bluuebunny/crossref_metadata_2025 huggingface dataset:
Intracellular Activity of Motoneurons of the Rostral Nucleus Ambiguus During Swallowing in Sheep
Authors: Zoungrana Ouinlassida R. , Amri Mohamed , Car Alexandre , Roman Claude
Published: December 2017

Zoungrana, Ouinlassida R., Mohamed Amri, Alexandre Car, and Claude Roman. Intracellular activity of motoneurons of the rostral nucleus ambiguus during swallowing in sheep. J. Neurophysiol. 77: 909–922, 1997. The nervous mechanisms that generate swallowing are still largely unknown. It has been suggested that a central pattern generator that contains a serial network of linked neurons must produce the successive excitation of motoneurons (Mns) and then the sequential activation of muscle through excitatory connections. Inhibitory connections have also been envisioned but never evidenced at the membrane level of the swallowing neurons. We investigated, by intracellular recordings, the behavior of 96 Mns in the rostral nucleus ambiguus during swallowing induced by application of superior laryngeal nerve stimulation to anesthetized sheep. The Mns were identified by antidromic activation following stimulation of glossopharyngeal, pharyngoesophageal, or cervical vagal nerves. Nine Mns showed a bell-shaped depolarization during the buccal or the early pharyngeal stage of swallowing. They probably projected to muscles of the soft palate (palatopharyngeal) and upper pharynx (stylopharyngeal, hyopharyngeal). Thirty-eight Mns exhibited a chloride-dependent hyperpolarization, indicating that they were under an active inhibition throughout the buccopharyngeal stage of swallowing. These Mns constitute a heterogeneous pool: some of them, producing spontaneous inspiratory discharges, probably innervated laryngeal or pharyngeal muscles; others might also be Mns of the esophagus, whose swallowing pattern was modified because of the anesthesia (suppression of the esophageal peristalsis). Forty-nine Mns showed a chloride-dependent hyperpolarization with a variable duration at the onset of swallowing, followed by a depolarization that could take place during either the buccopharyngeal (HD1-Mns) or the esophageal (HD2- and HD3-Mns) stage of deglutition. HD1-Mns probably projected to the median and inferior constrictors of the pharynx. HD2-Mns produced depolarizations with longer latencies and durations than those of the HD1-Mns. They probably projected to either the superior esophageal sphincter or the cervical esophagus (CE). HD3-Mns showed a buccopharyngeal hyperpolarization that was followed first by a lower-amplitude hyperpolarization accompanying the proximal CE contraction and then by a delayed depolarization. These Mns probably innervated the inferior CE or thoracic esophagus. We conclude that the initial inhibition exerted on the HD-Mns, by delaying the excitation of Mns, may play a role in the nervous mechanisms involved in temporal organization of the swallowing motor sequence. We suggest that swallowing disorders in humans such as dysphagia by failure of cricopharyngeal relaxation, diffuse esophageal spasm, and achalasia might be caused by impaired inhibitory mechanisms.
Eye Position Effects in Monkey Cortex. I. Visual and Pursuit-Related Activity in Extrastriate Areas MT and MST
Authors: Bremmer F. , Ilg U. J. , Thiele A. , Distler C. , Hoffmann K.-P.
Published: December 2017

Bremmer, F., U. J. Ilg, A. Thiele, C. Distler, and K.-P. Hoffmann. Eye position effects in monkey cortex. I. Visual and pursuit-related activity in extrastriate areas MT and MST. J. Neurophysiol. 77: 944–961, 1997. We studied the effect of eye position on visual and pursuit-related activity in neurons in the superior temporal sulcus of the macaque monkey. Altogether, 109 neurons from the middle temporal area (area MT) and the medial superior temporal area (area MST) were tested for influence of eye position on their stimulus-driven response in a fixation paradigm. In this paradigm the monitored eye position signal was superimposed onto the stimulus control signal while the monkey fixated at different locations on a screen. This setup guaranteed that an optimized stimulus was moved across the receptive field at the same retinal location for all fixation locations. For 61% of the MT neurons and 82% of the MST neurons the stimulus-induced response was modulated by the position of the eyes in the orbit. Directional selectivity was not influenced by eye position. One hundred sixty-eight neurons exhibited direction-specific responses during smooth tracking eye movements and were tested in a pursuit paradigm. Here the monkey had to track a target that started to move in the preferred direction with constant speed from five different locations on the screen in random order. Pursuit-related activity was modulated by eye position in 78% of the MT neurons as well as in 80% of the MST neurons tested. Neuronal activity varied linearly as a function of both horizontal and vertical eye position for most of the neurons tested in both areas, i.e., two-dimensional regression planes could be approximated to the responses of most of the neurons. The directions of the gradients of these regression planes correlated neither with the preferred stimulus direction tested in the fixation paradigm nor with the preferred tracking direction in the pursuit paradigm. Eighty-six neurons were tested with both the fixation and the pursuit paradigms. The directions of the gradients of the regression planes fit to the responses in both paradigms tended to correlate with each other, i.e., for more than two thirds of the neurons the angular difference between both directions was less than ±90°. The modulatory effect of the position of the eyes in the orbit proved to balance out at the population level for neurons in areas MT and MST, tested with the fixation as well as the pursuit paradigm. Results are discussed in light of the hypothesis of an ongoing coordinate transformation of the incoming sensory signals into a nonretinocentric representation of the visual field.
Physiological Identification of Pontomedullary Serotonergic Neurons in the Rat
Authors: Mason Peggy
Published: December 2017

Mason, Peggy. Physiological identification of pontomedullary serotonergic neurons in the rat. J. Neurophysiol. 77: 1087–1098, 1997. Spinal serotonin is derived entirely from bulbar sources and plays an important role in spinal modulatory processes, including pain modulation. Establishing the electrophysiological properties of serotonergic bulbospinal neurons in the pontomedullary raphe and reticular formation is critical to understanding the physiological role of serotonin in the spinal cord. Neurons were characterized by their responses to noxious stimulation and their background discharge pattern in the lightly anesthetized rat. Characterized cells were intracellularly labeled with Neurobiotin, which was visualized with a Texas Red fluorophore. Sections containing the labeled cells were processed for serotonin immunocytochemistry with the use of a Bodipy fluorophore. Forty-seven intracellularly labeled cells were tested for serotonin immunoreactivity. The labeled neurons were located in raphe magnus, the nucleus reticularis magnocellularis, and the adjacent reticular and raphe nuclei at levels from the inferior olivary complex to the superior olivary complex. serotonergic cells were located in the raphe nuclei, in nucleus reticularis magnocellularis pars alpha, and in nucleus reticularis paragigantocellularis lateralis, but not in nucleus reticularis magnocellularis pars beta or nucleus reticularis gigantocellularis. Thirteen intracellularly labeled cells contained serotonin immunoreactivity. The background discharge rate of serotonergic cells averaged 1.8 Hz (range: 0.5–3.1 Hz). Discharge was steady and without sustained pauses or bursts in firing. Most serotonin-immunoreactive cells were unaffected or slightly excited by pinch and were unaffected by noxious heat. Three serotonergic cells were weakly excited by both noxious pinch and heat, whereas two serotonergic cells were briefly inhibited by these stimuli. Cells that lacked serotonin immunoreactivity were heterogeneous and included on, off, and neutral cells. Nonserotonergic cells differed from serotonergic cells in having an irregular discharge pattern and/or a high mean discharge rate. A linear discriminant function, employing background discharge characteristics as independent variables, was calculated that successfully classified 13 of 13 serotonergic and 32 of 33 nonserotonergic neurons. The probability of misclassification with the use of this discriminant function was estimated to be <10%. Employing the discriminant function on a test group of cells whose immunochemical content was unknown revealed a population of serotonergic-like cells that resembled the labeled serotonergic cells in background discharge pattern, response to noxious stimulation, and nuclear location. The discharge of pontomedullary serotonergic neurons is slow and steady, suggesting that these neurons may have a role in the tonic, rather than phasic, modulation of spinal processes.
Endogenous Firing Patterns of Murine Spiral Ganglion Neurons
Authors: Mo Zun-Li , Davis Robin L.
Published: December 2017

Mo, Zun-Li and Robin L. Davis. Endogenous firing patterns of murine spiral ganglion neurons. J. Neurophysiol. 77: 1294–1305, 1997. Current-clamp recordings with the use of the whole cell configuration of the patch-clamp technique were made from postnatal mouse spiral ganglion neurons in vitro. Cultures contained neurons that displayed monopolar, bipolar, and pseudomonopolar morphologies. Additionally, a class of neurons having exceptionally large somata was observed. Frequency histograms of the maximum number of action potentials fired from 240-ms step depolarizations showed that neurons could be classified as either slowly adapting or rapidly adapting. Most neurons (85%) were in the rapidly adapting category (58 of 68 recordings). Measurements of elementary properties were used to define the endogenous firing characteristics of both neuron classes. Action potential number varied with step and holding potential, spike amplitude decayed during prolonged depolarizations, and spike frequency adaptation was observed in both rapidly and slowly adapting neurons. The apparent input resistance, spike amplitude decrement, and instantaneous firing frequency differed significantly between rapidly and slowly adapting neurons. Inward rectification was evaluated in response to hyperpolarizing constant current injections. Present in both electrophysiological classes, its magnitude was graded from neuron to neuron, reflecting differences in number, type, and/or voltage dependence of the underlying channels. These data suggest that spiral ganglion neurons possess intrinsic firing properties that regulate action potential number and timing, features that may be crucial to signal coding in the auditory periphery.
Dynorphin A-Mediated Reduction in Multiple Calcium Currents Involves a Goα-Subtype G Protein in Rat Primary Afferent Neurons
Authors: Wiley John W. , Moises Hylan C. , Gross Robert A. , Macdonald Robert L.
Published: December 2017

Wiley, John W., Hylan C. Moises, Robert A. Gross, and Robert L. Macdonald. Dynorphin A-mediated reduction in multiple calcium currents involves a Goα-subtype G protein in rat primary afferent neurons. J. Neurophysiol. 77: 1338–1348, 1997. We examined the effect of antisera directed at specific G-protein subtype(s) on dynorphin A (Dyn A)-mediated reduction of calcium currents in rat dorsal root ganglia (DRG) neurons. Whole cell patch-clamp recordings were performed on acutely dissociated neurons. Dyn A (1 μM)-mediated decrease in calcium currents was inhibited >90% by the preferential κ-receptor antagonist norbinaltorphimine. Dyn A (300–1,000 nM)-mediated reduction in calcium currents was examined during intracellular administration of antisera directed against specific regions of Goα, Gi1α/Gi2α, and Gi3αsubunits. Intracellular dialysis with an antiserum specific for Goα for 20 min decreased calcium current inhibition by Dyn A (1 μM) in 13 of 15 neurons by an average of 75%. Dialysis with nonimmune serum did not affect Dyn A's action to reduce calcium currents. Intracellular dialysis with either anti-Gi1α/Gi2αor anti-Gi3αantisera did not affect Dyn A-induced changes in calcium currents. In the presence of the N-type calcium channel antagonist ω-conotoxin GVIA, the P-type calcium channel antagonist ω-Aga IVA, and ω-Aga MVIIC applied subsequent to the other toxins, the effect of Dyn A to reduce calcium currents was inhibited by 52, 28, and 16%, respectively. The L channel antagonist nifedipine did not affect the ability of Dyn A to inhibit calcium currents. These results suggest that in rat DRG neurons coupling of κ-opioid receptors to multiple transient, high-threshold calcium currents involves the Goαsubclass of G proteins.
Correlation of Effects of General Anesthetics on Somatosensory Neurons in the Primate Thalamus and Cortical EEG Power
Authors: Dougherty P. M. , Li Y. J. , Lenz F. A. , Rowland L. , Mittman S.
Published: December 2017

Dougherty, P. M., Y. J. Li, F. A. Lenz, L. Rowland, and S. Mittman. Correlation of effects of general anesthetics on somatosensory neurons in the primate thalamus and cortical EEG power. J. Neurophysiol. 77: 1375–1392, 1997. The effects of two types of general anesthetic on the neurophysiological properties of the primate somatosensory thalamus were correlated with effects on frontal cortex electroencephalographic (EEG) power and spectral properties. Graded doses of the intravenous agent methohexital sodium (METH) were studied in 12 cells in three monkeys on a halothane baseline anesthetic. Low doses of METH (0.2–1.0 mg/kg) produced a reduction of EEG power but had no effects on spontaneous or evoked thalamic activity. EEG power showed maximal attenuation after 2.0 mg/kg METH, whereas decreases in thalamic activity were first noted over a similar moderate dose range (2.0–5.0 mg/kg). The physiological parameter most sensitive to METH was the spontaneous activity, which showed initial changes in rate and pattern at moderate doses followed by marked inhibition at higher doses. Finally, the high dose of METH (10.0 mg/kg) produced marked reduction in all neurophysiological parameters with recovery over the following 30–45 min. The effects of the volatile anesthetic halothane were studied on 15 cells in four monkeys anesthetized with pentobarbital sodium. The low dose of halothane (0.25%) produced a facilitation of responses to cutaneous stimuli as well as a decrease in the rate and burst patterns in the spontaneous activity. The power in the EEG was not affected at this concentration. The responses of the cells to the mechanical stimuli at moderate doses (0.5–1.0%) of halothane returned to the baseline magnitude, whereas spontaneous activity remained unaffected compared with initial effects. EEG power was reduced by 1% halothane. Finally, all neurophysiological parameters showed profound reduction at the highest halothane concentrations (2.0–3.0%) with recovery over the next 30–45 min. In conclusion, the two classes of anesthetics most commonly used for acute neurophysiological studies in the primate show well-defined thresholds at which changes in the response properties of thalamic neurons are produced. This threshold for the barbiturates and halothane can be predicted by monitoring of cortical EEG.
Muscimol and Midazolam Do Not Potentiate Each Other's Effects on Sleep EEG in the Rat
Authors: Lancel Marike , Faulhaber Johannes , Schiffelholz Thomas , Mathias Stefan , Deisz Rudolf A.
Published: December 2017

Lancel, Marike, Johannes Faulhaber, Thomas Schiffelholz, Stefan Mathias, and Rudolf A. Deisz. Muscimol and midazolam do not potentiate each other's effects on sleep EEG in the rat. J. Neurophysiol. 77: 1624–1629, 1997. The interaction of a γ-aminobutyric acid-A (GABAA) receptor agonist and a benzodiazepine-type modulator of GABAA receptors on sleep was investigated. Low doses of muscimol (0.3 mg/kg) and the benzodiazepine midazolam (1.5 mg/kg) were administered alone and incombination, in random order, to eight rats. All injections were given intraperitoneally at light onset. Electroencephalogram (EEG) and electromyogram were recorded during the first 6 h post injection. Compared with vehicle, muscimol hardly affected the time spent in non-rapid eye movement sleep (non-REMS) and REMS, but significantly enhanced EEG activity in the frequency range between 2 and 6 Hz during non-REMS. Midazolam significantly increased the time spent in non-REMS, reduced EEG activity at frequencies <12 Hz, and elevated EEG activity in most higher frequencies during this state. The combined administration of muscimol and midazolam affected non-REMS-specific EEG activity in an unexpected fashion: the effects were intermediate between those of muscimol and midazolam. These results indicate that muscimol and midazolam have dissimilar effects on EEG within non-REMS and demonstrate that midazolam does not augment but attenuates the muscimol-induced changes in sleep EEG. Our data are at variance with established mechanisms, according to which agonistic modulators would have similar effects and should potentiate the effects of GABAA agonists. The present data suggest that application of agonists and agonistic modulators of GABAA receptors causes differential net effects on sleep parameters.
Reverse Effects of Conditioning Produced by Two Different Unconditioned Stimuli on Thalamocortical Transmission
Authors: Meftah El Mehdi , Rispal-Padel Lucie
Published: December 2017

Meftah, El Mehdi and Lucie Rispal-Padel. Reverse effects of conditioning produced by two different unconditioned stimuli on thalamocortical transmission. J. Neurophysiol. 77: 1663–1678, 1997. Actions of cerebellothalamocortical (CTC) networks on the musculature can be modified by associative conditioning in adult animals. During conditioning, electrical stimulation of a CTC network involved in forearm flexion movements results in either flexion or extension responses, depending on the somatosensory information given by the unconditioned stimulus (UCS). In the present work we attempt to determine what kind of neurobiological changes induced in the CTC pathways as a consequence of distinct somesthetic messages could lead to different conditioned motor responses. Two conditioning procedures in which distinct UCSs were successively applied to awake cats in chronic preparation. The conditioned stimulus (CS) was an electrical subthreshold stimulation of an interpositus nucleus (IN) site at the origin of CTC circuits controlling forelimb flexion movements. It was first paired with a UCS applied to the skin above the wrist, also producing a forearm flexion reflex, and second with a UCS applied more proximally on the forearm, producing a backward withdrawal reflex of the forelimb. The two procedures, termed “concordant” and “discordant,” respectively, were carried out in a different order on the same cats, separated by 2 mo of rest. The effects of conditioning were assessed from the characteristics of the motor reponses induced by the CS and from the properties of the CTC transmission analyzed on the cortical field potentials induced by IN stimulation. The concordant procedure resulted in persistent enhancement of the amplitude and rate of occurrence of the forearm flexions induced by the CS. Concomitantly, an increase of the di- and/or trisynaptic excitatory negative component of the field potentials induced by the CS in layers III and V of the elbow motor cortical representation was observed. In contrast, during the discordant procedure, the forearm flexions initially induced by the IN stimulation were progressively abolished in favor of forearm extensions, and, in parallel, a depression of the excitatory negative component of the cortical responses and the appearance of a later large positive event were observed. The selectivity and the associative nature of the motor and synaptic changes were tested. The two kinds of events appeared to be linked. It was concluded that somesthetic information given by the UCS seems to be a critical factor in the determination of both the motor and synaptic CTC changes induced by associative conditioning. Alterations of cerebellocortical transmission appeared to constitute one of the neurobiological substrates for conditioned motor changes.
Functional Organization of Cone Bipolar Cells in the Rat Retina
Authors: Hartveit Espen
Published: December 2017

Hartveit, Espen. Functional organization of cone bipolar cells in the rat retina. J. Neurophysiol. 77: 1716–1730, 1997. The responses of cone bipolar cells in slices of rat retina to ionotropic glutamate receptor agonists were recorded with the whole cell voltage-clamp technique in the presence of 5 mM Co2+ and nominally 0 mM Ca2+ extracellularly. Application of the non- N-methyl-d-aspartate (non-NMDA) receptor agonists kainate and (S)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate had a series of effects on cone bipolar cells (types 1–9), and the different cell types could be classified as on- or off-type cells according to which type(s) of responses they displayed. First, direct responses were observed in cell types 1–4 as short-latency inward currents at −70 mV with reversal potentials ( E revs) close to 0 mV, characteristic of nonselective cation channels. Second, some cells, among types 5–9, did not display short-latency inward currents to kainate at −70 mV. Other type 5–8 cells displayed short-latency kainate responses, but the currents could not be reversed ( E rev of +40 mV or greater). I suggest that these responses are conveyed to the cone bipolar cells through gap junctions, most likely with AII amacrine cells. The lack of reversal is likely due to a substantial voltage drop across the gap junctions resulting in an inadequate voltage control of AII amacrine cells when the recording pipette is on the cone bipolar cell. Kainate responses recorded directly from AII amacrine cells had E rev ∼ 0 mV. Third, long-latency indirect responses selective for chloride ions ( E rev ∼ chloride equilibrium potential) were observed in many cone bipolar cells during longer-lasting application of kainate. The long-latency response component was suppressed by coapplication of the γ-aminobutyric acid-A (GABAA) receptor antagonist picrotoxin and the GABAC receptor antagonist 3-aminopropyl(methyl)phosphinic acid. This long-latency component was absent in axotomized bipolar cells, suggesting that it was due to external Ca2+-independent release of GABA onto the axon terminals of the cone bipolar cells. All kainate-evoked response components were blocked by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. Application of NMDA evoked no response in cone bipolar cells. These results suggest that cone bipolar cells types 1–4 are off cone bipolar cells, whereas cone bipolar cells types 5–9 are on cone bipolar cells.
Properties of Unitary IPSCs in Hippocampal Pyramidal Cells Originating From Different Types of Interneurons in Young Rats
Authors: Ouardouz Mohamed , Lacaille Jean-Claude
Published: December 2017

Ouardouz, Mohamed and Jean-Claude Lacaille. Properties of unitary IPSCs in hippocampal pyramidal cells originating from different types of interneurons in young rats. J. Neurophysiol. 77: 1939–1949, 1997. Whole cell recordings were used in hippocampal slices of young rats to examine unitary inhibitory postsynaptic currents (uIPSCs) evoked in CA1 pyramidal cells at room temperature. Loose cell-attached stimulation was applied to activate single interneurons of different subtypes located in stratum oriens (OR), near stratum pyramidale (PYR), and at the border of stratum radiatum and lacunosum-moleculare (LM). uIPSCs evoked by stimulation of PYR and OR interneurons had similar onset latency, rise time, peak amplitude, and decay. In contrast, uIPSCs elicited by activation of LM interneurons were significantly smaller in amplitude and had a slower time course. The mean reversal potential of uIPSCs was −53.1 ± 2.1 (SE) mV during recordings with intracellular solution containing potassium gluconate. With the use of recording solution containing the potassium channel blocker cesium, the reversal potential of uIPSCs was not significantly different (−58.5 ± 2.6 mV), suggesting that these synaptic currents were not mediated by potassium conductances. Bath application of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline (25 μM) reversibly blocked uIPSCs evoked by stimulation of all interneuron subtypes. In bicuculline, the mean peak amplitude of uIPSCs recorded with potassium gluconate was reduced to 3.5 ± 4.4% of control ( n = 7). Similarly, with cesium methanesulfonate, the mean amplitude in bicuculline was 2.9 ± 3.1% of control ( n = 13). Application of the GABAB receptor antagonist CGP 55845A (5 μM) resulted in a significant and reversible increase in the mean amplitude of uIPSCs recorded with cesium-containing intracellular solution. Thus uIPSCs from all cell types appeared under tonic presynaptic inhibition by GABAB receptors. Paired stimulation of individual interneurons at 100- to 200-ms intervals did not result in paired pulse depression of uIPSCs. For individual responses, a significant negative correlation was observed between the amplitude of the first and second uIPSCs. A significant paired pulse facilitation (154.0 ± 8.0%) was observed when the first uIPSC was smaller than the mean of all first uIPSCs. A small, but not significant, paired pulse depression (90.8 ± 4.0%) was found when the first uIPSC was larger than the mean of all first uIPSCs. Our results indicate that these different subtypes of hippocampal interneurons generate Cl−-mediated GABAA uIPSCs. uIPSCs originating from different types of interneurons may have heterogeneous properties and may be subject to tonic presynaptic inhibition via heterosynaptic GABAB receptors. These results suggest a specialization of function for inhibitory interneurons and point to complex presynaptic modulation of interneuron function.
Modeling Neural Mechanisms for Genesis of Respiratory Rhythm and Pattern. I. Models of Respiratory Neurons
Authors: Rybak Ilya A. , Paton Julian F. R. , Schwaber James S.
Published: December 2017

Rybak, Ilya A., Julian F. R. Paton, and James S. Schwaber. Modeling neural mechanisms for genesis of respiratory rhythym and pattern. I. Models of respiratory neurons. J. Neurophysiol. 77: 1994–2006, 1997. The general objectives of our research, presented in this series of papers, were to develop a computational model of the brain stem respiratory neural network and to explore possible neural mechanisms that provide the genesis of respiratory oscillations and the specific firing patterns of respiratory neurons. The present paper describes models of single respiratory neurons that have been used as the elements in our network models of the central respiratory pattern generator presented in subsequent papers. The models of respiratory neurons were developed in the Hodgkin-Huxley style employing both physiological and biophysical data obtained from brain stem neurons in mammals. Two single respiratory neuron models were developed to match the two distinct firing behaviors of respiratory neurons described in vivo: neuron type I shows an adapting firing pattern in response to synaptic excitation, and neuron type II shows a ramp firing pattern during membrane depolarization after a period of synaptic inhibition. We found that a frequency ramp firing pattern can result from intrinsic membrane properties, specifically from the combined influence of calcium-dependent KAHP(Ca), low-threshold CaT and KA channels. The neuron models with these ionic channels (type II) demonstrated ramp firing patterns similar to those recorded from respiratory neurons in vivo. Our simulations show that KAHP(Ca) channels in combination with high-threshold CaL channels produce spike frequency adaptation during synaptic excitation. However, in combination with low-threshold CaT channels, they cause a frequency ramp firing response after release from inhibition. This promotes a testable hypothesis that the main difference between the respiratory neurons that adapt (for example, early inspiratory, postinspiratory, and decrementing expiratory) and those that show ramp firing patterns (for example, ramp inspiratory and augmenting expiratory) consists of a ratio between the two types of calcium channels: CaL channels predominate in the former and CaT channels in the latter respiratory neuron types. We have analyzed the dependence of adapting and ramp firing patterns on maximal conductances of different ionic channels and values of synaptic drive. The effect of adjusting specific membrane conductances and synaptic interactions revealed plausible neuronal mechanisms that may underlie modulatory effects on respiratory neuron firing patterns and network performances. The results of computer simulation provide useful insight into functional significance of specific intrinsic membrane properties and their interactions with phasic synaptic inputs for a better understanding of respiratory neuron firing behavior.
Efferent Neurons and Vestibular Cross Talk in the Frog
Authors: Myers S. F. , Salem H. H. , Kaltenbach J. A.
Published: December 2017

Myers, S. F., H. H. Salem, and J. A. Kaltenbach. Efferent neurons and vestibular cross talk in the frog. J. Neurophysiol. 77: 2061–2070, 1997. A galvanic stimulus (30- to 120-s, 0.3-mA constant current pulse) was used to depolarize the spike-generating region of horizontal and anterior canal afferent neurons. The galvanically induced spike activity from these neurons served as a driving input to the efferent vestibular system in the bullfrog. Efferent-mediated effects were assessed by intracellular recordings of posterior canal afferent spike activity, either ipsilateral or contralateral to the driving stimulus. Ipsilateral to the driving stimulus, efferent-mediated spike rate changes occurred in 62 (39%) of 158 posterior canal afferent neurons. Ipsilateral efferent-mediated effects were overwhelmingly excitatory (92%). Of responding units, 3% were inhibited during stimulus application and 5% showed mixed responses involving 3–20 s of inhibition followed by facilitation. Contralateral to the driving stimulus, efferent-mediated spike rate changes occurred in 18 (23%) of 77 posterior canal afferent neurons. Contralateral efferent-mediated effects were overwhelmingly inhibitory (95%). Only one unit was facilitated during stimulation and no mixed responses to contralateral stimulation were observed. Analysis of the coefficient of variation in interspike intervals (CV) before and during stimulation showed no significant efferent-mediated effects on spike train noise. Comparisons of resting spike rates between units showing efferent-mediated effects and those that did not were in general agreement with previous studies. Responding units had a lower mean spike rate (6.8 ± 0.70 spikes/s, mean ± SE) than did nonresponding units (10.7 ± 0.42 spikes/s, mean ± SE; P < 0.001; 2-tailed t-test of log-normalized data). Comparison between groups in the regularity of their resting spike rates, as quantified by CV, showed considerable overlap. When responding and nonresponding units with similar resting spike rates were compared, responding units had more irregular resting spike rates than did nonresponding units ( P < 0.004; 2-tailed, paired t-test). In most cases (77%) the temporal pattern and general shapes of efferent-mediated responses mirrored the driving input of the galvanically activated afferent neurons. The other 23% of efferent-mediated responses exhibited a marked adaptation of the response. Adapting and nonadapting units were not significantly different in their mean resting spike rates or in the regularity of their resting spike rates.
Prediction of Complex Two-Dimensional Trajectories by a Cerebellar Model of Smooth Pursuit Eye Movement
Authors: Kettner R. E. , Mahamud S. , Leung H.-C. , Sitkoff N. , Houk J. C. , Peterson B. W. , Barto A. G.
Published: December 2017

Kettner, R. E., S. Mahamud, H.-C. Leung, N. Sitkoff, J. C. Houk, B. W. Peterson, and A. G. Barto. Prediction of complex two-dimensional trajectories by a cerebellar model of smooth pursuit eye movement. J. Neurophysiol. 77: 2115–2130, 1997. A neural network model based on the anatomy and physiology of the cerebellum is presented that can generate both simple and complex predictive pursuit, while also responding in a feedback mode to visual perturbations from an ongoing trajectory. The model allows the prediction of complex movements by adding two features that are not present in other pursuit models: an array of inputs distributed over a range of physiologically justified delays, and a novel, biologically plausible learning rule that generated changes in synaptic strengths in response to retinal slip errors that arrive after long delays. To directly test the model, its output was compared with the behavior of monkeys tracking the same trajectories. There was a close correspondence between model and monkey performance. Complex target trajectories were created by summing two or three sinusoidal components of different frequencies along horizontal and/or vertical axes. Both the model and the monkeys were able to track these complex sum-of-sines trajectories with small phase delays that averaged 8 and 20 ms in magnitude, respectively. Both the model and the monkeys showed a consistent relationship between the high- and low-frequency components of pursuit: high-frequency components were tracked with small phase lags, whereas low-frequency components were tracked with phase leads. The model was also trained to track targets moving along a circular trajectory with infrequent right-angle perturbations that moved the target along a circle meridian. Before the perturbation, the model tracked the target with very small phase differences that averaged 5 ms. After the perturbation, the model overshot the target while continuing along the expected nonperturbed circular trajectory for 80 ms, before it moved toward the new perturbed trajectory. Monkeys showed similar behaviors with an average phase difference of 3 ms during circular pursuit, followed by a perturbation response after 90 ms. In both cases, the delays required to process visual information were much longer than delays associated with nonperturbed circular and sum-of-sines pursuit. This suggests that both the model and the eye make short-term predictions about future events to compensate for visual feedback delays in receiving information about the direction of a target moving along a changing trajectory. In addition, both the eye and the model can adjust to abrupt changes in target direction on the basis of visual feedback, but do so after significant processing delays.
Reducing Extracellular Cl−Suppresses Dihydropyridine-Sensitive Ca2+Currents and Synaptic Transmission in Amphibian Photoreceptors
Authors: Thoreson Wallace B. , Nitzan Ron , Miller Robert F.
Published: December 2017

Thoreson, Wallace B., Ron Nitzan, and Robert F. Miller. Reducing extracellular Cl−suppresses dihydropyridine-sensitive Ca2+currents and synaptic transmission in amphibian photoreceptors. J. Neurophysiol. 77: 2175–2190, 1997. A reduction in extracellular chloride suppresses light-evoked currents of second-order retinal neurons (bipolar and horizontal cells) by reducing release of glutamate from photoreceptors. The underlying mechanisms responsible for this action of reduced extracellular Cl−were studied with a combination of electrophysiological recordings from single neurons in a retinal slice preparation and image analyses of intracellular Ca2+(Fura-2) and pH [2′,7′-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein, acetoxymethyl ester] in dissociated photoreceptors. The results show that reducing extracellular Cl−suppresses a dihydropyridine (DHP)-sensitive Ca2+current ( ICa) in photoreceptors. It is proposed that suppression of ICaresults in suppression of photoreceptor neurotransmission. The suppressive effect of low Cl−on ICais not due to antagonism by the substituting anion nor is it mediated by changes in extracellular or intracellular pH. We conclude that normal extracellular levels of Cl−are important for maintenance of the voltage-gated Ca2+channels that support neurotransmission from photoreceptors. Several ideas are presented about the mechanisms by which Cl−supports photoreceptor neurotransmission and the possibility that modulations of Cl−might play a physiological role in the regulation of Ca2+channels in photoreceptors and, hence, photoreceptor function.
Endogenous GABA Activates Small-Conductance K+ Channels Underlying Slow IPSCs in Rat Hippocampal Neurons
Authors: De Koninck Yves , Mody Istvan
Published: December 2017

De Koninck, Yves and Istvan Mody. Endogenous GABA activates small-conductance K+ channels underlying slow IPSCs in rat hippocampal neurons. J. Neurophysiol. 77: 2202–2208, 1997. The objective of this study was to determine the properties of K+ channels activated by endogenously released trasmitter under synaptic conditions. First, the levels of γ-aminobutyric acid (GABA) were depleted in hippocampal nerve endings to establish the relative contribution of endogenously released GABA to the activation of GABAB receptors mediating slow inhibitory postsynaptic currents (IPSCs). Inhibition of glutamic acid decarboxylase and GABA reuptake effectively depleted >85% of the releasable GABA pool, producing parallel reductions of GABAA and GABAB receptor-mediated IPSCs, indicating that both classes of receptors are activated synaptically by endogenously released GABA. Whole cell patch-clamp recordings of stimulus-evoked slow IPSCs at potentials hyperpolarized from the potassium reversal potential were consistent with the activation of a nonrectifying ( n = 3) or slightly outwardly rectifying ( n = 4) K+ conductance by the endogenously released GABA. Spectral analysis of the decay phase of GABAB IPSCs revealed several time constants indicating complex underlying channel kinetics. Nonstationary variance analysis yielded a small unitary conductance in the range of 5–13 pS, consistent with a large number of channels activated during evoked currents. These results indicate that in granule cells of the dentate gyrus, GABA released synaptically from interneuron terminals activates an unusually small K+ conductance, with no or slight outward rectification. This conductance is therefore unlike those typically reported for neuronal G protein-coupled K+ channels or those activated by exogenously applied baclofen with larger, inwardly rectifying conductances.
NT-3 Increases Amplitude of EPSPs Produced by Axotomized Group Ia Afferents
Authors: Munson John B. , Johnson Richard D. , Mendell Lorne M.
Published: December 2017

We thank K. Foli for technical support and Regeneron Pharmaceuticals for providing NT-3.

This research was supported by National Institute of Neurological Disorders and Stroke Grants NS-15913 (Javits Neuroscience Award) to J. B. Munson and NS-16996 (Javits Neuroscience Award) to L. M. Mendell. Additional support was furnished by NS-14899 and NS-32264 to L. M. Mendall.

Present addresses: R. D. Johnson, Dept. of Physiological Sciences, University of Florida College of Veterinary Medicine, Gainesville, FL 32610; L. M. Mendell, Dept. of Neurobiology and Behaviour, SUNY at Stony Brook, Stony Brook, NY 11794.
Posttetanic Excitation Mediated by GABAA Receptors in Rat CA1 Pyramidal Neurons
Authors: Taira Tomi , Lamsa Karri , Kaila Kai
Published: December 2017

Taira, Tomi, Karri Lamsa, and Kai Kaila. Posttetanic excitation mediated by GABAA receptors in rat CA1 pyramidal neurons. J.Neurophysiol. 77: 2213–2218, 1997. The contributions of γ-aminobutyric acid (GABA) receptors to posttetanic excitation of CA1 pyramidal neurons in rat hippocampal slices were studied using extracellular and intracellular recording techniques. Synaptic responses were evoked on tetanic stimulation (100–200 Hz, 40–100 pulses) applied in stratum radiatum close (300–600 μm) to the recording site. Under control conditions, tetanic stimulation resulted in a triphasic depolarization/hyperpolarization/sustained depolarization sequence in area CA1 pyramidal cells. The late depolarization usually gave rise to a prolonged (≤3 s) spike firing. The late depolarization and the associated spike firing were blocked both specifically and completely (within a time window of 3–6 min starting from picrotoxin application) by the GABAA receptor antagonist picrotoxin (PiTX, 100 μM). Paradoxically, at this early stage of PiTX application, overall neuronal firing was attenuated to a higher degree than what was achieved by ionotropic glutamate antagonists. Complete block of ionotropic glutamate receptors by the antagonists d-2-amino-5-phosphonopentoate (AP5, 80 μM), 6-nitro-7-sulphamoylbenzo[f]quinoxaline-2,3-dione (NBQX, 10 μM), and ketamine (50 μM) blocked the initial fast depolarization and suppressed the late one. Exposure to a permeable inhibitor of carbonic anhydrase, ethoxyzolamide (EZA, 50 μM) inhibited the late, apparently GABA-mediated depolarization. It is concluded that GABA can provide the main posttetanic excitatory drive in the adult hippocampus. The present results suggest that intense activation of GABAergic interneurons may accentuate the excitation of principal neurons and, hence, play an important facilitatory role in the induction of long-term potentiation (LTP) and epileptogenesis.
Ionotropic GABA Receptor From Lobster Olfactory Projection Neurons
Authors: Zhainazarov A. B. , Wachowiak M. , Boettcher A. , Elenes S. , Ache B. W.
Published: December 2017

Zhainazarov, A. B., M. Wachowiak, A. Boettcher, S. Elenes, and B. W. Ache. Ionotropic GABA receptor from lobster olfactory projection neurons. J. Neurophysiol. 77: 2235–2251, 1997. This study reports an ionotropic GABA (γ-aminobutyric acid) receptor in projection neurons acutely dissociated from the olfactory lobe of the brain of the spiny lobster and analyzed by whole cell and cell-free patch-clamp recording. GABA evokes a macroscopic current in the cells that is linear from −100 to +100 mV, reverses at the imposed chloride equilibrium potential, has a permeability sequence of Cl−> acetate > bicarbonate > phosphate > propionate and SCN−> Br−> I−> Cl−> F−, and is reversibly blocked by the Cl channel blocker picrotoxin but not tert-butylbicyclophosphorothionate (TBPS). The current is bicuculline insensitive and activated by muscimol, isoguvacine, cis-4-aminocrotonic acid (CACA), and trans-aminocrotonic acid (TACA), as well as by the GABAC-receptor antagonists 4,5,6,7-tetrahydroisoxazolo [5,4,-c]pyridin-3-ol (THIP), 3-amino-1-propanesulfonic acid(3-APS), and imidazole-4-acetic acid (I-4AA), but not theGABAB-receptor agonists baclofen and 3-aminopropylphosphonic acid (3-APA). Agonist potency for the receptor is TACA > muscimol > GABA > I-4AA > isoguvacine > 3-APS > CACA > THIP. Unitary chloride currents in cell-free, outside-out patches from the cells share enough of these pharmacological properties to indicate that the channel underlies the macroscopic current. The receptor mediates an inhibitory current in the cells in vivo. The receptor is similar, if not identical, to one from neurons cultured from the thoracic ganglia of the clawed lobster. The more extensive pharmacological characterization of the receptor reported here indicates that this lobster CNS receptor is pharmacologically distinct from previously characterized ionotropic GABA receptors.
Activation and Detection of Facilitation as Studied by Presynaptic Voltage Control at the Inhibitor of the Crayfish Opener Muscle
Authors: Vyshedskiy Andrey , Lin Jen-Wei
Published: December 2017

Vyshedskiy, Andrey and Jen-Wei Lin. Activation and detection of facilitation as studied by presynaptic voltage control at the inhibitor of the crayfish opener muscle. J. Neurophysiol. 77: 2300–2315, 1997. Facilitation at the crayfish neuromuscular inhibitor synapse was investigated with the use of a presynaptic voltage control method in which 5-ms presynaptic pulses were used to activate and monitor facilitation. A single 5-ms pulse was able to activate facilitation with a decay time constant similar to that of the F2 component of facilitation activated by action potentials. The quality of the control of presynaptic potential during F2 facilitation was evaluated by measuring the amplitude of presynaptic pulses and by analyzing the shape of the depolarization-release coupling plot during facilitation. Both approaches suggested that neither the amplitude of presynaptic depolarizations nor the space clamp of the presynaptic axon was changed during F2 facilitation. The activation of facilitation was examined by changing the amplitude of conditioning pulses systematically and using a test pulse of a constant amplitude to monitor facilitation. We found that a significant amount of facilitation could be activated by conditioning pulses that were subthreshold to the activation of transmitter release. Facilitation plateaued before the inhibitory postsynaptic potentials (IPSPs) activated by conditioning pulses reached their maximum. A double logarithm plot of facilitation magnitude against the conditioning IPSP amplitude yielded a slope of 0.34, which implies that the calcium ion cooperativity of activating facilitation is about one third of the secretion process. These findings enabled us to activate near maximal facilitation, by a burst of subthreshold conditioning pulses, without any conditioning transmitter release, and, therefore, to avoid complications associated with previous transmitter release. The detection of facilitation was examined by changing test pulse amplitude systematically to evaluate the ability of the test pulse to detect a constant level of facilitation. The magnitude of normalized facilitation decreased with increasing test pulse amplitude. The magnitude of absolute facilitation (the amplitude of the facilitated minus the control IPSP) increased with increasing test pulse amplitude. A double logarithm plot between facilitated and control IPSPs gave rise to a slope of 0.77, which suggests that the calcium cooperativity of transmitter release was decreased during facilitation.
Rapid Kinetics and Inward Rectification of Miniature EPSCs in Layer I Neurons of Rat Neocortex
Authors: Zhou Fu-Ming , Hablitz John J.
Published: December 2017

Zhou, Fu-Ming and John J. Hablitz. Rapid kinetics and inward rectification of miniature EPSCs in layer I neurons of rat neocortex. J. Neurophysiol. 77: 2416–2426, 1997. With the use of the whole cell patch-clamp technique combined with visualization of neurons in brain slices, we studied the properties of miniature excitatory postsynaptic currents (mEPSCs) in rat neocortical layer I neurons. At holding potentials (−50 to −70 mV) near the resting membrane potential (RMP), mEPSCs had amplitudes of 5–100 pA and were mediated mostly by α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA) receptors. Amplitude histograms were skewed toward large events. An N-methyl-d-aspartate (NMDA) component was revealed by depolarization to −30 mV or by the use of a Mg2+-free bathing solution. At RMP, averaged AMPA mEPSCs had a 10–90% rise time of ∼0.3 ms (uncorrected for instrument filtering). The decay of averaged mEPSCs was best fit by double-exponential functions in most cases. The fast, dominating component had a decay time constant of ∼1.2 ms and comprised ∼80% of the total amplitude. A small slow component had a decay time constant of ∼4 ms. Positive correlations were found between rise and decay times of both individual and averaged mEPSCs, indicative of dendritic filtering. Some large-amplitude mEPSCs and spontaneous EPSCs (recorded in the absence of tetrodotoxin) had slower kinetics, suggesting a role of asynchronous transmitter release in shaping EPSCs. The amplitudes of mEPSCs were much smaller at +60 mV than at −60 mV, indicating that synaptic AMPA-receptor-mediated currents were inwardly rectifying. These results suggest that neocortical layer I neurons receive both NMDA- and AMPA-receptor-mediated synaptic inputs. The rapid decay of EPSCs appears to be largely determined by AMPA receptor deactivation. The observed rectification of synaptic responses suggests that synaptic AMPA receptors in layer I neurons may lack GluR-2 subunits and may be Ca2+ permeable.