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Results for “Cochlear Nucleus”

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PubMed1997

Synaptophysin immunoreactivity in the cochlear nucleus after unilateral cochlear or ossicular removal.

This study determined if unilateral cochlear removal in adult guinea pigs led to synaptic loss followed by synaptogenesis in the cochlear nucleus (CN) and if unilateral middle ear ossicle removal led to synaptic loss in the CN. Synaptic endings were identified immunohistochemically, using a monoclonal antibody to synaptophysin. Immunolabeling was quantified densitometrically in the CN 4-161 days after cochlear removal and 161 days after ossicle removal. Fiber degeneration was visualized with the Nauta-Rasmussen silver method. Tissue shrinkage was measured from drawings of CN sections. Compared to the contralateral side, immunolabeling density ipsilaterally was reduced by 4 days in the anterior division of the anteroventral CN (a-AVCN) and by 7 days in the anterior part of the posteroventral CN (a-PVCN). At 7 days, preterminal fiber degeneration was abundant in both areas. These findings were consistent with the loss of cochlear nerve endings and fibers. At later times, immunolabeling density recovered. In the a-AVCN, tissue shrinkage explained approximately half the recovery of staining density; the rest was attributed to synaptogenesis. In the a-PVCN, the entire recovery was attributed to tissue shrinkage. In the polymorphic layer of the dorsal CN, immunostaining density increased transiently at 4 days, while at 7 days preterminal fiber degeneration was abundant. A net loss of synaptic endings was not detected immunohistochemically. The increased immunostaining density may reflect a transient growth of immature processes or presynaptic endings. Ossicle removal produced a deficit in immunolabeling density only in the ipsilateral a-PVCN, without fiber degeneration, suggesting a loss of presynaptic endings or of synaptophysin expression.

Afferent Pathways↗

PubMed1998

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↗

PubMed1997

Collateral projections from single neurons in the dorsal column nucleus to both the cochlear nucleus and the ventrobasal thalamus: a retrograde double-labeling study in the rat.

In the rats which were injected with Fluoro-Gold into the cochlear nucleus and simultaneously with tetramethylrhodamine-dextran amine into the ventrobasal thalamus, a number of neurons in the gracile and the cuneate nuclei of the dorsal column nucleus (DCN) and in the interpolar and caudal subnuclei of the spinal trigeminal nucleus (STN) were double-labeled retrogradely with the both tracers. The results indicated the existence of single DCN/STN-neurons which provided axons to the cochlear nucleus, mainly ipsilaterally, and to the contralateral ventrobasal thalamus.

Animals↗

PubMed2004

Cochlear ablation in mice lacking SHP-1 results in an extended period of cell death of anteroventral cochlear nucleus neurons.

Cochlear ablation results in the death of anteroventral cochlear nucleus (AVCN) neurons from birth to approximately postnatal day 14 (P14) in the murine brainstem. It is not known whether microglial activation contributes to AVCN neuronal death following deafferentation. In order to determine whether microglial activation helps to define the period of neuronal susceptibility within AVCN, we performed unilateral cochlear ablation on mice lacking the protein tyrosine phosphatase SHP-1 (me/me). These mice have been shown to have an exaggerated microglial response following ischemic injury. In the present study, the glial and neuronal response to deafferentation within AVCN was examined in wild-type and me/me mice at P5, P14, and P21. Lack of SHP-1 results in robust microglial but not astrocyte activation within the ablated P14 me/me AVCN. These mice also exhibit approximately 28% neuronal death at P14, a time when normal wild-type littermate controls show little cell death. Glial activation and neuronal loss at P5 and P21 were similar between the two phenotypes, suggesting a role of activated microglia in inducing neuronal death beyond P14 but not P21. These results indicate that activated microglia may participate in determining whether neurons in AVCN live or die following deafferentation.

Afferent Pathways↗

PubMed1997

Glycinergic and GABAergic inputs affect short-term suppression in the cochlear nucleus.

Most cochlear nucleus (CN) neurons exhibit short-term response suppression to a second stimulus in a paired-pulse (click), forward-masking, paradigm. The magnitude of suppression, which appears to be greater than that observed in acoustic nerve, is dependent on the temporal separation and/or relative intensities of the two stimuli. Recent evidence suggests that inhibitory circuitry ending on CN neurons may mediate this response suppression. Using extracellular recordings from single CN neurons, suppression was evaluated using a forward-masking paradigm. Responses to paired acoustic clicks (i.e., a 'masker' followed by an identical 'probe' click) were measured while the time interval between the masker and probe was varied systematically. The role of inhibitory circuitry in forward-masking in the CN was assessed by pharmacologic manipulation of the GABA(A) and glycine(I) (strychnine-sensitive) receptors. Blockade of glycinergic or GABAergic receptors by iontophoretic application of the antagonists, strychnine and bicuculline methiodide, decreased the effects of forward-masking by shortening recovery times of the probe response in 2/3 of the neurons tested. Conversely, agonist application (glycine, and GABA or muscimol) increased the magnitude of suppression and delayed recovery of the probe response relative to control values. These findings suggest that known circuits releasing glycine and/or GABA mediate short-term response suppression in some CN neurons.

Acoustic Stimulation↗

PubMed1997

Granule cell activation of complex-spiking neurons in dorsal cochlear nucleus.

Dorsal cochlear nucleus (DCN) principal cells receive, in addition to their well known auditory inputs, various nonauditory inputs via a cerebellar-like granule cell circuit located in the superficial layers of the DCN. Activation of this circuit (granule cell axons make excitatory synapses on the principal cells but also contact inhibitory interneurons that project to the principal cells) produces strong inhibition of the principal cells. Here we investigate the role of cartwheel cells, homologs of cerebellar Purkinje cells, in producing this inhibition. The responses of type IV units (one type of principal cells) and of cartwheel cells were recorded to ortho- and antidromic activation of the granule cells (i. e., by stimulation of their inputs from the somatosensory cuneate and spinal trigeminal nuclei and by direct stimulation of their parallel fiber axons). Cartwheel cells were identified on the basis of recording depth and complex action potential shape. A four-pulse facilitation paradigm (four pulses at 50 msec intervals) was used; this stimulus allows separation of the apparently simple inhibitory somatosensory response of type IV units into a three-component (inhibition-excitation-inhibition) response. As expected, cartwheel cells are excited by granule cell activation; the latencies and four-pulse amplitudes of these responses correspond to the properties of the second, long-latency inhibitory component of type IV responses. The source of the first, short-latency inhibitory response is still unknown. Nevertheless, these results show that cartwheel cells convey inhibitory polysensory information to DCN principal cells.

Animals↗

PubMed2002

Morphometric changes in the cochlear nucleus in patients who had undergone cochlear implantation for bilateral profound deafness.

We have investigated the morphometric changes in the cochlear nucleus of patients who had undergone cochlear implantation following profound deafness. The brain stems of 11 adult patients who had undergone implantation and four non-implanted control cases with varying degrees of hearing loss were studied. The volumes of the ventral cochlear nucleus (VCN) and dorsal cochlear nucleus (DCN), and the maximal cross-sectional area and densities of cell bodies in the anterior ventral cochlear nucleus (AVCN) were measured bilaterally by light microscopy assisted by the Neurolucida 2000 image analysis system. In addition, the density of synapses on cells of the AVCN were estimated using immunostaining for the synaptosome-associated protein (SNAP-25) by light microscopy. There was no significant difference in volumes of VCN and DCN, maximal cross-sectional area and density of cell bodies of the AVCN, and SNAP-25 immunostaining between the cochlear nucleus ipsilateral and contralateral to cochlear implantation. In addition, there was no significant correlation between these morphometric parameters and clinical performance. Peripheral deafness seems to reduce the size of neurons in the AVCN in that the maximum diameter of cell bodies was greater in the ear with better hearing preoperatively (chi-square test P<0.05). However, electrical stimulation provided by the cochlear implantation did not alter these morphometric changes in adult cochlear implant patients.

Aged↗

PubMed1992

Changes in the tonotopic map of the dorsal cochlear nucleus following induction of cochlear lesions by exposure to intense sound.

Hamsters were exposed to intense tones (10 kHz) at levels and durations sufficient to cause stereocilia lesions. The purpose was to determine how the tonotopic map of the dorsal cochlear nucleus (DCN) readjusts to loss of receptor sensitivity. Neural population thresholds and tonotopic organization was mapped over the surface of the DCN in normal unexposed animals and those showing tone-induced lesions. The results indicate that cochlear lesions characterized mainly by loss of stereocilia in a restricted portion of the organ of Corti cause changes in a corresponding region of the tonotopic map which reflect primarily changes in the shape and thresholds of neural tuning curves. In many cases the center of the lesion was represented in the DCN as a distinct characteristic frequency (CF) gap in the tonotopic map in which responses were either extremely weak or absent. In almost all cases the map area representing the center of the lesion was bordered by an expanded region of near-constant CF, a feature superficially suggestive of map reorganization. These expanded map areas had abnormal tip thresholds and showed other features suggesting that their CFs had been shifted downward by distortion and deterioration of their original tips. Such changes in neural tuning are similar to those observed by others in the auditory nerve following acoustic trauma, and thus would seem to have a peripheral origin. Thus, it is not necessary to invoke plastic changes in the cochlear nucleus to explain the changes observed in the tonotopic map.

Animals↗

PubMed1981

Quantitative distribution of choline acetyltransferase and acetylcholinesterase activities in the rat cochlear nucleus.

Within the cochlear nucleus of the rat, as well as some nearby regions, quantitative histochemical mapping procedures were used to construct maps of the distributions of choline acetyltransferase and acetylcholinesterase activities. The results were in some ways consistent with results previously reported for cat, e.g., very low activities of both enzymes were found in the auditory nerve root, and also in the vestibular nerve root, except where acetylcholinesterase-positive centrifugal fibers are located, very high activities were found in the facial nerve system. In many ways, however, the results for the rat cochlear nucleus contrasted with those for the cat. Notably, choline acetyltransferase activities in some regions of the rat cochlear nucleus were as much as 30- to 60-fold higher than for the comparable regions in the cat, and both enzymes had much more uniform distributions in the rat cochlear nucleus than in the cat. The more prominent cholinergic system in the rat cochlear nucleus might relate to a proportionately larger population of cholinergic interneurons, or, more probably, a more significant innervation by cholinergic, centrifugal pathways, or both, as well as, perhaps, generally higher choline acetyltransferase activities in cholinergic neurons of rat.

Acetylcholinesterase↗

PubMed1995

Inositol 1,4,5-trisphosphate receptors: immunocytochemical localization in the dorsal cochlear nucleus.

In the cochlear nucleus of mammals, the relatively homogeneous responses of auditory nerve fibers are transformed into a variety of different response patterns by the different classes of resident neurons. The spectrum of these responses is hypothesized to depend on the types and distribution of receptors, ion channels, G proteins, and second messengers that form the signaling capabilities in each cell class. In the present study, we examined the immunocytochemical distribution of the inositol 1,4,5-triphosphate (IP3) receptor in the dorsal cochlear nucleus to better understand how this second messenger might be involved in shaping the neural signals evoked by sound. Affinity-purified polyclonal antibodies directed against the IP3 receptor labeled a homogeneous population of neurons in the dorsal cochlear nucleus of rats, guinea pigs, mustache bats, cats, New World owl monkeys, rhesus monkeys, and humans. These cells were all darkly immunostained except in the human where the labeling was less intense. Immunoblots of dorsal cochlear nucleus tissue from the rat revealed a single band of protein of molecular weight approximately 260 kD, which is the same size as the purified receptor, indicating that our antibodies reacted specifically with the IP3 receptor. These immunolabeled neurons were identified as cartwheel cells on the basis of shared characteristics across species, including cell body size and distribution, the presence of a highly invaginated nucleus, and a well-developed system of cisternae. Reaction product was localized along the membranes of rough and smooth endoplasmic reticulum, subsurface cisternae, and the nuclear envelope. This label was distributed throughout the cartwheel cell body and dendritic shafts but not within dendritic spines, axons, or axons terminals. The regular pattern of immunolabeling across mammals suggests that IP3 and cartwheel cells are conserved in evolution and that both play an important but as yet unknown role in hearing.

Aged↗

PubMed1995

Re-emergence of GAP-43 in cochlear nucleus and superior olive following cochlear ablation in the rat.

The effect of cochlear lesion on the expression of the growth associated protein GAP-43 in superior olive and cochlear nucleus was studied in the rat. In normal development of these auditory brainstem nuclei, GAP-43 immunoreactivity is high perinatally but low 10 days postnatally or thereafter. Removal of one spiral ganglion in grown-up animals caused a substantial re-emergence of GAP-43 immunoreactivity in varicose fibers of the ipsilateral ventral cochlear nucleus and cell bodies of the lateral superior olive. These findings suggest that a reactive synaptogenesis takes place in the cochlear nucleus as a consequence of deafening through spiral ganglion loss.

Animals↗

PubMed1996

Why do cats need a dorsal cochlear nucleus?

The dorsal cochlear nucleus (DCN), one of the three major divisions of the cochlear nucleus (CN), has a complex internal structure, multiple inputs (some of them non-auditory), and multiple output pathways. Response properties of DCN units are accordingly complex. The principal cells of the DCN have type IV response characteristics, characterized by relatively high levels of spontaneous activity and inhibition by high level best frequency (BF) tones. We showed previously that type IV units are inhibited by two separate inhibitory mechanisms, one of them sensitive to narrow band stimuli and the other to wide band stimuli. One result of the wide band inhibition of type IV units is their sensitivity to spectral notches in the region of their BF - stimuli with such notches inhibit type IV units. The source of the narrow band inhibition is an interneuron in the DCN which has type II response characteristics - it does not have spontaneous activity and is strongly activated by BF tones. The neurons giving rise to type II responses are presumably vertical cells, which also project to other divisions of the CN. From anatomical studies, it is known that type IV units are also inhibited by a third system, which carries non-auditory information; movements of the pinna inhibit type IV units through this system. We hypothesize that type IV units signal important events to the auditory system by being inhibited. Such events are either auditory, e.g. spectral maxima and minima, or non-auditory, such as the somatosensory inputs from the pinnae. We hypothesize that the projection of type II units to the ventral cochlear nucleus (VCN) plays a role in reducing the effects of spectral notches introduced by the pinnae in the core auditory pathway. We conclude that although the DCN lies close to the auditory periphery, it already performs sophisticated tasks of auditory processing.

Animals↗

PubMed1994

Effect of altered neuronal activity on cell size in the medial nucleus of the trapezoid body and ventral cochlear nucleus of the gerbil.

Activity-dependent transneuronal regulation of neuronal soma size has been studied in the medial nucleus of the trapezoid body and ventral cochlear nucleus of adolescent gerbils. Cochlear ablation or tetrodotoxin has been used to eliminate afferent electrical activity in auditory nerve fibers permanently or for 24 or 48 hours. Previous studies have shown that the cross-sectional area of spherical cell somata in the ipsilateral anteroventral cochlear nucleus decreases within 24 hours of electrical activity blockade with tetrodotoxin, which is fully reversible when activity is restored. The present findings extend this work by directly comparing the results of unilateral blockade of auditory nerve action potentials or unilateral cochlear ablation on the size of spherical and globular cell bodies in the ventral cochlear nucleus with changes produced by the same manipulations in third-order cells, principal neurons in the medial nucleus of the trapezoid body. Soma size in both ventral cochlear nucleus cell types decreases reliably by 24 hours after cochlear removal or eighth nerve activity blockade by tetrodotoxin. Soma size of neurons in the contralateral medial nucleus of the trapezoid body decreases 48 hours, but not 24 hours, after either manipulation. When activity in auditory nerve fibers is allowed to resume for 7 days following a 48-hour activity blockade, soma size fully recovers in the medial nucleus of the trapezoid body as well as in ventral cochlear nucleus neurons. We also report that the cross-sectional area of neuronal soma in the medial nucleus of the trapezoid body is larger in lateral regions of medial nucleus of the trapezoid body (low-frequency representation) than in the medial regions of the nucleus (high-frequency representation). We conclude that cell body size changes in brainstem auditory neurons are reversible and that the signals associated with the loss and subsequent recovery of soma size are activity related. However, the delayed effect of activity deprivation in the medial nucleus of the trapezoid body suggests that trophic substances released by afferent axons may contribute to the maintenance of anatomical characteristics.

Action Potentials↗

PubMed2005

Contralateral effects and binaural interactions in dorsal cochlear nucleus.

The dorsal cochlear nucleus (DCN) receives afferent input from the auditory nerve and is thus usually thought of as a monaural nucleus, but it also receives inputs from the contralateral cochlear nucleus as well as descending projections from binaural nuclei. Evidence suggests that some of these commissural and efferent projections are excitatory, whereas others are inhibitory. The goals of this study were to investigate the nature and effects of these inputs in the DCN by measuring DCN principal cell (type IV unit) responses to a variety of contralateral monaural and binaural stimuli. As expected, the results of contralateral stimulation demonstrate a mixture of excitatory and inhibitory influences, although inhibitory effects predominate. Most type IV units are weakly, if at all, inhibited by tones but are strongly inhibited by broadband noise (BBN). The inhibition evoked by BBN is also low threshold and short latency. This inhibition is abolished and excitation is revealed when strychnine, a glycine-receptor antagonist, is applied to the DCN; application of bicuculline, a GABAA-receptor antagonist, has similar effects but does not block the onset of inhibition. Manipulations of discrete fiber bundles suggest that the inhibitory, but not excitatory, inputs to DCN principal cells enter the DCN via its output pathway, and that the short latency inhibition is carried by commissural axons. Consistent with their respective monaural effects, responses to binaural tones as a function of interaural level difference are essentially the same as responses to ipsilateral tones, whereas binaural BBN responses decrease with increasing contralateral level. In comparison to monaural responses, binaural responses to virtual space stimuli show enhanced sensitivity to the elevation of a sound source in ipsilateral space but reduced sensitivity in contralateral space. These results show that the contralateral inputs to the DCN are functionally relevant in natural listening conditions, and that one role of these inputs is to enhance DCN processing of spectral sound localization cues produced by the pinna.

Acoustic Stimulation↗

PubMed1993

The projections of intracellularly labeled auditory nerve fibers to the dorsal cochlear nucleus of cats.

The cochlear nucleus receives incoming auditory nerve discharges, preserves or transforms the signals, and distributes outgoing activity to higher centers. The organization of auditory nerve input to the cochlear nucleus will heavily influence the mechanisms by which acoustic information is processed. In order to study structure-function relationships between auditory nerve and cochlear nucleus, the axonal arborizations of type I spiral ganglion cells were labeled with intracellular injections of horseradish peroxidase after first being electrophysiologically characterized by recording with a micropipette inserted into the axon. For each auditory nerve fiber, spontaneous discharge rate (SR) and a frequency tuning curve were determined. The tuning curve yielded the characteristic frequency (CF, that frequency to which the fiber is most sensitive) and CF threshold in dB SPL. Individual axonal arborizations including all terminal swellings were reconstructed through serial sections with the aid of a light microscope and drawing tube. On average, 13.4 +/- 8.1% of the terminal swellings were found in the dorsal cochlear nucleus (DCN) and the remaining terminal swellings were located in the ventral cochlear nucleus. In the DCN, the terminal fields of auditory nerve fibers were restricted to layer III, contributed to cytoarchitectonic striations, and exhibited a systematic relationship between fiber CF and position along the strial (or long) axis of the nucleus. Computer-aided rotations revealed that the terminal fields were anisotropic, being flattened within the trans-strial axis. The maximal width of the terminal fields along the strial axis ranged from 31-321 microns and was inversely related to fiber CF and SR. Variation in the number of terminals or depth of the terminal field within layer III was not related to SR grouping or CF of the fiber.

Animals↗

PubMed1993

Glial populations in the juvenile and adult Mongolian gerbil: relationship to spongiform degeneration of the ventral cochlear nucleus.

The gerbil cochlear nucleus is subject to a spongiform degeneration, the progression of which is dependent on auditory functional activity. The most affected region is the ventrolateral aspect of the caudal posterior ventral cochlear nucleus (PVCN). Lesion density and glial changes were quantified in this region for two age groups. Spongiform lesions increased significantly in area density from 4% in 60-day-old gerbils to 14% in 6-month-old gerbils. In spite of this significant increase in tissue damage, no gliosis was found. A significant age-related decrease in oligodendrocyte density was found in the PVCN.

Acoustic Stimulation↗

PubMed1981

Neuronal organization of the rabbit cochlear nucleus: some anatomical and electrophysiological observations.

The cochlear nucleus of the young adult rabbit was studied using both anatomical and electrophysiological techniques. The cytoarchitecture of the cochlear nucleus, as revealed by Nissl-staining and Bodian's Protargol method, was quite similar to that of the cat. The cell types observed by the Golgi-Cox method were very similar to those observed in the cat cochlear nucleus. Bushy and stellate cells were predominant in the anterior ventral cochlear nucleus, and multipolar and globular cells were observed throughout the posterior ventral cochlear nucleus, surrounding a region containing mainly octopus cells. The dorsal cochlear nucleus was revealed as a limited structure with a prominent band of fusiform cells. The polymorphic layers continued varieties of giant neurons similar to those observed in the cat. Units in the cochlear nucleus were classified electrophysiologically, in terms of their discharge pattern, and located histologically. The ventral cochlear nucleus contained mainly "primarylike," "chopper" and "onset" units, but the dorsal cochlear nucleus contained a greater variety of response patterns. "Buildup," "pauser" and "chopper" response patterns were predominant, and the dorsal cochlear nucleus also obtained more inhibitory units than the ventral cochlear nucleus. Both the types of units observed and their location in each nucleus were very similar to those reported for the cat. Both divisions of the ventral cochlear nucleus and the dorsal cochlear nucleus were found to be tonotopically organized in a dorsal (high frequency) to ventral (low frequency) direction. A trend for an organization in a medial to lateral direction was also apparent, particularly in the dorsal cochlear nucleus.

Animals↗

PubMed1984

Development of the cochlear innervation of the dorsal cochlear nucleus of the hamster.

The development of cochlear fibers and terminals in the dorsal cochlear nucleus of the hamster was studied with light and electron microscopic techniques. Like the dorsal cochlear nucleus of most other mammals, the dorsal cochlear nucleus of the adult hamster is a laminated structure. Three distinct layers can be identified in cresyl-violet-stained sections: the molecular layer, the fusiform cell layer, and the deep layer. The deep layer consists of a superficial zone, free of large cell bodies, and a deep zone which contains the somas of giant cells. Horseradish peroxidase and degeneration studies reveal that the cochlear fibers ramify throughout the deep and fusiform cell layers of the adult hamster but do not enter the molecular layer. In the electron microscope, three types of terminals that contact the fusiform and the giant cells can be distinguished. Only one type of terminal (type LR) degenerates after cochlear ablation and is, therefore, thought to be of cochlear origin. Type LR terminals are found throughout the deep and fusiform cell layers and contact the somas of giant and fusiform cells, as well as their intermingled dendrites in the deep layer. In Golgi-impregnated material, cochlear fibers are not found in the dorsal cochlear nucleus of the neonatal hamster, although they have entered the ventral cochlear nucleus. Ingrowth of cochlear fibers into the dorsal cochlear nucleus occurs over the first postnatal week and one-half. A spatial gradient is evident during the ingrowth of the fibers in that they invade the dorsomedial parts of the dorsal cochlear nucleus before they invade the ventrolateral parts. In all parts of the nucleus, the fibers enter the deepest layer and grow progressively more superficially. In the electron microscope, the first appearance of type LR terminals at each depth lags behind the ingrowth of the fibers by about two days. In hamsters, fibers from the basal turns of the cochlea terminate in the dorsomedial dorsal cochlear nucleus, while fibers from the apical turns terminate in the ventrolateral dorsal cochlear nucleus (DCN). The dorsomedial to ventrolateral gradient in the ingrowth of the cochlear fibers into the DCN indicates that the fibers from the basal turn are the first to arrive. Several components of the mammalian cochlea have been shown to mature at the base of the cochlea before they mature at the apex. The present study suggests that maturation gradients in the cochlear nucleus parallel those observed in the cochlea.

Animals↗