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PubMed2004

Co-induction of growth-associated protein GAP-43 and neuronal nitric oxide synthase in the cochlear nucleus following cochleotomy.

In adult animals, cochlear lesioning leads to a reactive synaptogenesis with a reemergence of growth-associated protein, GAP-43, in the auditory brainstem nuclei. In addition, nitric oxide (NO) is also implicated in synaptogenesis. Three isoforms of nitric oxide synthase (NOS) responsible for generating NO have been identified and, in neurons, the predominant isoform is neuronal NOS (nNOS). Studies in visual or olfactory systems have found that the NOS expression often correlates with periods of axonal outgrowth and synapse formation; whether NO plays a similar role in the auditory brainstem needs to be examined. In the present study, a unilateral cochleotomy was performed in adult mice to examine the relationship between the reemergence of GAP-43 and the expression pattern of nNOS. Following surgery, GAP-43 re-emerged in the ipsilateral anterior ventral cochlear nucleus (AVCN) and the immunoreactivity reached a climax around postoperative day (POD) 8; the same expression pattern as that reported in the previous literature is the indicator of synaptogenesis. As for the nNOS immunoreactivity, a dramatic redistribution from a mostly cytoplasmal to a predominantly membranous localization in the ipsilateral AVCN was found especially at POD 4. A similar redistribution pattern in the ipsilateral AVCN for the N-methyl-D-aspartate (NMDA) receptor was also observed at POD 4, corresponding to the fact that the activation of nNOS is coupled to calcium influx via the NMDA-receptor. Furthermore, the expression of cyclic guanosine monophosphate (cGMP) is an indicator for activity of soluble guanylyl cyclase (sGC), the substrate of NO, which reveals the target area of NO. Therefore, cGMP immunoreactivity was also examined and an obvious increase of cytoplasmal cGMP expression was observed around POD 4. Accordingly, it is suggested that nNOS activity correlates closely with the reactive synaptogenesis following a cochleotomy. Further evidence is shown by the results of fluorescent double staining; nNOS-positive cells were surrounded by GAP-43 labeled regions that appeared to be presynaptic boutons, and the vast majority of nNOS-positive cells also expressed cGMP. The former result indicates that, after surgery, there should be new terminal endings projecting onto the nNOS-positive cells in the AVCN. Furthermore, the latter result suggests a possible role of an autocrine mediator for nNOS in the AVCN.

Animals↗

PubMed1998

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

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

Animals↗

PubMed2001

Potassium currents in octopus cells of the mammalian cochlear nucleus.

Octopus cells in the posteroventral cochlear nucleus (PVCN) of mammals are biophysically specialized to detect coincident firing in the population of auditory nerve fibers that provide their synaptic input and to convey its occurrence with temporal precision. The precision in the timing of action potentials depends on the low input resistance (approximately 6 MOmega) of octopus cells at the resting potential that makes voltage changes rapid (tau approximately 200 micros). It is the activation of voltage-dependent conductances that endows octopus cells with low input resistances and prevents repetitive firing in response to depolarization. These conductances have been examined under whole cell voltage clamp. The present study reveals the properties of two conductances that mediate currents whose reversal at or near the equilibrium potential for K(+) over a wide range of extracellular K(+) concentrations identifies them as K(+) currents. One rapidly inactivating conductance, g(KL), had a threshold of activation at -70 mV, rose steeply as a function of depolarization with half-maximal activation at -45 +/- 6 mV (mean +/- SD), and was fully activated at 0 mV. The low-threshold K(+) current (I(KL)) was largely blocked by alpha-dendrotoxin (alpha-DTX) and partially blocked by DTX-K and tityustoxin, indicating that this current was mediated through potassium channels of the Kv1 (also known as shaker or KCNA) family. The maximum low-threshold K(+) conductance (g(KL)) was large, 514 +/- 135 nS. Blocking I(KL) with alpha-DTX revealed a second K(+) current with a higher threshold (I(KH)) that was largely blocked by 20 mM tetraethylammonium (TEA). The more slowly inactivating conductance, g(KH), had a threshold for activation at -40 mV, reached half-maximal activation at -16 +/- 5 mV, and was fully activated at +30 mV. The maximum high-threshold conductance, g(KH), was on average 116 +/- 27 nS. The present experiments show that it is not the biophysical and pharmacological properties but the magnitude of the K(+) conductances that make octopus cells unusual. At the resting potential, -62 mV, g(KL) contributes approximately 42 nS to the resting conductance and mediates a resting K(+) current of 1 nA. The resting outward K(+) current is balanced by an inward current through the hyperpolarization-activated conductance, g(h), that has been described previously.

Animals↗

PubMed2000

Hyperpolarization-activated, mixed-cation current (I(h)) in octopus cells of the mammalian cochlear nucleus.

Octopus cells in the posteroventral cochlear nucleus of mammals detect the coincidence of synchronous firing in populations of auditory nerve fibers and convey the timing of that coincidence with great temporal precision. Earlier recordings in current clamp have shown that two conductances contribute to the low input resistance and therefore to the ability of octopus cells to encode timing precisely, a low-threshold K(+) conductance and a hyperpolarization-activated mixed-cation conductance, g(h). The present experiments describe the properties of g(h) in octopus cells as they are revealed under voltage clamp with whole-cell, patch recordings. The hyperpolarization-activated current, I(h), was blocked by extracellular Cs(+) (5 mM) and 4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyridinium chloride (50-100 nM) but not by extracellular Ba(2+) (2 mM). The reversal potential for I(h) in octopus cells under normal physiological conditions was -38 mV. Increasing the extracellular potassium concentration from 3 to 12 mM shifted the reversal potential to -26 mV; lowering extracellular sodium concentration from 138 to 10 mM shifted the reversal potential to -77 mV. These pharmacological and ion substitution experiments show that I(h) in octopus cells is a mixed-cation current that resembles I(h) in other neurons and in heart muscle cells. Under control conditions when cells were perfused intracellularly with ATP and GTP, I(h) had an activation threshold between about -35 to -40 mV and became fully activated at -110 mV. The maximum conductance associated with hyperpolarizing voltage steps to -112 mV ranged from 87 to 212 nS [150 +/- 30 (SD) nS, n = 36]. The voltage dependence of g(h) obtained from peak tail currents is fit by a Boltzmann function with a half-activation potential of -65 +/- 3 mV and a slope factor of 7. 7 +/- 0.7. This relationship reveals that g(h) was activated 41% at the mean resting potential of octopus cells, -62 mV, and that at rest I(h) contributes a steady inward current of between 0.9 and 2.1 nA. The voltage dependence of g(h) was unaffected by the extracellular application of dibutyryl cAMP but was shifted in hyperpolarizing direction, independent of the presence or absence of dibutyryl cAMP, by the removal of intracellular ATP and GTP.

4-Aminopyridine↗

PubMed1997

[Effect of monaural cochlear ablation on cell areas of ventral cochlear nucleus neurons in neonatal and adult guinea pigs].

The changes of the cross-sectional areas of anteroventral cochlear nucleus (AVCN) and posteroventral cochlear nucleus (PVCN) were studied in neonatal and adult guinea pigs after monaural cochlear ablation with computer imaging analysis system. The cross-sectional areas of neurons in AVCN and PVCN were not significantly changed after 24 h of monaural cochlear ablation in neonatal guinea pigs. But the cell areas of AVCN neurons of ablated side were respectively reduced by 20.93%, 25.70% and 28.72% compared to non-ablated side in 4 d, 7 d, 60 d after cochlear ablation, the cell areas of PVCN neurons were reduced by 17.58%, 20.30% and 38.55% respectively. The area reduction of AVCN and PVCN neurons of ablated side in 60 d group with monaural cochlear ablation were 51.00% and 32.75% relative to normal control group. Our results showed that cochlear ablation could results in rapid cell area reduction of VCN neurons in guinea pigs. Our investigation implied that it is important to stimulate the auditory nerve early in the patients with hearing loss.

Animals↗

PubMed2006

Site-specific interactions of neurotrophin-3 and fibroblast growth factor (FGF2) in the embryonic development of the mouse cochlear nucleus.

Neurotrophins and FGF2 contribute to formation of the cochlea, but their roles in cochlear nucleus development are unknown. The effects of these factors may differ in the cochlea and cochlear nucleus, which may influence each other's development. It is important to analyze the effects of these factors on cellular structures at well-defined steps in the normal morphogenetic sequence. The present study used immunohistochemistry to localize factors in situ and to test hypotheses about their roles in an in vitro model. Specific antibody staining revealed that TrkC, the NT3 receptor, is present in neural precursors prior to embryonic day E11 until after birth. NT3 appeared in precursor cells during migration (E13-E15) and disappeared at birth. TrkC and NT3 occurred in the same structures, including growing axons, terminals, and their synaptic targets. Thus, NT3 tracks the migration routes and the morphogenetic sequences within a window defined by TrkC. In vitro, the cochlear nucleus anlage was explanted from E11 embryos. Cultures were divided into groups fed with defined medium, with or without FGF2, BDNF, and NT3 supplements, alone or in combinations, for 7 days. When neuroblasts migrated and differentiated, immunostaining was used for locating NT3 and TrkC in the morphogenetic sequence, bromodeoxyuridine for proliferation, and synaptic vesicle protein for synaptogenesis. By time-lapse imaging and quantitative measures, the results support the hypothesis that FGF2 promotes proliferation and migration. NT3 interacts with FGF2 and BDNF to promote neurite outgrowth, fasciculation, and synapse formation. Factors and receptors localize to the structural sites undergoing critical changes.

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PubMed1991

Electrical stimulation of the auditory nerve in deaf kittens: effects on cochlear nucleus morphology.

The present study examines the effects of long-term electrical stimulation of the auditory nerve on the morphology of neurons in the cochlear nucleus in young, sensorineural deaf animals. Kittens, systemically deafened using kanamycin and ethacrynic acid, received bilateral cochlear implants and were stimulated unilaterally for periods of up to four months. After sacrifice, cross-sectional areas of neuron somata were measured with an image-analysis system and compared using nonparametric statistics. The areas of cell somata within the anteroventral cochlear nucleus (AVCN) on the stimulated side were significantly larger than those of corresponding somata on the control, unstimulated side (P less than 0.001). However, there was no statistically significant difference among dorsal cochlear nucleus (DCN) neurons. These results indicate that long-term electrical stimulation of the auditory nerve can at least partially negate some effects of early postnatal auditory deprivation at the level of the cochlear nucleus.

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PubMed1993

Varieties of inhibition in the processing and control of processing in the mammalian cochlear nucleus.

Seven-barrel micropipettes were used to apply drugs microiontophoretically to single units in the dorsal cochlear nucleus (DCN) in chloralose-anaesthetised guinea-pigs. While both agonists and antagonists of putative neurotransmitters in the cochlear nucleus have been investigated in these experiments, the main thrust has been to explore the influence of specific antagonists on cells' spectral and temporal properties, thus elucidating the effects of naturally occurring inhibitory transmitters. At least five types of inhibition appear to be pharmacologically/physiologically separable: (1) Stimulus-evoked tonic "lateral/sideband" inhibition: glycinergic; (blocked by strychnine); responsible for the lateral inhibition of dorsal cochlear nucleus (DCN) type III and IV cells. Strychnine has its predominant effect on sustained (lateral) inhibition compared with the more transient forms of inhibition. Subtraction of receptive field maps enables us to visualise the extent of the inhibitory receptive field. It extends virtually throughout the unit's response field for both these classes but is generally, especially in type IV cells, maximal at the characteristic frequency (CF). This type of inhibition will primarily be responsible for enhancing spectral contrasts in the way that, in the visual system, surround inhibition enhances visual contrast. Furthermore, lateral inhibitory sidebands can "bias" the "working point" of a cell's response so that the dynamic range of effective stimuli and response can be extended. (2) "Background" tonic inhibition: GABAAergic; (blocked by bicuculline). Blocking this inhibition generally results in an increase in the background (i.e., spontaneous) activity. This inhibition is probably responsible for adjusting excitatory-inhibitory contrasts in both spectral and temporal domains. (3) Stimulus-related off-inhibition appears to be neither glycinergic nor GABAAergic. Blocking these receptors actually enhances off-inhibition. Nicotinic cholinergic blockers may have a small effect on off-inhibition, but so far we have not been able to block it entirely. This off-inhibition is important for enhancing temporal contrast. This inhibition must, therefore, be mediated by other transmitters, yet undetermined, or by a local feedback circuit or, less likely, be a membrane-based after-effect of stimulation. (4) Pre-synaptic inhibition, mediated by GABAB receptors presumed to act on primary afferent terminals, thus controlling afferent input to DCN principal cells. (5) Short-latency contralateral inhibition, mediated by glycine.

Animals↗

PubMed1998

Redistribution of NMDA receptors in the cochlear nucleus following cochleotomy.

The major input to neurons of the cochlear nucleus comes from the glutamatergic cells of the spiral ganglion. We have studied the effect of unilateral destruction of the inner ear, including the spiral ganglion, with two antibodies against different types of NMDA receptor subunits, NMDAR1 and NMDAR2A/B, in the cochlear nucleus of the rat. Following cochleotomy, a dramatic redistribution of the receptor subunits was observed from a mostly perikaryal to a predominantly dendritic localization. Moreover, distinct changes in the composition of NMDA receptor complexes occurred. These effects were interpreted as compensatory responses to the massive loss of presynaptic release of the transmitter glutamate.

Animals↗

PubMed2005

Deafness-related decreases in glycine-immunoreactive labeling in the rat cochlear nucleus.

There is increasing evidence of activity-related plasticity in auditory pathways. The present study examined the effects of decreased activity on immunolocalization of the inhibitory neurotransmitter glycine in the cochlear nucleus of the rat after bilateral cochlear ablation. Specifically, glycine-immunoreactive puncta adjacent to somatic profiles were compared in normal hearing animals and animals deafened for 14 days. The number of glycine-immunoreactive puncta surrounding somatic profiles of spherical and globular bushy cells, glycine-immunoreactive type I stellate multipolar cells, radiate neurons (type II stellate multipolar cells), and fusiform cells decreased significantly. In addition, the number of glycine immunopositive tuberculoventral (vertical or corn) cells in the deep layer of the dorsal cochlear nucleus also decreased significantly. These results suggest that decreased inhibition reported in cochlear nucleus after deafness may be due to decreases in glycine.

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PubMed1981

Histogenesis of the cochlear nucleus of the mouse.

In Nissl-stained preparations of the cochlear nucleus there are nine recognizable cell types. These cells are born during three periods of histogenesis prenatally. On gestation days 10.0, 10.5, and 11.0 the pyramidal, giant, and dark-staining cells are born. The spherical, globular, multipolar, and horizontal cells are formed on gestation days 12.0, 12.5, and 13.0 and small cells follow on gestation day 14.5. The onset of granule cell formation is gestation day 14.5 continues to birth on gestation day 19. At birth, and for at least the first 2 postnatal weeks, glial cells are born. There are no regional gradients in cell birth dates, cells from all birth dates being intermixed. Cell birth proceeds in an orderly sequence that is related only to cell size. Although there were no apparent spatiotemporal patterns, some clustering of labeled cells was evident. These observations do not support the hypothesis that Golgi Type I cells precede Golgi Type II cells in their order of birth since both large and small neurons project beyond the nucleus. There is, nonetheless, a sequential pattern in the onset of cell birth for the auditory system, with cochlear nucleus neurons preceding cochlear neurons.

Aging↗

PubMed1992

Presbycusis: correlations of clinical audiology with morphological changes in the cochlea and the ventral cochlear nucleus.

Five cases of presbycusis are presented. Analysis included audiological tests, cochlear hair cell and ganglion cell counts, assessment of degree of strial atrophy, and ventral cochlear nucleus neuron counts. One case showed a reduction in cochlear nucleus neuron counts without significant cochlear changes, indicating that this pattern of pathological changes is a possible cause of high tone sensorineural deafness.

Aged↗

PubMed1995

Distribution of calbindin D-28k immunoreactivity in the cochlear nucleus of the young adult chinchilla.

Calbindin is a 28 kD calcium-binding protein found in neural tissue. Although its functional role in nerve cell physiological processing is still uncertain, previous investigations have suggested that because of its intracellular calcium buffering and regulation properties, it could influence temporal precision of neuronal firing to subserve temporal processing in the auditory brainstem, or could mediate monaural versus binaural coding, or be involved in synaptic plasticity (learning). The present study demonstrates differential calbindin immunoreactivity in the cochlear nuclear complex of the chinchilla, a rodent with exceptionally good low-frequency hearing. The most intense labeling in the cochlear cochlear nucleus was in somata of cartwheel and fusiform cells of the fusiform cell layer, and somata and process of the molecular layer of the dorsal cochlear nucleus (DCN). Only a relatively few scattered neurons were stained in the deep layers of DCN. In contrast, moderate labeling of neurons and neuropil throughout the ventral cochlear nucleus was seen. For instance, moderately stained spherical and elongate cells of the anteroventral cochlear nucleus were observed in contact with labeled puncta and amidst stained fibers. In the cochlear nerve root region, stained auditory nerve fibers and global cells were noted. In the posteroventral cochlear nucleus, principal cells of elongate and octopus shape were observed, in contact with labeled swellings and surrounded by labeled neuropil.

Animals↗

PubMed2004

Postsynaptic targets of type II auditory nerve fibers in the cochlear nucleus.

Type II auditory nerve fibers, which provide the primary afferent innervation of outer hair cells of the cochlea, project thin fibers centrally and form synapses in the cochlear nucleus. We investigated the postsynaptic targets of these synapses, which are unknown. Using serial-section electron microscopy of fibers labeled with horseradish peroxidase, we examined the border of the granule-cell lamina in mice, an area of type II termination that receives branches having swellings with complex shapes. About 70% of the swellings examined with the electron microscope formed morphological synapses, which is a much higher value than found in previous studies of type II swellings in other parts of the cochlear nucleus. The high percentage of synapses enabled a number of postsynaptic targets to be identified. Most of the targets were small dendrites. Two of these dendrites were traced to their somata of origin, which were cochlear-nucleus "small cells" situated at the border of the granule-cell lamina. These cells did not appear to receive any terminals containing synaptic vesicles that were large and round, indicating a lack of input from type I auditory nerve fibers. Nor did type II swellings or targets participate in the synaptic glomeruli formed by mossy terminals and the dendrites of granule cells. Other type II synapses were axosomatic and their targets were large cells, which were presumed multipolar cells and one cell with characteristics of a globular bushy cell. These large cells almost certainly receive additional input from type I auditory nerve fibers, which provide the afferent innervation of the cochlear inner hair cells. A few type II postsynaptic targets-the two small cells as well as a large dendrite-received synapses that had accompanying postsynaptic bodies, a likely marker for synapses of medial olivocochlear branches. These targets thus probably receive convergent input from type II fibers and medial olivocochlear branches. The diverse nature of the type II targets and the examples of segregated convergence of other inputs illustrates the synaptic complexity of type II input to the cochlear nucleus.

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PubMed1996

Membrane properties of mouse anteroventral cochlear nucleus neurons in vitro.

Intracellular recordings were made from neurons of the mouse anteroventral cochlear nucleus (AVCN) in vitro. The whole cochlear nucleus was dissected out and maintained submerged in rapidly flowing artificial CSF. This preparation has the advantages of maintaining cell-to-cell connections and dendritic trees whereas slices and enzymatically separated preparations do not. Recordings were made using current clamp technique in the presence and absence of the ion channel blockers, tetrodotoxin (TTX 1 microM), tetraethylammonium (TEA 20 mM), 4-aminopyridine (4-AP 5 mM) or verapamil (150 microM). Two distinct types of neurons were observed when tested with depolarizing current pulses: one which fired only a single action potential at the onset of stimulation followed by a relative depolarization for the remainder of the stimulus period, and the other which fired a sustained train of action potentials, each followed by a large undershoot, then a rapid recovery phase and the slower depolarization to threshold. The single spike cells (n = 24) had resting membrane potentials of -63.4 +/- 4.7 mV, resistance of 48.4 +/- 29.6 M omega, time constant of 3.47 +/- 3.1 ms, capacitance of 0.081 +/- 0.079 nF. The I/V plot was non-linear above the resting membrane potential and linear below. Spike train cells (n = 24) had resting membrane potentials of -64.2 +/- 4.54 mV, resistance of 69.8 +/- 28.9 M omega, time constant of 6.51 +/- 3.09 ms, capacitance of 0.11 +/- 0.087 nF. The I/V plot was linear both below resting membrane potential and up to threshold for spike firing. TTX abolished spike firing in both cell types. TEA significantly increased the spike duration in both cell types. 4-AP increased the spike duration in spike train cells but not in single spike cells. Verapamil had no effect on the firing properties of both cells but it significantly increased the spike duration of spike train cells. The single spike cells are known to fire rapidly and repetitively in vivo. Injection of sine wave currents caused rapid and repetitive firing suggesting that these cells require hyperpolarization to allow for removal of inactivation. There was a linear relationship between injected depolarizing current and the rate of action potential firing in spike train cells.

4-Aminopyridine↗

PubMed2001

Immunohistochemical localization of nitric oxide synthase and soluble guanylyl cyclase in the ventral cochlear nucleus of the rat.

The diffusible messenger nitric oxide (NO) is implicated in auditory processing. It acts in the brain largely through activation of soluble guanylyl cyclase (sGC), a heterodimer comprised of alpha and beta subunits. The authors used immunohistochemistry to study the NO/guanosine 3',5'-cyclic monophosphate (cGMP) pathway in the cochlear nucleus of Sprague-Dawley rats. Central fibers of the cochlear nerve were stained for neuronal nitric oxide synthase (NOS-I) but not for sGCbeta. Within the ventral cochlear nucleus, a large fraction of principal cells were immunopositive for both NOS-I and sGCbeta; these cells could be seen at times receiving contacts from NOS-I-positive fibers. sGC staining of somatic cytoplasm extended into the distal dendritic tree. At variance with this pattern, NOS-I was concentrated mainly in somata. Double-labeling experiments showed that most of the principal neurons expressed both antigens. By contrast, in the granule cell domain, small cells that were immunopositive for NOS-I rarely corresponded to those that were immunopositive for sGC. To assess whether NOS-I and sGC immunoreactivities colocalize with their respective catalytic activities, the authors performed multiple labeling with L-citrulline (a by-product of the formation of NO from L-arginine) and cGMP, respectively. L-citrulline was restricted to NOS-I-positive elements, and the large majority of NOS-expressing neurons were positive for citrulline. Multiple labeling revealed that almost all sGC-positive neurons also accumulated cGMP both in the ventral cochlear nucleus and in the granule cell domain. These data suggest that NO is a signaling molecule in the cochlear nucleus, perhaps functioning in both a paracrine manner and an autocrine manner.

Animals↗

PubMed1981

Immunocytochemical localization of aspartate aminotransferase immunoreactivity in cochlear nucleus of the guinea pig.

There is substantial evidence supporting the role of aspartate or glutamate as the neurotransmitter of the auditory nerve. The concentration of aspartate aminotransferase (L-aspartate:2-oxoglutarate aminotransferase, EC 2.6.1.1), an enzyme associated with the metabolism of these amino acids, is high in axons and terminals of the auditory nerve. Antibodies were raised against aspartate aminotransferase and used in immunocytochemical studies to determine its localization in the cochlear nucleus of the guinea pig. Indirect immunofluorescence techniques were used for light microscopic localization of aspartate aminotransferase-like immunoreactivity in normal guinea pigs and guinea pigs with auditory nerve lesions. Fluorescent rings of aspartate aminotransferase-like immunoreactivity were seen around spherical cells in the anteroventral cochlear nucleus. In animals with auditory nerve lesions, rings were no longer seen in the ipsilateral cochlear nucleus. Immunoreactivity was also seen on cells in the posteroventral cochlear nucleus and in auditory nerve fibers. Ultrastructural studies were done in the rostral anteroventral cochlear nucleus, using the peroxidase-antiperoxidase technique. Aspartate aminotransferase-like immunoreactivity was seen at axosomatic synapses on large spherical cells in terminals with the morphological characteristics of auditory nerve terminals. Other classes of terminals on the soma of large spherical cells showed no immunoreactivity. It was concluded that aspartate aminotransferase-like immunoreactivity is present in axons and terminals of the auditory nerve. These findings indicate that aspartate aminotransferase-like immunoreactivity may serve as a marker at terminals where aspartate or glutamate is a neurotransmitter.

Animals↗

PubMed2002

Putative inhibitory collicular boutons contact large neurons and their dendrites in the dorsal cochlear nucleus of the rat.

Within the circuits of the acoustic nuclei, the inferior colliculus sends descending (collicular) terminals to control with a feedback mechanism, part of the activity of the dorsal cochlear nucleus (DCN). It is not known whether this descending projection is prevalently excitatory or inhibitory. Using the neuronal tracer Wheat Germ Agglutinin conjugated to Horse Radish Peroxidase (WGA-HRP) the connections between the inferior colliculus and the DCN of the rat have been investigated. By far most retrograde labelled large neurons were glycine and GABA negative (pyramidal and giant neurons) and rare medium-size cells were glycine positive. The ultrastructural immunocytochemical analysis for glycine and GABA shows that mainly large, excitatory, neurons innervate the inferior colliculus. Rare medium-size glycine-positive cells with intermediate characteristics between pyramidal and cartwheel cells, seem also to project to the colliculus. Few WGA-HRP labelled boutons contact the large cells or their dendrites, have symmetric pre- and post-synaptic thickenings, contain pleomorphic and/or flat vesicles, and are labelled for GABA or glycine. Since no GABA labelled cells in both the dorsal and ventral cochlear nucleus were retrograde labelled from the colliculus, the source of these intrinsic anterograde labelled boutons must be external to the cochlear nucleus. GABA positive neurons are both present in the inferior colliculus (injected with the tracer) and superior olivary complex (not injected with the tracer). This suggests that the double labelled boutons (WGA-HRP and GABA) are inhibitory GABA-ergic collicular terminals contacting the excitatory neurons of the DCN. Other few boutons or mossy fibers containing round vesicles and immunonegative for both glycine and GABA, were also seen contacting the large neurons and their dendrites in the DCN. As the round vesicles boutons may be derived from other retrograde cells of the cochlear nucleus (pyramidal and stellate cells) and those glycine positive from the glycinergic neurons in paraolivary nuclei, it is more likely that only the WGA-HRP and GABA labelled boutons are true collicular terminals.

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