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D Oertel

Publications and source records attributed to D Oertel.

At least 19 recordsLinked to original sources
PubMed2001

Cholinergic modulation of stellate cells in the mammalian ventral cochlear nucleus.

The main source of excitation to the ventral cochlear nucleus (VCN) is from glutamatergic auditory nerve afferents, but the VCN is also innervated by two groups of cholinergic efferents from the ventral nucleus of the trapezoid body. One arises from collaterals of medial olivocochlear efferents, and the other arises from neurons that project solely to the VCN. This study examines the action of cholinergic inputs on stellate cells in the VCN. T stellate cells, which form one of the ascending auditory pathways to the inferior colliculus, and D stellate cells, which inhibit T stellate cells, are distinguished electrophysiologically. Whole-cell recordings from stellate cells in slices of the VCN of mice demonstrate that most T stellate cells are excited by cholinergic agonists through three types of receptors, whereas all D stellate cells tested were insensitive to cholinergic agonists. Nicotinic excitation in T stellate cells has two components. The faster component was blocked by alpha-bungarotoxin and methyllycaconitine, suggesting that receptors contained alpha7 subunits; the slower component was insensitive to both. Muscarinic receptors excite T stellate cells by blocking a voltage-insensitive, "leak" potassium conductance. Our results suggest that cholinergic efferent innervation enhances excitation by sounds of T stellate cells, opposing the inhibitory action of cholinergic innervation in the cochlea that is conveyed indirectly through the glutamatergic afferents. The inhibitory action of D stellate cells on their targets is probably not affected by cholinergic inputs. Excitation of T stellate cells by cholinergic efferents would be expected to enhance the encoding of spectral peaks in noise.

Acetylcholine↗
PubMed2001

Correlation of AMPA receptor subunit composition with synaptic input in the mammalian cochlear nuclei.

The composition of AMPA receptors in patches excised from somata and dendrites of six cell types in the mammalian cochlear nuclei was probed and compared electrophysiologically and pharmacologically with the rapid application of glutamate. Cells excited predominantly by auditory nerve fibers had AMPA receptors with exceptionally rapid gating (submillisecond deactivation and desensitization time constants). The nonlinear current-voltage relationship in the presence of spermine showed that few of these receptors had GluR2 subunits, and the insensitivity of desensitization to cyclothiazide indicated that they contained mostly flop splice variants. At synapses made by parallel fibers, AMPA receptors were slowly gating (time constants of deactivation and desensitization >1 msec) and contained higher levels of GluR2 and flip isoforms. However, receptors at auditory nerve synapses on cells that also receive parallel fiber input, the fusiform cells, had intermediate properties with respect to kinetics and contained GluR2 and flip isoforms. Given the diverse biophysical properties, patterns of innervation, patterns of electrical activity, and targets of each cell type in vivo, these data indicate that the kinetics and permeation properties of AMPA receptors are linked to factors associated with synaptic connectivity.

Alternative Splicing↗
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

Detection of synchrony in the activity of auditory nerve fibers by octopus cells of the mammalian cochlear nucleus.

The anatomical and biophysical specializations of octopus cells allow them to detect the coincident firing of groups of auditory nerve fibers and to convey the precise timing of that coincidence to their targets. Octopus cells occupy a sharply defined region of the most caudal and dorsal part of the mammalian ventral cochlear nucleus. The dendrites of octopus cells cross the bundle of auditory nerve fibers just proximal to where the fibers leave the ventral and enter the dorsal cochlear nucleus, each octopus cell spanning about one-third of the tonotopic array. Octopus cells are excited by auditory nerve fibers through the activation of rapid, calcium-permeable, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate receptors. Synaptic responses are shaped by the unusual biophysical characteristics of octopus cells. Octopus cells have very low input resistances (about 7 M Omega), and short time constants (about 200 microsec) as a consequence of the activation at rest of a hyperpolarization-activated mixed-cation conductance and a low-threshold, depolarization-activated potassium conductance. The low input resistance causes rapid synaptic currents to generate rapid and small synaptic potentials. Summation of small synaptic potentials from many fibers is required to bring an octopus cell to threshold. Not only does the low input resistance make individual excitatory postsynaptic potentials brief so that they must be generated within 1 msec to sum but also the voltage-sensitive conductances of octopus cells prevent firing if the activation of auditory nerve inputs is not sufficiently synchronous and depolarization is not sufficiently rapid. In vivo in cats, octopus cells can fire rapidly and respond with exceptionally well-timed action potentials to periodic, broadband sounds such as clicks. Thus both the anatomical specializations and the biophysical specializations make octopus cells detectors of the coincident firing of their auditory nerve fiber inputs.

Acoustic Stimulation↗
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↗
PubMed1999

Time course and permeation of synaptic AMPA receptors in cochlear nuclear neurons correlate with input.

AMPA receptors mediate rapid glutamatergic synaptic transmission. In the mammalian cochlear nuclei, neurons receive excitatory input from either auditory nerve fibers, parallel fibers, or both fiber systems. The functional correlates of differences in the source of input were examined by recording AMPA receptor-mediated, miniature EPSCs (mEPSCs) in whole-cell voltage-clamp mode from identified neurons. Bushy, octopus, and T-stellate cells of the ventral cochlear nucleus (VCN) and tuberculoventral cells of the dorsal cochlear nucleus (DCN) receive most of their excitatory input from the auditory nerve; fusiform cells receive excitatory inputs from both the auditory nerve and parallel fibers; cartwheel cells receive excitatory input from parallel fibers alone. mEPSCs from bushy, octopus, T-stellate, and tuberculoventral cells had significantly faster decay time constants (0.35-0.40 msec) than did those from fusiform and cartwheel cells (1.32-1.79 msec). Some fusiform cells had two populations of mEPSCs with distinct time courses. mEPSCs in cells with auditory nerve input alone were inhibited by philanthotoxin, a blocker of calcium-permeable AMPA receptors, whereas mEPSCs in cells with parallel fiber input were not. Thus AMPA receptors postsynaptic to the auditory nerve differ from those postsynaptic to parallel fibers both in channel-gating kinetics and in their permeability to calcium. These results confirm the conclusion that synaptic AMPA receptors are specialized according to the source of input (Hunter et al., 1993; Rubio and Wenthold, 1997; Wang et al., 1998).

Animals↗
PubMed1999

Role of intrinsic conductances underlying responses to transients in octopus cells of the cochlear nucleus.

Recognition of acoustic patterns in natural sounds depends on the transmission of temporal information. Octopus cells of the mammalian ventral cochlear nucleus form a pathway that encodes the timing of firing of groups of auditory nerve fibers with exceptional precision. Whole-cell patch recordings from octopus cells were used to examine how the brevity and precision of firing are shaped by intrinsic conductances. Octopus cells responded to steps of current with small, rapid voltage changes. Input resistances and membrane time constants averaged 2.4 MOmega and 210 microseconds, respectively (n = 15). As a result of the low input resistances of octopus cells, action potential initiation required currents of at least 2 nA for their generation and never occurred repetitively. Backpropagated action potentials recorded at the soma were small (10-30 mV), brief (0.24-0.54 msec), and tetrodotoxin-sensitive. The low input resistance arose in part from an inwardly rectifying mixed cationic conductance blocked by cesium and potassium conductances blocked by 4-aminopyridine (4-AP). Conductances blocked by 4-AP also contributed to the repolarization of the action potentials and suppressed the generation of calcium spikes. In the face of the high membrane conductance of octopus cells, sodium and calcium conductances amplified depolarizations produced by intracellular current injection over a time course similar to that of EPSPs. We suggest that this transient amplification works in concert with the shunting influence of potassium and mixed cationic conductances to enhance the encoding of the onset of synchronous auditory nerve fiber activity.

4-Aminopyridine↗
PubMed1999

The role of timing in the brain stem auditory nuclei of vertebrates.

Vertebrate animals gain biologically important information from environmental sounds. Localization of sound sources enables animals to detect and respond appropriately to danger, and it allows predators to detect and localize prey. In many species, rapidly fluctuating sounds are also the basis of communication between conspecifics. This information is not provided directly by the output of the ear but requires processing of the temporal pattern of firing in the tonotopic array of auditory nerve fibers. The auditory nerve feeds information through several parallel ascending pathways. Anatomical and electrophysiological specializations for conveying precise timing, including calyceal synaptic terminals and matching axonal conduction times, are evident in several of the major ascending auditory pathways through the ventral cochlear nucleus and its nonmammalian homologues. One pathway that is shared by all higher vertebrates makes an ongoing comparison of interaural phase for the localization of sound in the azimuth. Another pathway is specifically associated with higher frequency hearing in mammals and is thought to make use of interaural intensity differences for localizing high-frequency sounds. Balancing excitation from one ear with inhibition from the other in rapidly fluctuating signals requires that the timing of these synaptic inputs be matched and constant for widely varying sound stimuli in this pathway. The monaural nuclei of the lateral lemniscus, whose roles are not understood (although they are ubiquitous in higher vertebrates), receive input from multiple pathways that encode timing with precision, some through calyceal endings.

Animals↗
PubMed1998

Golgi cells in the superficial granule cell domain overlying the ventral cochlear nucleus: morphology and electrophysiology in slices.

Golgi cells are poised to integrate multimodal influences by participating in circuits involving granule cells in the cochlear nuclei. To understand their physiological role, intracellular recordings were made from anatomically identified Golgi cells in slices of the cochlear nuclei from mice. Cell bodies, dendrites, and terminals for all seven labeled cells were restricted to the narrow plane of the superficial granule cell domain over the ventral cochlear nucleus. The axonal arborization was the most striking feature of all Golgi cells; a dense plexus of terminals covered an area 200-400 microm in diameter in the vicinity of the cell body and dendrites. Axonal beads often surrounded granule cell bodies, indicating that granule cells are probable targets. Cells had input resistances up to 130 M omega and fired regular, overshooting action potentials. Golgi cells probably receive auditory nerve input, because shocks to the cut end of the auditory nerve excited Golgi cells with excitatory postsynaptic potentials (EPSPs). The latency of EPSPs shortened to a minimum and the amplitude of EPSPs grew in several steps as the strength of shocks was increased. The minimum latency of EPSPs in Golgi cells was on average 1.3 milliseconds, 0.6 milliseconds longer than the minimum latencies of EPSPs in nearby octopus and T stellate cells. The long latency raises the possibility that Golgi cells receive input from slowly conducting, unmyelinated auditory nerve fibers. Golgi cells are also excited by interneurons with N-methyl-D-aspartate receptors, probably granule cells, because repetitive shocks and single shocks in the absence of extracellular Mg2+ evoked late EPSPs that were reversibly blocked by DL-2-amino-5-phosphono-valeric acid.

Animals↗
PubMed1998

Synaptic inputs to stellate cells in the ventral cochlear nucleus.

Auditory information is carried from the cochlear nuclei to the inferior colliculi through six parallel ascending pathways, one of which is through stellate cells of the ventral cochlear nuclei (VCN) through the trapezoid body. To characterize and identify the synaptic influences on T stellate cells, intracellular recordings were made from anatomically identified stellate cells in parasagittal slices of murine cochlear nuclei. Shocks to the auditory nerve consistently evoked five types of synaptic responses in T stellate cells, which reflect sources intrinsic to the cochlear nuclear complex. 1) Monosynaptic excitatory postsynaptic potentials (EPSPs) that were blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX), an antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, probably reflected activation by auditory nerve fibers. Electrophysiological estimates indicate that about five auditory nerve fibers converge on one T stellate cell. 2) Disynaptic, glycinergic inhibitory postsynaptic potentials (IPSPs) arise through inhibitory interneurons in the VCN or in the dorsal cochlear nucleus (DCN). 3) Slow depolarizations, the source of which has not been identified, that lasted between 0.2 and 1 s and were blocked by -2-amino-5-phosphonovaleric acid (APV), the N-methyl-D-aspartate (NMDA) receptor antagonist. 4) Rapid, late glutamatergic EPSPs are polysynaptic and may arise from other T stellate cells. 5) Trains of late glycinergic IPSPs after single or repetitive shocks match the responses of D stellate cells, showing that D stellate cells are one source of glycinergic inhibition to T stellate cells. The source of late, polysynaptic EPSPs and IPSPs was assessed electrophysiologically and pharmacologically. Late synaptic responses in T stellate cells were enhanced by repetitive stimulation, indicating that the interneurons from which they arose should fire trains of action potentials in responses to trains of shocks. Late EPSPs and late IPSPs were blocked by APV and enhanced by the removal of Mg2+, indicating that the interneurons were driven at least in part through NMDA receptors. Bicuculline, a gamma-aminobutyric acid-A (GABAA) receptor antagonist, enhanced the late PSPs, indicating that GABAergic inhibition suppresses both the glycinergic interneurons responsible for the trains of IPSPs in T-stellate cells and the interneuron responsible for late EPSPs in T stellate cells. The glycinergic interneurons that mediate the series of IPSPs are intrinsic to the ventral cochlear nucleus because long series of IPSPs were recorded from T stellate cells in slices in which the DCN was removed. These experiments indicate that T stellate cells are a potential source of late EPSPs and that D stellate cells are a potential source for trains of late IPSPs.

Action Potentials↗
PubMed1997

Physiological identification of the targets of cartwheel cells in the dorsal cochlear nucleus.

The integrative contribution of cartwheel cells of the dorsal cochlear nucleus (DCN) was assessed with intracellular recordings from anatomically identified cells. Recordings were made, in slices of the cochlear nuclei of mice, from 58 cartwheel cells, 22 fusiform cells, 3 giant cells, 5 tuberculoventral cells, and 1 cell that is either a superficial stellate or Golgi cell. Cartwheel cells can be distinguished electrophysiologically from other cells of the cochlear nuclei by their complex spikes, which comprised two to four rapid action potentials superimposed on a slower depolarization. The rapid action potentials were blocked by tetrodotoxin (n = 17) and were therefore mediated by voltage-sensitive sodium currents. The slow spikes were eliminated by the removal of calcium from the extracellular saline (n = 3) and thus were mediated by voltage-sensitive calcium currents. The spontaneous and evoked firing patterns of cartwheel cells were distinctive. Cartwheel cells usually fired single and complex spikes spontaneously at irregular intervals of between 100 ms and several seconds. Shocks to the DCN elicited firing that lasted tens to hundreds of milliseconds. With the use of these distinctive firing patterns, together with a pharmacological dissection of postsynaptic potentials (PSPs), possible targets of cartwheel cells were identified and the function of the connections was examined. Not only cartwheel and fusiform cells, but also giant cells, received patterns of synaptic input consistent with their having originated from cartwheel cells. These cell types responded to shocks of the DCN with variable trains of PSPs that lasted hundreds of milliseconds. PSPs within these trains appeared both singly and in bursts of two to four, and were blocked by 0.5 or 1 microM strychnine (n = 4 cartwheel, 4 fusiform, and 2 giant cells), indicating that cartwheel cells are likely to be glycinergic. In contrast with cartwheel cells, which are weakly excited by glycinergic input, glycinergic PSPs consistently inhibited fusiform and giant cells. Tuberculoventral cells and the putative superficial stellate cell received little or no spontaneous synaptic activity. Shocks to the DCN evoked synaptic activity that lasted approximately 5 ms. These cells therefore probably do not receive input from cartwheel cells. In addition, the brief firing of tuberculoventral cells and of the putative superficial stellate cell in response to shocks indicates that these cells are unlikely to contribute to the late, glycinergic synaptic potentials observed in cartwheel, fusiform, and giant cells.

Action Potentials↗
PubMed1996

Context-dependent synaptic action of glycinergic and GABAergic inputs in the dorsal cochlear nucleus.

Cartwheel cells are prominent interneurons in the dorsal cochlear nucleus (DCN) that bear considerable homology to cerebellar Purkinje cells. They contact other cartwheel cells as well as fusiform cells, the principal cells of the DCN. In fusiform cells, the inhibition from cartwheel cells interacts with excitation mediated by granule cells and auditory nerve fibers, and shapes the output of the DCN in its ascent to the inferior colliculi. With intracellular recordings from anatomically identified cells in slices, synaptic inputs to fusiform and cartwheel cells were analyzed pharmacologically. Shocks to the auditory nerve and granule cell domains evoked glutamatergic, glycinergic, and GABA(A)ergic postsynaptic potentials (PSPs) in both cartwheel and fusiform cells. The temporal patterns of spontaneous and evoked glycinergic PSPs in fusiform and cartwheel cells were similar and mirrored the pattern of firing of cartwheel cells, probably reflecting the anatomical connections between these cell types and supporting the conclusion that cartwheel cells are glycinergic. In fusiform cells, glycinergic and GABA(A)ergic IPSPs evoked with shocks reversed at -68 mV on average. In marked contrast, glycinergic and GABA(A)ergic PSPs in cartwheel cells, as well as responses to exogenous application of 50-100 mM glycine or 100 microns muscimol, were depolarizing. Reversal potentials of PSPs and responses to glycine and muscimol were similar and averaged -52 mV. Glycinergic and GABA(A)ergic PSPs could elicit firing from cartwheel cells at their resting potentials, but could also reduce rapid firing during strong depolarizations. Thus, the action of glycinergic and GABA(A)ergic inputs on cartwheel cells depends on the electrophysiological context in which they occur.

2-Amino-5-phosphonovalerate↗
PubMed1995

Recordings from slices indicate that octopus cells of the cochlear nucleus detect coincident firing of auditory nerve fibers with temporal precision.

Acoustic information in auditory nerve discharges is integrated in the cochlear nuclei, and ascends through several parallel pathways to higher centers. Octopus cells of the posteroventral cochlear nucleus form a pathway known to carry information in the timing of action potentials. Octopus cells have dendrites oriented to receive converging input from many auditory nerve fibers. In all 34 intracellular recordings from anatomically identified octopus cells in slices, shocks to the auditory nerve evoked brief, consistent, graded EPSPs. EPSPs were about 1 msec in duration. At all but the lowest shock strengths, the delays between shocks and the peaks of resultant EPSPs had SDs of 0.02 msec. Polysynaptic excitation, perhaps arising from the axon collaterals of octopus cells, was observed. No detectable glycinergic or GABAergic inhibition was evoked with shocks. The input resistances were low, around 10 M omega, voltage changes were rapid, with time constants of about 1 msec, and action potentials were small. The low input resistance resulted in part from a Cs(+)-sensitive conductance. In the presence of 10 or 15 mM extracellular Cs+ the time constants increased 20-fold in the hyperpolarizing voltage range. As several subthreshold inputs were required to produce suprathreshold responses, octopus cells detect the coincident firing of auditory nerve fibers. Under physiological conditions the low input resistance and resulting short time constant limit the time over which temporal summation of excitation from auditory nerve fibers can occur and thus provide temporal precision to electrical signaling.

Action Potentials↗
PubMed1994

In vitro modulation of somatic glycine-like immunoreactivity in presumed glycinergic neurons.

Previous studies indicate that tuberculoventral and cartwheel cells in the dorsal cochlear nucleus as well as a group of stellate cells in the ventral cochlear nucleus are likely to be glycinergic. To test whether these neurons contain higher levels of free glycine than cells that are probably not glycinergic, immunocytochemical studies with antibodies against glycine conjugates were undertaken on slices of the murine cochlear nuclear complex. Present results show that the cell bodies of all three groups of neurons are immunolabeled. However, the somatic labeling of the tuberculoventral and cartwheel cells can be modulated by experimental conditions. In slices fixed immediately after cutting, many cell bodies in the deep layer of the dorsal cochlear nucleus (DCN), presumably tuberculoventral neurons, are labeled. As a slice is incubated in vitro, cell bodies in the deep layer of the DCN lose their glycine-like immunoreactivity. After 7 hours in vitro, labeled cells are absent in the deep DCN, but the immunoreactivity can be regained by electrically stimulating the auditory nerve for 20 minutes. The loss of immunoreactivity is prevented by electrical stimulation, by axotomy, and by inclusion of 0.8 microM tetrodotoxin, or 1 microM strychnine, or 50 microM colchicine or 50 microM beta-lumicolchicine in the bathing saline. Cartwheel cells retain their immunoreactivity during incubation in vitro without electrical stimulation, but lose it under two conditions. One is following a cut across the ventral cochlear nucleus (VCN) that severs most of their granule cell input, and the other is the inclusion of tetrodotoxin in the bathing saline. The labeling of cell bodies in the ventral cochlear nucleus and of puncta and processes is not changed by any of these experimental manipulations.

Animals↗
PubMed1994

Neuronal circuits associated with the output of the dorsal cochlear nucleus through fusiform cells.

1. Intracellular recordings were made from 21 anatomically identified fusiform cells in the dorsal cochlear nucleus (DCN) of mice in slices. The aim of the experiments was to dissect the synaptic responses to shocks of the auditory nerve to correlate functional characteristics with the different classes of synaptic inputs. 2. When depolarized from rest (-57 +/- 5 mV) with current pulses, fusiform cells fired regular, overshooting action potentials that were followed by two undershoots. The frequency of firing increased with the strength of injected current by between 100 and 300 spikes/s/nA. The current-voltage relationship rectified between 10 and 15 mV below the resting potential. The slopes of current-voltage relationships of fusiform cells in the range between the resting potential and 10 mV hyperpolarization indicated an average input resistance of 86 +/- 37 M omega. 3. In each of the labeled fusiform cells frequent, spontaneous inhibitory postsynaptic potentials (IPSPs) were recorded singly or in bursts. Some, but not all, IPSPs were preceded by a slowly rising excitatory postsynaptic potential (EPSP). The temporal association of spontaneous EPSPs and IPSPs suggests that they are driven by a common source, possibly granule cells. 4. Shocks to the auditory nerve evoked synaptic responses consisting of early (1 to approximately 10 ms) and late (approximately 10 to 100 ms) components. 6,7-Dinitroquinoxaline-2,3-dione (DNQX) at 20 to 40 microM eliminated all detectable excitation and all late IPSPs. Late bursts of IPSPs, therefore, are mediated through a polysynaptic pathway that includes a DNQX-sensitive stage. Strong shocks to the nerve root elicited single monosynaptic IPSPs, indicating that inhibitory interneurons have processes close to the auditory nerve. Strychnine at 0.5 microM eliminated all detectable inhibition. 6. Cuts through the posteroventral cochlear nucleus (PVCN), which severed the descending branches of auditory nerve fibers, eliminated early EPSPs and IPSPs leaving late, slowly rising EPSPs and bursts of IPSPs in responses to shocks of the auditory nerve. Late, slowly rising EPSPs and bursts of IPSPs, as well as monosynaptic IPSPs, could also be evoked by stimulating the anteroventral cochlear nucleus (AVCN). 7. Focal applications of glutamate evoked excitation and inhibition from many parts of a slice, with patterns varying among cells, indicating that fusiform cells receive inputs through several groups of interneurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Cartwheel and superficial stellate cells of the dorsal cochlear nucleus of mice: intracellular recordings in slices.

1. Intracellular recordings were made from identified cartwheel and stellate cells in the molecular and fusiform cell layers of the murine dorsal cochlear nucleus (DCN). The aim of the study was to identify and characterize their synaptic inputs and to learn how synaptic inputs and intrinsic electrical properties interact to generate firing patterns. 2. Eight cells labeled by the intracellular injection of biocytin were cartwheel cells. Their axon terminals extended from the deep part of the molecular layer through the fusiform cell layer. Their dendrites extended through the molecular layer and had spines. Both the dendritic and axonal arbors were small, having diameters of approximately 150 microns in the parasagittal plane. 3. When depolarized, cartwheel cells often fired bursts of rapid action potentials superimposed on a slow depolarization. The peaks of action potentials were usually overshooting. Individually occurring action potentials were followed by two afterhyperpolarizations, as in other cells of the DCN. During bursts, action potentials did not have two distinct repolarizing phases. 4. Excitatory postsynaptic potentials (EPSPs) were recorded from cartwheel cells spontaneously and after shocks to the nerve root or to the ventral cochlear nucleus (VCN). The EPSPs rose slowly. When they were suprathreshold they evoked action potentials singly or in bursts. EPSPs evoked by shocks to the nerve root or to the VCN had long latencies, the rise of EPSPs beginning between 5 and 10 ms after the shock. No inhibitory synaptic potentials, either spontaneous or driven with electrical stimulation, were detected in cells whose resting potentials were between -50 and -70 mV. 5. The locations from which excitatory input can be driven electrically are consistent with cartwheel cells receiving excitatory synaptic input from granule cells. 6. One labeled cell was a superficial stellate cell. It had smooth, straight dendrites that radiated parallel to the layers of the DCN; its axonal arbor was also planar and was restricted to the molecular layer. Both the dendritic and axonal arbors of this stellate cell were large, > 500 microns diam in the parasagittal plane. 7. The superficial stellate cell fired trains of action potentials at regular intervals that, like other cells of the DCN, were overshooting and were followed by double undershoots. 8. Shocks to the nerve root and to the surface of the VCN evoked EPSPs after 3.5 and 2 ms, respectively, in the superficial stellate cell. Chemical stimulation of the VCN also evoked excitation. No inhibitory synaptic input, spontaneous or driven, was detected.

Animals↗
PubMed1993

Giant cells of the dorsal cochlear nucleus of mice: intracellular recordings in slices.

1. In slices of the murine cochlear nuclear complex, intracellular recordings were made from five giant cells that were identified by intracellular labeling with biocytin. Giant cells form one of the two output pathways of the dorsal cochlear nucleus (DCN). Understanding how neuronal circuits and intrinsic electrical properties interact to control the firing of giant cells is a step toward understanding what acoustic information is conveyed through these cells. 2. Cell bodies of the labeled giant cells lay in the deep layer of the DCN. Dendrites, widespread both along the isofrequency axis and along the tonotopic axis, occupied mainly the deep layer, but some distal ends strayed into the molecular layer. Axons of giant cells were large, varying between 1 and 2 microns diam, and left through the dorsal acoustic stria. They were not observed to branch in the cochlear nuclei. 3. Giant cells fired large, overshooting action potentials that were followed by two afterhyperpolarizations. The first brought the membrane potential below rest, independent of the strength of injected current. The more variable second one produced either an undershoot or an inflection in the membrane potential between action potentials. 4. In each of the five labeled giant cells, shocks to the nerve root or to the anteroventral cochlear nucleus (AVCN) evoked a monosynaptic excitatory postsynaptic potential and two tandem inhibitory postsynaptic potentials (IPSPs) in the first 10 ms. Later IPSPs followed after latencies of between 10 and 50 ms. Monosynaptic excitation was usually cut short by the inhibition. 5. Strychnine, at 1 microM, blocked all IPSPs in the one giant cell tested, indicating that inhibitory input to this giant cell from circuits intrinsic to the cochlear nuclear complex was glycinergic. 6. The location of afferents was mapped for two giant cells. Both excitatory and inhibitory inputs to giant cells could be driven by the local application of glutamate to many loci in the AVCN and posteroventral cochlear nucleus, indicating that the ventral cochlear nucleus VCN contains interneurons that are monosynaptically or polysynaptically connected to giant cells. 7. An interpretation consistent with the results is that giant cells are excited by auditory nerve fibers and are inhibited by tuberculoventral cells. Giant cells may also be excited by granule or T stellate cells.

Animals↗