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PubMed1978

Survey of intracellular recording in the cochlear nucleus of the cat.

Intracellular recordings were made in the cochlear nucleus of anesthetized cats. In anterior passes, one never obtained sustained depolarizations from 'primary-like' units. For 'chopper' units, however, it was possible to record sustained depolarizations accompaneid by spikes that lasted as long as the tone burst. 'Pauser, 'buildup' and 'on' units also had spike responses that could be accompanied by sustained depolarizations. For 'pauser', 'buildup' and 'on' units, hyperpolarization was not seen during the times when no spike discharges appeared so long as the tone bursts were at the characteristic frequency of the units.

Acoustic Stimulation↗
PubMed1972

Response decrements in the cochlear nucleus of decerebrate cats during repeated acoustic stimulation.

In the cochlear nucleus of decerebrate, paralyzed cats, multiple-unit responses to an acoustic stimulus showed significant decrements when the stimulus was repeatedly presented once every 5 seconds. These decrements developed in the absence of peripheral receptor adaptation. The responses recovered to the level prior to stimulation when stimulation was withheld for 5 to 10 minutes. Dishabituation by somatic stimulation of the forepaw, however, was less effective than in the intact cat. The continued development of response decrements after strychnine blockade of peripheral olivocochlear influences and central postsynaptic inhibition suggests a mechanism of decreased synaptic effectiveness, which has previously been postulated for neuronal habituation in brainstem and spinal cord.

Animals↗
PubMed1982

Response properties of type II and type III units in dorsal cochlear nucleus.

Type II and type III units in the dorsal cochlear nucleus (DCN) of unanesthetized (decerebrate) cats are those with excitatory responses to best frequency (BF) tones at all levels above threshold. They are distinguished from type IV units which give predominantly inhibitory responses to tones. Type II and type III units are distinguished from one another by their rates of spontaneous activity. Type II units have low rates of spontaneous activity (below 2.5 spikes/s), whereas type III units are spontaneously active at rates up to 95 spikes/s. In this paper we show that segregation of units according to spontaneous activity produces a segregation of several other properties as well. A typical type II unit responds vigorously to BF tones (median maximum rate of 242 spikes/s), has slightly nonmonotonic rate versus level function, and responds weakly or not at all to broadband noise. These units tend to be located in the deep layer of the DCN. Type III units tend to respond to BF tones at moderate rates (median maximum driven rate of 124 spikes/s), have monotonic or nonmonotonic rate versus level functions, and respond to noise at rates comparable to their tone rates. They are distributed somewhat more uniformly in all DCN layers, but a majority were found in the fusiform cell and molecular layers. Most evidence indicates that type II units are recorded from inhibitory interneurons in the DCN.

Acoustic Stimulation↗
PubMed2006

Lithium increases bcl-2 expression in chick cochlear nucleus and protects against deafferentation-induced cell death.

Approximately 20-30% of neurons in the avian cochlear nucleus (nucleus magnocellularis) die following deafferentation (i.e. deafness produced by cochlea removal) and the remaining neurons show a decrease in soma size. Cell death is generally accepted to be a highly regulated process involving various pro-survival and pro-death molecules. One treatment that has been shown to modify the expression of these molecules is chronic administration of lithium. The present experiments examined whether lithium treatment can protect neurons from deafferentation-induced cell death. Post-hatch chicks were treated with LiCl or saline for 17 consecutive days, beginning on the day of hatching. On the 17th day, a unilateral cochlea ablation was performed. Five days following surgery, the nucleus magnocellularis neurons were counted stereologically on opposite sides of the same brains. Lithium reduced deafferentation-induced cell death by more than 50% (9.8% cell death as compared with 22.4% in saline-treated subjects). Lithium did not affect cell number on the intact side of the brain. Lithium also did not prevent the deafferentation-induced decrease in soma size, suggesting a dissociation between the mechanisms involved in the afferent control of soma size and those involved in the afferent control of cell viability. A possible mechanism for lithium's neuroprotective influence was examined in a second set of subjects. Previous studies suggest that the pro-survival molecule, bcl-2, may play a role in regulating cell death following deafferentation. Tissues from lithium- and saline-treated subjects were examined using immunocytochemistry. Chronic administration of lithium dramatically increased the expression of bcl-2 protein in nucleus magnocellularis neurons. These data suggest that lithium may impart its neuroprotective effect by altering the expression of molecules that regulate cell death.

Afferent Pathways↗
PubMed1995

Evidence for glutamatergic projections from the cochlear nucleus to the superior olive and the ventral nucleus of the lateral lemniscus.

This study attempts to determine if projections ascending from the guinea pig cochlear nucleus (CN) could be glutamatergic and/or aspartatergic. Multiple radio frequency lesions were made to ablate the right CN. The ablation was verified histologically. To identify the principal targets of CN efferents, silver impregnation methods were used to localize the preterminal degeneration of fibers in transverse sections of the brainstem 5 and 7 days after CN ablation. CN efferents projected heavily to the lateral superior olive (LSO) ipsilaterally, the medial superior olive (MSO) bilaterally, and contralaterally to the medial (MNTB) and ventral (VNTB) nuclei of the trapezoid body, the ventral (VNLL) and intermediate nuclei of the lateral lemniscus and the central nucleus of the inferior colliculus (ICc). There were smaller projections to the lateral nucleus of the trapezoid body ipsilaterally, the dorsal and dorsomedial periolivary nuclei bilaterally, and the dorsal nucleus of the lateral lemniscus contralaterally. There were sparse projections to the VNLL and ICc ipsilaterally and the CN contralaterally, and a very sparse projection to the contralateral LSO. To determine if CN efferents were glutamatergic and/or aspartatergic, the fresh brainstem was sectioned transversely and samples of the LSO, MSO, MNTB, VNLL, and ICc were taken to measure the electrically evoked release and the uptake of D-[3H]Asp and [14C]Gly or [14C]GABA 3-5 days after the CN ablation. The release studies suggest that only certain of the histologically identified projections ascending from the CN may be glutamatergic and/or aspartatergic. CN ablation depressed D-[3H]Asp release in the MSO bilaterally and in the contralateral MNTB and VNLL, suggesting that the CN efferents to these nuclei may use glutamate or aspartate as a transmitter. It was unclear whether a marginal depression of D-[3H]Asp release in the ipsilateral LSO reflected the presence of glutamatergic CN projections to this nucleus. D-[3H]Asp release in the ICc was unaffected, suggesting that CN efferents to this nucleus may not be glutamatergic. There were no deficits in D-[3H]Asp uptake. [14C]Gly release from the LSO and MSO was unchanged. [14C]Gly uptake was unchanged in the MSO and depressed only in the contralateral LSO, possibly reflecting subnormal uptake activity in endings contributed by contralateral MNTB cells that had lost their CN efferents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

GABA alters the discharge pattern of chopper neurons in the rat ventral cochlear nucleus.

The effect of microiontophoretically applied gamma-aminobutyric acid (GABA) on chopper neurons in the ventral cochlear nucleus of the rat is described. The predominantly inhibitory effect of GABA resulted in a change of the regular discharge pattern. The interspike interval increased and the pattern became less regular as indicated by an increase of its coefficient of variation. These results suggest that the release of GABA may be responsible for the transient chopper behavior of some neurons which loose their regular discharge pattern within 20 ms after onset of the response to pure-tone stimulation.

Acoustic Stimulation↗
PubMed1978

Discharge patterns in the cochlear nucleus of the chinchilla following noise induced asymptotic threshold shift.

Chinchillas were exposed to an 86 dB SPL octave band of noise centered at 4.0 kHz for 3.5--5 days. The noise elevated the hearing thresholds between 4.0 and 16.0 kHz to between 60 and 75 dB SPL. Measurements from single neurons in the cochlear nucleus revealed abnormalities in the response properties of neurons with characteristic frequencies (CF) above 2.0 kHz. Units above 2.0 kHz had elevated thresholds (between 50 and 90 dB SPL) and broad tuning curves due to a greater loss in sensitivity near CF than at lower frequencies. The tuning curve Q10dB values for high frequency neurons were generally less than 3.0 and approached the Q10dB values for basilar membrane displacement. Spontaneous activity rates in units above 2.0 kHz were also low. In a few units, the threshold for single tone inhibition was significantly lower than that for excitation; the best inhibitory frequencies were always below 2.0 kHz. Two-tone inhibition was present in both low and high threshold neurons, but its strength was not assessed. Cochleagrams obtained 12 hours postexposure revealed discrete hair cell lesions in the basal third of the cochlea. The locations of the lesions were consistent with the frequencies of maximum hearing loss. The behavioral thresholds and the thresholds at CF of the most sensitive units were within 10--15 dB of each other. The results indicate that intense sounds reduce the sensitivity, frequency selectivity and spontaneous activity of units in the cochlear nucleus. The findings are similar to those obtained in auditory nerve fibers with ototoxic drugs and hypoxia.

Acoustic Stimulation↗
PubMed2005

Hyperpolarization-activated currents regulate excitability in stellate cells of the mammalian ventral cochlear nucleus.

The differing biophysical properties of neurons the axons of which form the different pathways from the ventral cochlear nucleus (VCN) determine what acoustic information they can convey. T stellate cells, excitatory neurons the axons of which project locally and to the inferior colliculus, and D stellate cells, inhibitory neurons the axons of which project to the ipsi- and contralateral cochlear nuclei, fire tonically when they are depolarized, and, unlike other cell types in the VCN, their firing rates are sensitive to small changes in resting currents. In both types of neurons, the hyperpolarization-activated current (I(h)) reversed at -40 mV, was activated at voltages negative to -60 mV, and half-activated at approximately -88 mV; maximum hyperpolarization-activated conductances (g(h max)) were 19.1 +/- 2.3 nS in T and 30.3 +/- 2.6 nS in D stellate cells (means +/- SE). Activation and deactivation were slower in T than in D stellate cells. In both types of stellate cells, 50 microM 4(N-ethyl-N-phenylamino)1,2-dimethyl-6-(methylamino) pyridinium chloride (ZD7288) and 2 mM Cs(+) blocked a 6- to 10-fold greater conductance than the voltage-dependent g(h) determined from Boltzmann analyses at -62 mV. The voltage-insensitive, ZD7288-sensitive conductance was proportional to g(h max) and g(input). 8-Br-cAMP shifted the voltage dependence of I(h) in the depolarizing direction, increased the rate of activation, and slowed its deactivation in both T and D stellate cells. Reduction in temperature did not change the voltage dependence but reduced the maximal g(h) with a Q(10) of 1.3 and slowed the kinetics with a Q(10) of 3.3.

Action Potentials↗
PubMed2000

Plasticity of spontaneous neural activity in the dorsal cochlear nucleus after intense sound exposure.

Increases in multiunit spontaneous activity (hyperactivity) can be induced in the dorsal cochlear nucleus (DCN) by intense sound exposure. This hyperactivity has been observed in the hamster and rat following exposure to a 10 kHz tone at a level of 125-130 dB SPL for a period of 4 h. The present study demonstrates that the onset of this hyperactivity is not immediate, but develops in the DCN between 2 and 5 days after exposure. Mean rates of multiunit spontaneous activity increased sharply from below normal levels at day 2 to higher than normal levels at day 5. The mean magnitude of activity continued to increase more gradually over the next 6 months. During this period, changes in the distribution of hyperactivity across the tonotopic array were also noted. The hyperactivity was more broadly distributed across the DCN at the early post-exposure times (5 and 14 days) than at later post-exposure recovery times (30 and 180 days), and peak activity was found at increasingly more medial positions over this time frame. These changes over time indicate that the mechanisms leading to hyperactivity following intense sound exposure are more complex than previously realized.

Animals↗
PubMed2004

Transient expression of acetylcholinesterase in the posterior ventral cochlear nucleus of rat brain.

In this report we partially characterize a pathway projecting to the posterior ventral cochlear nucleus (PVCN) of the rat brain that transiently expresses a high level of acetylcholinesterase (AChE). The AChE-positive axons form a network that envelops a discrete region of the PVCN that includes the octopus cell region and some cells rostral to it. AChE is first detectable by postnatal day 3 (P3), peaks in expression at about P7-10, and is barely detectable in our preparations by P15. We previously reported that neurons in the octopus cell region express high levels of alpha7 nAChR mRNA and alpha-bungarotoxin binding during the same time period. In light microscopic immunocytochemical studies using antibodies to the vesicular acetylcholine transporter (VAChT), we could not identify immunopositive boutons in the developing regions of the PVCN that express high levels of AChE-positive fibers despite distinct punctate labeling in other brain regions. Systematic electron microscopic examination of AChE histochemical staining throughout the PVCN revealed intense labeling of axons, but synaptic sites were devoid of reaction product. The source of the AChE-positive fibers is not known, but the fibers are not auditory nerve axons and probably not collaterals of the olivocochlear bundle.

Acetylcholine↗
PubMedDate not supplied

Wideband inhibition of dorsal cochlear nucleus type IV units in cat: a computational model.

A computational model of a portion of dorsal cochlear nucleus neural circuitry was used to investigate relationships between connectivity and response properties of type IV units. The model in this study consists of four neural populations. The pattern of convergence from one population to another and the strengths of those connections are the most important model parameters. Lumped parameter electrical circuit models represent individual cells. Interconnections are achieved by activating variable conductances in post-synaptic cells according to spike activity in pre-synaptic cells. Auditory nerve fibers are incorporated as a bank of logarithmically spaced gammatone filters that drive compartmental models of inner hair cell function. While it might be possible to configure the model without wideband inhibition to simulate type IV unit notch noise responses, the resulting parameters would likely be physiologically implausible. The model with wideband inhibition, however, shows the appropriate notch noise behavior. A wide variety of simulated rate versus cutoff-frequency plots are achieved varying three model parameters. The model was fit to physiological data by finding values of these three parameters that minimize the sum of squared errors. The results show that wideband inhibition can quantitatively account for the responses of type IV units to notch noise.

Acoustic Stimulation↗
PubMed2004

Glutamate-induced cytoplasmic Ca2+ transients in neurones isolated from the rat dorsal cochlear nucleus.

Extracellular application of glutamate elicited cytoplasmic Ca2+ transients in freshly dissociated rat neurones of the dorsal cochlear nucleus (DCN) (identified as pyramidal cells) with half-maximal concentration of 513 micromol/l while saturating doses (5 mmol/l) of this neurotransmitter caused transients of 46.1 +/- 3.0 nmol/l on an average. The genesis of these glutamate-evoked Ca2+ transients required extracellular Ca2+. When [Mg2+]o was 1 mmol/l, the NMDA receptor antagonist AP5 (100 micromol/l) had no effects while 100 micromol/l CNQX and 10 micromol/l NBQX, inhibitors of the AMPA receptors, greatly decreased the glutamate-induced Ca2+ transients (a decrease of 92 and 57%, respectively). When facilitating the activation of the NMDA receptors (50 micromol/l glycine, 20 micromol/l [Mg2+]o) in the presence of 100 micromol/l CNQX, Ca2+ transients of 55.4 +/- 13.1 nmol/l could be produced. Block of the voltage-gated Ca2+ channels (200 micromol/l Cd2+) decreased the Ca2+ transients to approx. 50%. The data indicate that under our control experimental circumstances the glutamate-induced Ca2+ transients of the isolated DCN neurones are produced mainly by Ca2+ entry through voltage-gated Ca2+ channels and AMPA receptors. However, when the activation of the NMDA receptors may take place, these receptors also contribute significantly to the genesis of the glutamate-evoked cytoplasmic [Ca2+] elevations.

Animals↗
PubMed1998

Changes in spontaneous neural activity in the dorsal cochlear nucleus following exposure to intense sound: relation to threshold shift.

Previous studies have shown that the dorsal cochlear nucleus exhibits increased spontaneous activity after exposure to intense sound. Such increases were apparent 1-2 months after the exposure and were generally proportional to the shift in response thresholds induced by the same exposure. The purpose of the present study was to determine whether this sound-induced increase in spontaneous activity is an early event which can be observed shortly after exposure. As in previous studies, anesthetized hamsters ranging in postnatal age from 60-70 days were exposed to a 10-kHz tone at levels between 125 and 130 dB SPL for a period of 4 h. Control animals were similarly anesthetized but were not exposed to the intense tone. Exposed animals were examined in two groups, one at 30 days after exposure, the other at 2 days after exposure. Time of exposure was adjusted so that all animals were between 90 and 100 days of age when spontaneous activity was studied electrophysiologically. The results showed that the increases in spontaneous activity, which were evident at 30 days after exposure, were not observed in animals studied 2 days after exposure. This result contrasted with the effect of the intense tone exposure on neural response thresholds. That is, the shifts in response thresholds seen 2 days after exposure were similar to those observed in animals studied 30 days after exposure. These results indicate that changes in spontaneous activity reflect a more slowly developing phenomenon and occur secondarily after induction of threshold shift.

Animals↗
PubMed1997

Marginal shell of the anteroventral cochlear nucleus: single-unit response properties in the unanesthetized decerebrate cat.

The marginal shell of the anteroventral cochlear nucleus (AVCN) is anatomically different from its central core. We investigated 38 single units in the shells of 10 cats and contrasted them with 62 single units in the cores of 15 cats. The sites of all shell units were localized with the use of reconstructed electrode tracks. The shell units were divided into acoustically well-driven (68%) and weakly/not-driven (32%) subgroups. The shell units mostly exhibited low spontaneous rates (SRs). Among the well-driven shell units, a large majority (68%) exhibited wide dynamic ranges (> or = 50 dB) to tones, noise, or both, with some ranges as wide as 89 dB. In contrast, a large majority (80%) of the core units exhibited narrow dynamic ranges (< 50 dB) to tones and noise. The poststimulus time histograms (PSTHs) of the well-driven shell units included pause-build (29%), onset (24%), and unusual (33%) types, whereas those of the core units included mainly primary-like (47%) and chopper (29%) types. The excitatory-inhibitory areas (EIAs) of the well-driven shell units included types I/III (47%), III (22%), IV (13%), and II (9%), whereas those of the core units included mainly types III (52%) and I/III (32%). On the basis of Fisher's exact tests, we conclude that the shell and core neural groups of the AVCN are significantly different regarding all of the following physiological characteristics: SR, maximum driven rate, threshold and dynamic range to tones and noise, frequency response area, PSTH type, latency, and EIA type. Wide dynamic ranges of the well-driven shell units suggest that they may play a role in encoding absolute intensity of acoustic stimulus.

Acoustic Stimulation↗
PubMed1996

Amplitude and time course of spontaneous and evoked excitatory postsynaptic currents in bushy cells of the anteroventral cochlear nucleus.

1. Spontaneous and evoked excitatory postsynaptic currents (EPSCs) were recorded in slices of the rat anteroventral cochlear nucleus (AVCN) at the endbulb-bushy cell synaptic connection. 2. The amplitudes of alpha-amino-3-hydroxy-5-methy-4-isoxa-zolepropionic acid (AMPA)-receptor-mediated spontaneous EPSCs were large (54 +/- 6 pA, mean +/- SD; membrane potential = -70 mV, 22-25 degrees C) and, in the same cell, exhibited a very wide range of peak amplitudes (CM = 0.42 +/- 0.01, n - 15 cells). There was no significant correlation between rise times or decay time constants and the peak amplitudes of spontaneous EPSCs recorded in the same cell, demonstrating that electrotonic attenuation is not responsible for the large amplitude variability of spontaneous EPSCs. 3. Cyclothiazide, a potent blocker of AMPA-receptor desensitization, did not affect the amplitude of spontaneous EPSCs in AVCN bushy cells, suggesting that background desensitization of AMPA receptors is not significant in these cells. However, the decay time constant of spontaneous EPSCs was prolonged significantly (2.6-fold increase). In addition, cyclothiazide produced a marked increase (approximately 40%, n = 6 cells) in the frequency of spontaneous EPSCs, indicating a likely presynaptic site of action of this drug. 4. Cyclothiazide produced a small increase (approximately 10%, n = 7 cells) in the peak amplitude of the evoked endbulb EPSC, but this effect could be explained by the action of cyclothiazide to increase the decay time constant of the underlying quantal EPSCs in conjunction with the asynchrony of quantal transmitter release at the endbulb synapse. 5. These results indicate that neither electrotonic attenuation nor receptor desensitization are responsible for the wide range of peak amplitudes of spontaneous EPSCs in bushy cells. The large quantal variability therefore is likely to be due entirely to intrinsic fluctuations at each release site and site-to-site variability in the numbers of available receptors.

Animals↗
PubMed1998

Activity-dependent regulation of [Ca2+]i in avian cochlear nucleus neurons: roles of protein kinases A and C and relation to cell death.

Neurons of the cochlear nucleus, nucleus magnocellularis (NM), of young chicks require excitatory afferent input from the eighth nerve for maintenance and survival. One of the earliest changes seen in NM neurons after deafferentation is an increase in intracellular calcium concentration ([Ca2+]i). This increase in [Ca2+]i is due to loss of activation of metabotropic glutamate receptors (mGluR) that activate second-messenger cascades involved in [Ca2+]i regulation. Because mGluRs are known to act via the phospholipase C and adenylate cyclase signal transduction pathways, the goal of this study was to determine the roles of protein kinases A (PKA) and C (PKC) activities in the regulation of NM neuron [Ca2+]i by eighth nerve stimulation. Additionally, we sought to determine the relationship between increased [Ca2+]i and cell death as measured by propidium iodide incorporation. [Ca2+]i of individual NM neurons in brain stem slices was monitored using fura-2 ratiometric fluorescence imaging. NM field potentials were monitored in experiments in which the eighth nerve was stimulated. Five hertz orthodromic stimulation maintained NM neuron [Ca2+]i at approximately 110 nM for 180 min. In the absence of stimulation, NM neuron [Ca2+]i increased steadily to a mean of 265 nM by 120 min. This increase was attenuated by superfusion of PKC activators phorbol-12,13-myristate acetate (100 nM) or dioctanoylglycerol (50 microM) and by activators of PKA: 1 mM 8-bromoadenosine-3',5'-cyclophosphate sodium (8-Br-cAMP), 50 microM forskolin or 100 microM Sp-adenosine 3',5'-cyclic monophosphothioate triethylamine. Inhibition of PKA (100 microM Rp-cAMPS) or PKC (50 nM bisindolymaleimide or 10 microM U73122) during continuous orthodromic stimulation resulted in an increase in NM neuron [Ca2+]i that exceeded 170 and 180 nM, respectively, by 120 min. Nonspecific kinase inhibition with 1 microM staurosporine during stimulation resulted in an [Ca2+]i increase that was greater in magnitude than that seen with either PKA or PKC inhibition alone, equal to that seen in the absence of stimulation, but much smaller than that seen with inhibition of mGluRs. In addition, manipulations that resulted in a [Ca2+]i increase >/=250 nM resulted in an increase in number and percentage of propidium iodide-labeled NM neurons. These results suggest that eighth nerve activity maintains [Ca2+]i of NM neurons at physiological levels in part via mGluR-mediated activation of PKA and PKC and that increases in [Ca2+]i due to activity deprivation or interruption of the PKA and PKC [Ca2+]i regulatory mechanisms are predictive of subsequent cell death.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Central projections of auditory-nerve fibers of differing spontaneous rate. I. Anteroventral cochlear nucleus.

Auditory nerve fibers have been subdivided into three functional groups (Liberman, M.C. [1978] J. Acoust. Soc. Am. 63:442-455) differing in acoustic sensitivity and spontaneous discharge rate (SR). Using intracellular injection of horseradish peroxidase, the present study analyzes the projections of these three neuronal subclasses to the various subdivisions of the anteroventral cochlear nucleus (AVCN) and to the different cell types found therein. The average number of swellings and number of cells contacted decreased from low- to medium- to high-SR groups. However, these differences in terminal elaboration were not evenly distributed throughout the AVCN. The small cell cap was almost exclusively innervated by low- and medium-SR fibers, i.e., those with the highest acoustic thresholds. Within anterior AVCN, spherical-cell innervation was seen from all SR groups, whereas almost all multipolar cell innervation was from low- and medium-SR fibers. In the posterior AVCN, multipolar-cell innervation was equally likely from all SR groups, whereas globular cells were preferentially contacted by high-SR fibers. These SR-based trends in cochlear nucleus innervation help explain some of the known physiological properties of cell-types in each subdivision. They also suggest that additional physiological study of the small cell cap may be key in elucidating the functional significance of the low-SR population.

Action Potentials↗
PubMed2005

Role of cochlear integrity in cochlear nucleus glucose metabolism and neuron number after cochlea removal in aging broiler chickens.

In the chicken auditory system, cochlear nucleus (nucleus magnocellularis, NM) neurons receive their only excitatory input from the ipsilateral cochlea. Cochlea removal (CR) results in an immediate decrease in NM neuron electrical activity, followed by death of approximately 30% of NM neurons. Previous work showed a decrease in NM activity and subsequent loss of NM neurons in all chicks. Egg layer adults showed NM neuron loss after CR, while neuron number remained stable in broiler adults. This suggested that effects of CR on NM were age- and breed-dependent. We now know that most aging egg layer chickens maintain largely normal cochleae throughout adulthood. Some exhibit cochlear damage with age. The converse is true of broiler chickens. Most aging broiler chickens display cochlear degeneration, with some maintaining normal cochlear anatomy throughout adulthood. The presence of extensive cochlear damage may alter the effect of CR on NM, leading to the described differences. Here, we examine the effect of unilateral CR on NM glucose metabolism and neuron number in 2, 30, 39, and 52 week-old broiler chickens found to have normal cochleae. Chickens with damaged cochleae were excluded. Using 2-deoxyglucose uptake to evaluate bilateral NM glucose metabolism, we found significantly decreased uptake ipsilateral to CR at each age examined. Bilateral cell counts revealed significant neuron loss ipsilateral to CR at each age examined. This suggests that NM glucose metabolism decreases and subsequent neuron death occurs in aging broiler chickens when a normal cochlea is removed. The status of the cochlea must play a role in the effect of deafferentation on NM glucose metabolism and neuron survival. The effect of CR appears to be dependent upon neither age nor breed, but upon cochlear integrity instead.

Aging↗