynaptic EPSPs evoked from the pial surface are probably generated by parallel fibres. Apparently the inhibitory interneurones are also excited by a circuit including parallel fibres. 6. The putative neurotransmitter of parallel fibres, glutamate, excited all neurones tested. 7. Cells were sensitive both to glycine and to gamma-aminobutyric acid (GABA). Only strychnine, however, not picrotoxin or bicuculline, blocked IPSPs.

Action Potentials↗
PubMed1997

Evidence for functional metabotropic glutamate receptors in the dorsal cochlear nucleus.

The parallel fibers (PFs) of the dorsal cochlear nucleus (DCN) molecular layer use glutamate as a neurotransmitter. Although metabotropic glutamate receptors (mGluRs) have been identified on cells postsynaptic to the PFs, little is known about the effects of mGluR activation in PF synaptic transmission in the DCN. To investigate these effects, PF-evoked field potentials were recorded from the DCN in guinea pig brain stem slice preparations. The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated components of the field response were reversibly depressed by bathing the slice in the mGluR agonists (+/-)-aminocyclopentane-1,3-dicarboxylic acid (trans-ACPD) or (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD]. A similar depression was produced by the mGluR1/5 agonist (RS)-3,5-dihydroxyphenylglycine, but not by the mGluR2/3 agonist (2S,1'S,2'S)-2-(carboxycyclopropyl)glycine or by the mGluR4/6/7/8 agonist L(+)-2-amino-4-phosphonobutyric acid. In addition to the AMPA component, an N-methyl-D-aspartate (NMDA) receptor-dependent component of the field potentials could be identified when the slices were bathed in a low magnesium solution. Under these conditions, the ACPD-induced depression of the AMPA component did not completely recover, whereas the depression of the NMDA component usually recovered and potentiated in some slices. Intracellular recordings of PF-evoked responses were obtained to ascertain which neuronal populations were affected by mGluR activation. Activation of mGluRs produced a reversible depression of PF-evoked responses in cartwheel cells that was not accompanied by any changes in paired-pulse facilitation. The PF-evoked responses recorded from pyramidal cells were unaffected by mGluR activation. Both cell types exhibited a reversible depolarization during (1S,3R)-ACPD application. Subsequent experiments explored the involvement of protein kinases in mediating the effects of mGluRs. The protein kinase C (PKC) activator phorbol-12,13-diacetate partially inhibited the mGluR-mediated depression of the field response; however, the PKC inhibitor 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl)-maleimide or the protein kinase A inhibitor N-[2-((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide had little effect on the actions of (1S,3R)-ACPD. These results demonstrate that functional mGluRs are present at PF synapses and are capable of modulating PF synaptic transmission in the DCN.

Animals↗
PubMed1989

Immunocytochemical localization of the GABAA/benzodiazepine receptor in the guinea pig cochlear nucleus: evidence for receptor localization heterogeneity.

Immunocytochemistry with a monoclonal antibody against the GABAA/benzodiazepine receptor showed labeled axo-dendritic synapses in the anteroventral cochlear nucleus. In the dorsal cochlear nucleus, label was seen apposing both axo-somatic and axo-dendritic terminals. The results suggest a heterogeneous distribution of GABA receptors, together with a possible segregation of receptor subtypes between somata and dendrites in certain neurons. The presence of cytoplasmic labeling in some neurons might reflect a higher receptor turnover rate in these neurons.

Animals↗
PubMed2004

An immunogold investigation of the distribution of GABA and glycine in nerve terminals on the somata of spherical bushy cells in the anteroventral cochlear nucleus of guinea pig.

Spherical bushy neurons in the anteroventral cochlear nucleus receive glutamatergic primary terminals from the cochlear nerve and terminals of noncochlear (i.e. nonprimary) origin, many of which colocalize gamma-aminobutyric acid (GABA) and glycine. Here the relationship between GABA and glycine in these terminals has been investigated using postembedding immunogold labelling. A significant negative correlation was found between the density of terminal labelling for GABA and for glycine in four guinea pigs. Terminals could be divided into three categories, GABA-only, glycine-only, or colocalizing depending on whether they had a significantly higher labelling density for either amino acid than the primary terminals. The overall labelling density in all four animals was significantly greater for GABA in GABA-only terminals than colocalizing ones but similar for glycine in both. Within the terminals, the labelling density over synaptic vesicles, nonvesicular regions of cytoplasm and mitochondria was also investigated. No significant difference was detected in the labelling density of vesicles compared with nonvesicular regions for either amino acid. However, a significant difference was found between the overall labelling density over mitochondria and nonvesicular regions for both. There was also significantly more mitochondrial GABA labelling in GABA-only terminals compared to colocalizing terminals but mitochondrial glycine labelling was similar in glycine-only and colocalizing terminals. Thus the level of GABA is higher in single than in colocalizing terminals, particularly in the mitochondria, but similar for glycine in both. It is possible therefore that the presence of glycine affects the level of GABA in the nonprimary terminals but that the presence of GABA does not affect the level of glycine.

Animals↗
PubMed1994

Mesencephalic projections of the cochlear nucleus in the frog, Rana esculenta.

The lectin Phaseolus vulgaris leucoagglutinin was injected into chochlear nucleus in order to study the trajectory and projections of the auditory pathway in the frog. A strong contralateral and a weak ipsilateral fiber bundle representing the lemniscus lateralis could be followed to the torus semicircularis. The following areas of termination could be discerned in the mesencephalon: (1) Each of the five subnuclei of the torus semicircularis received fibers from the cochlear nucleus, the largest number of fibers terminated in the principal nucleus. (2) Nuclei of the mesencephalic tegmentum were supplied by fibers from the cochlear nucleus on both sides. (3) The nucleus isthmi was innervated by a few small caliber fibers, and (4) the nucleus visceralis secundarius was richly supplied by large caliber fibers. Two ill-defined neuron groups in the mesencephalic tegmentum, the nucleus reticularis isthmi (5) and (6) the nucleus profundus mesencaphali were conspicuously outlined by the terminals of auditory fibers. Their positions suggested homology to the mammalian nucleus of the lemniscus lateralis. (7) A few fibers and boutons were labelled in the fifth and sixth layers of the optic tectum. Retrogradely labelled cells were found in the nucleus laminaris of the torus semicircularis and in the nuclei of mesencephalic tegmentum. Our results indicate that the frog auditory pathway is more complex at the level of the secondary fiber projections than has been previously recognized. The retrogradely labelled neurons suggest a descending control of the cochlear nucleus from higher structures of the auditory pathway.

Affinity Labels↗
PubMed1997

Susceptibility of developing cochlear nucleus neurons to deafferentation-induced death abruptly ends just before the onset of hearing.

To investigate the ability of developing cochlear nucleus (CN) neurons to survive in the absence of afferent input, left cochlear removals were performed on gerbils at 2 day intervals from postnatal (P)3 to P11, and at P18 and P93. After a 3 month postsurgical survival period, Nissl-stained frontal sections through the brainstem were analyzed under the light microscope. CN volume, anteroventral cochlear nucleus (AVCN) neuron cross-sectional area, and total number of neurons in the CN were measured on both sides of the brain. Mean volume reduction of the deafferented CN relative to the intact CN ranged between 76% in the P3 group to 33% in the P11 group and did not differ significantly between P11 and P93. Cochlear removal at all ages reduced AVCN neuron cross-sectional area by approximately 40% in the deafferented CN relative to the intact CN, except for the P93 group where neuron atrophy was significantly less severe (23% mean reduction). Massive loss of CN neurons (>50% of the intact side) was observed following cochlear removal performed during the first postnatal week. However, between P7 and P9, neurons in all areas of the CN lose susceptibility to deafferentation-induced neuron death. No significant neuron loss was observed following cochlear removal after P7. This study shows that an abrupt transition in the ability of CN neurons to survive in the absence of afferent input is coincident with events leading to the onset of hearing.

Afferent Pathways↗
PubMed1996

Marginal shell of the anteroventral cochlear nucleus: acoustically weakly-driven and not-driven units in the unanesthetized decerebrate cat.

The ventral cochlear nucleus (VCN) of the cat is encapsulated by a marginal shell which is anatomically distinct from the central core of the VCN. Physiologically, little is known about the marginal shell. We report here a new finding that the marginal shell of the anteroventral cochlear nucleus (AVCN) in the unanesthetized decerebrate cat contains neural units which were weakly driven or not driven acoustically. The locations of the single units were histologically determined. Our observations also included other neural units of the marginal shell which were strongly driven acoustically; the latter results will be reported separately. The present physiological findings, together with previous anatomical findings of vestibular and somatosensory inputs to the AVCN marginal shell, suggest that some neurons of the AVCN marginal shell receive non-auditory sensory inputs besides weak auditory inputs and that these may play a role in multi-sensory processing.

Acoustic Stimulation↗
PubMed2000

Olivocochlear neurons sending axon collaterals into the ventral cochlear nucleus of the rat.

The olivocochlear projection constitutes the last stage of the descending auditory system in the mammalian brain. Its neurons reside in the superior olivary complex (SOC) and project to the inner and outer hair cell receptors in the cochlea. Olivocochlear neurons were also reported to send axon collaterals into the cochlear nucleus, but controversies about their number and about species differences persist. By injecting the fluorescent retrograde axonal tracers diamidino yellow and fast blue into the cochlea and the ventral cochlear nucleus (VCN), we studied the distribution and number of olivocochlear neurons with and without axon collaterals into the VCN of the rat. We found that olivocochlear neurons residing in the lateral superior olive (LSO), the intrinsic lateral olivocochlear cells (intrinsic LOCs), do not send axon collaterals into the VCN. By contrast, a majority, and possibly all, olivocochlear neurons residing in the ventral nucleus of the trapezoid body (VNTB), the medial olivocochlear cells (MOCs), do have such axon collaterals. These cells may thus affect processing in the ascending auditory pathway at the level of the receptors and concurrently at the level of the secondary sensory neurons in the cochlear nucleus. Belonging to the lateral olivocochlear system, shell neurons reside around the LSO and form a third group of olivocochlear cells (shell LOCs). Like intrinsic LOCs, they innervate the inner hair cells, but like MOCs they do, by means of axon collaterals, project into the VCN. These findings have implications for understanding both auditory signal processing and the plasticity responses that occur following loss of cochlear function.

Animals↗
PubMed2004

Contributions of age, cochlear integrity, and auditory environment to avian cochlear nucleus metabolism.

Most commercially raised broiler chickens display progressive cochlear degeneration with age [Hear. Res. 166 (2002) 82]. Recent work examining the effects of age and cochlear degeneration on avian cochlear nucleus (nucleus magnocellularis, NM) metabolism showed that changes in metabolic activity occur with age and cochlear damage [Hear. Res. 175 (2003) 101]. The auditory environment also differed between facilities housing young and adult birds. The relative contributions of age, cochlear degeneration, and auditory environment to these changes in NM metabolism are unknown. Using cytochrome oxidase (CO) histochemistry, NM neuron metabolism is examined in several age groups of birds under varying conditions. When normal cochlear integrity and auditory environment are held constant, CO staining is significantly decreased in adult vs. young birds. When age and auditory environment are held constant, CO staining is significantly decreased in birds with damaged vs. normal cochleae. When age and normal cochlear integrity are held constant, CO staining is significantly decreased in birds living in a quiet vs. noisy environment. All factors examined cause changes in CO staining, which is indicative of NM metabolic activity. Results are discussed in the context of mitochondrial aging, afferent regulation, and auditory deprivation and enrichment.

Aging↗
PubMed2002

Effects of acoustic trauma on dorsal cochlear nucleus neuron activity in slices.

Previous studies found increased multi-unit spontaneous activity in the dorsal cochlear nucleus (DCN) of animals that had been exposed to intense sound. Such activity may be related to tinnitus. Our study examined effects of previous exposure to intense sound on single neurons in the DCN, by measuring spontaneous activities and sensitivities to acetylcholine, an important neurotransmitter of centrifugal pathways to the cochlear nucleus, in brain slices. Spontaneous discharges were recorded extracellularly in the DCN portion of brain slices from control and intense-tone-exposed rats. Slices from exposed rats showed increased prevalence of bursting and decreased regular spontaneous activity. Since regular neurons include fusiform cells, and bursting neurons include cartwheel cells, intense tone exposure may lead to increased activity of DCN cartwheel cells and decreased activity of fusiform cells. Alternatively, the activity of some fusiform cells might change to bursting. Intense tone exposure also appeared to increase bursting neuron sensitivity to carbachol. This suggests that changes in DCN cartwheel cell spontaneous activity may reflect changes in effects of cholinergic centrifugal pathways following intense tone exposure. We conclude that acoustic trauma may lead to changes in the physiology and pharmacology of DCN neurons. These changes may be related to underlying mechanisms of central tinnitus.

Animals↗
PubMed1995

Small neurons in the vestibular nerve root project to the marginal shell of the anteroventral cochlear nucleus in the cat.

We injected biotinylated dextran amine (BDA) into marginal shell regions of the anteroventral cochlear nucleus (AVCN) of the cat. These injections led to retrograde labeling of cells including small cells (median some area = 111 micron2, equivalent diameter = 11.9 microns) in the vestibular nerve root (VNR), just ventral to an anterior part of the AVCN. This is an unexpected new finding. The cells were scattered among BDA-labeled fibers and were oriented parallel to the course of the VNR fibers. We suggest that the small neurons of the VNR might serve as second-order vestibular neurons conveying information from vestibular end organs to the cochlear nucleus (CN) and/or act as interneurons between the olivocochlear fibers in the VNR and the CN.

Animals↗