bluuebunny/crossref_metadata_2025 huggingface dataset:
Facilitation of a Nociceptive Flexion Reflex in Man by Nonnoxious Radiant Heat Produced by a Laser
Authors: Plaghki Léon , Bragard Dominique , Bars Daniel Le , Willer Jean-Claude , Godfraind Jean-Marie
Published: December 2017

Plaghki, Léon, Dominique Bragard, Daniel Le Bars, Jean-Claude Willer, and Jean-Marie Godfraind. Facilitation of a nociceptive flexion reflex in man by nonnoxious radiant heat produced by a laser. J. Neurophysiol. 79: 2557–2567, 1998. Electromyographic recordings were made in healthy volunteers from the knee-flexor biceps femoris muscle of the nociceptive RIIIreflex elicited by electrical stimulation of the cutaneous sural nerve. The stimulus intensity was adjusted to produce a moderate pricking-pain sensation. The test responses were conditioned by a nonnoxious thermal (≤40°C) stimulus applied to the receptive field of the sural nerve. This stimulus was delivered by a CO2laser stimulator and consisted of a 100-ms pulse of heat with a beam diameter of 20 mm. Its power was 22.7 ± 4.2 W (7.2 mJ/mm2), and it produced a sensation of warmth. The maximum surface temperature reached at the end of the period of stimulation was calculated to be 7°C above the actual reference temperature of the skin (32°C). The interval between the laser (conditioning) and electrical (test) stimuli was varied from 50 to 3,000 ms in steps of 50 ms. It was found that the nociceptive flexion reflex was facilitated by the thermal stimulus; this modulation occurred with particular conditioning-test intervals, which peaked at 500 and 1,100 ms with an additional late, long-lasting phase between 1,600 and 2,300 ms. It was calculated that the conduction velocities of the cutaneous afferent fibers responsible for facilitating the RIIIreflex, fell into three ranges: one corresponding to Aδ fibers (3.2 m/s) and two in the C fiber range (1.3 and 0.7 m/s). It is concluded that information emanating from warm receptors and nociceptors converges. In this respect, the present data show, for the first time, that in man, conditioning nonnociceptive warm thermoreceptive Aδ and C fibers results in an interaction at the spinal level with a nociceptive reflex. This interaction may constitute a useful means whereby signals add together to trigger flexion reflexes in defensive reactions and other basic motor behaviors. It also may contribute to hyperalgesia in inflammatory processes. The methodology used in this study appears to be a useful noninvasive tool for exploring the thermoalgesic mechanisms in both experimental and clinical situations.
Differential Effects of Morphine on Corneal-Responsive Neurons in Rostral Versus Caudal Regions of Spinal Trigeminal Nucleus in the Rat
Authors: Meng Ian D. , Hu James W. , Bereiter David A.
Published: December 2017

Meng, Ian D., James W. Hu, and David A. Bereiter. Differential effects of morphine on corneal-responsive neurons in rostral versus caudal regions of spinal trigeminal nucleus in the rat. J. Neurophysiol. 79: 2593–2602, 1998. The initial processing of corneal sensory input in the rat occurs in two distinct regions of the spinal trigeminal nucleus, at the subnucleus interpolaris/caudalis transition (Vi/Vc) and in laminae I-II at the subnucleus caudalis/spinal cord transition (Vc/C1). Extracellular recording was used to compare the effects of morphine on the evoked activity of corneal-responsive neurons located in these two regions. Neurons also were characterized by cutaneous receptive field properties and parabrachial area (PBA) projection status. Electrical corneal stimulation-evoked activity of most (10/13) neurons at the Vi/Vc transition region was increased [146 ± 16% (mean ± SE) of control, P < 0.025] after systemic morphine and reduced after naloxone. None of the Vi/Vc corneal units were inhibited by morphine. By contrast, all corneal neurons recorded at the Vc/C1 transition region displayed a naloxone-reversible decrease (55 ± 10% of control, P < 0.001) in evoked activity after morphine. None of 13 Vi/Vc corneal units and 7 of 8 Vc/C1 corneal units tested projected to the PBA. To determine if the Vc/C1 transition acted as a relay for the effect of intravenous morphine on corneal stimulation-evoked activity of Vi/Vc units, morphine was applied topically to the dorsal brain stem surface overlying the Vc/C1 transition. Local microinjection of morphine at the Vc/C1 transition increased the evoked activity of 4 Vi/Vc neurons, inhibited that of 2 neurons, and did not affect the remaining 12 corneal neurons tested. In conclusion, the distinctive effects of morphine on Vi/Vc and Vc/C1 neurons support the hypothesis that these two neuronal groups contribute to different aspects of corneal sensory processing such as pain sensation, autonomic reflex responses, and recruitment of descending controls.
Intrinsic and Thalamic Excitatory Inputs Onto Songbird LMAN Neurons Differ in Their Pharmacological and Temporal Properties
Authors: Boettiger Charlotte A. , Doupe Allison J.
Published: December 2017

Boettiger, Charlotte A. and Allison J. Doupe. Intrinsic and thalamic excitatory inputs onto songbird LMAN neurons differ in their pharmacological and temporal properties. J. Neurophysiol. 79: 2615–2628, 1998. In passerine songbirds, the lateral portion of the magnocellular nucleus of the anterior neostriatum (LMAN) plays a vital role in song learning, possibly by encoding sensory information and providing sensory feedback to the vocal motor system. Consistent with this, LMAN neurons are auditory, and, as learning progresses, they evolve from a broadly tuned initial state to a state of strong preference for the bird's own song and acute sensitivity to the temporal order of this song. Moreover, normal synaptic activity in LMAN is required during sensory learning for accurate tutor song copying to occur ( Basham et al. 1996 ). To explore cellular and synaptic properties of LMAN that may contribute to this crucial stage of song acquisition, we developed an acute slice preparation of LMAN from zebra finches in the early stages of sensory learning (18–25 days posthatch). We used this preparation to examine intrinsic neuronal properties of LMAN neurons at this stage and to identify two independent excitatory inputs to these neurons and compare each input's pharmacology and short-term synaptic plasticity. LMAN neurons had immature passive membrane properties, well-developed spiking behavior, and received excitatory input from two sources: afferents from the medial portion of the dorsolateral thalamus (DLM), and recurrent axon collaterals from LMAN itself (“intrinsic” input). These two inputs differed in both their pharmacology and temporal properties. Both inputs were glutamatergic, but LMAN responses to intrinsic inputs exhibited a larger N-methyl-d-aspartate component than responses to DLM inputs. Both inputs elicited temporal summation in response to pairs of stimuli delivered at short intervals, but dl-2-amino-5-phosphonovalerate (APV) significantly reduced the temporal summation only of the responses to intrinsic inputs. Moreover, responses to DLM inputs showed consistent paired-pulse depression, whereas the responses to intrinsic inputs did not. The differences between these two inputs suggest that intrinsic circuitry plays an important role in transforming DLM input patterns into the appropriate LMAN output patterns, as has been suggested for mammalian thalamocortical networks. Moreover, in LMAN, such interactions may contribute to the profound temporal and spectral selectivity that these neurons will acquire during learning.
Electrophysiological Properties of Human Astrocytic Tumor Cells In Situ: Enigma of Spiking Glial Cells
Authors: Bordey Angélique , Sontheimer Harald
Published: December 2017

Bordey, Angélique and Harald Sontheimer. Electrophysiological properties of human astrocytic tumor cells in situ: enigma of spiking glial cells. J. Neurophysiol. 79: 2782–2793, 1998. To better understand physiological changes that accompany the neoplastic transition of astrocytes to become astrocytoma cells, we studied biopsies of low-grade, pilocytic astrocytomas. This group of tumors is most prevalent in children and the tumor cells maintain most antigenic features typical of astrocytes. Astrocytoma cells were studied with the use of whole cell patch-clamp recordings in acute biopsy slices from 4-mo- to 14-yr-old pediatric patients. Recordings from 53 cells in six cases of low-grade astrocytomas were compared to either noncancerous peritumoral astrocytes or astrocytes obtained from other surgeries. Astrocytoma cells almost exclusively displayed slowly activating, sustained, tetraethylammonium (TEA)-sensitive outward potassium currents (delayed rectifying potassium currents; IDR) and transient, tetrodotoxin (TTX)-sensitive sodium currents ( INa). By contrast, comparison glial cells from peritumoral regions or other surgeries showed IDRand INa, but in addition these cells also expressed transient “A”-type K+currents and inwardly rectifying K+currents ( IIR), both of which were absent in astrocytoma cells. IIRconstituted the predominant conductance in comparison astrocytes and was responsible for a high-resting K+conductance in these cells. Voltage-activated Na+currents were observed in 37 of 53 astrocytoma cells. Na+current densities in astrocytoma cells, on average, were three- to fivefold larger than in comparison astrocytes. Astrocytoma cells expressing INacould be induced to generate slow action potential-like responses (spikes) by current injections. The threshold for generating such spikes was −34 mV (from a holding potential of −70 mV). The spike amplitude and time width were 52.5 mV and 12 ms, respectively. No spikes could be elicited in comparison astrocytes, although some of them expressed Na+currents of similar size. Comparison of astrocytes to astrocytoma cells suggests that the apparent lack of IIR, which leads to high-input resistance (>500 MΩ), allows glioma cells to be sufficiently depolarized to generate Na+spikes, whereas the high resting K+conductance in astrocytes prevents their depolarization and thus generation of spikes. Consistent with this notion, Na+spikes could be induced in spinal cord astrocytes in culture when IIRwas experimentally blocked by 10 μM Ba2+, suggesting that the absence of IIRin astrocytoma cells is primarily responsible for the unusual spiking behavior seen in these glial tumor cells. It is unlikely that such glial spikes ever occur in vivo.
Effect of Motion Contrast on Human Cortical Responses to Moving Stimuli
Authors: Shulman Gordon L. , Schwarz Jacob , Miezin Francis M. , Petersen Steven E.
Published: December 2017

Shulman, Gordon L., Jacob Schwarz, Francis M. Miezin, and Steven E. Petersen. Effect of motion contrast on human cortical responses to moving stimuli. J. Neurophysiol. 79: 2794–2803, 1998. The cortical areas activated by motion-defined contours were studied in humans using positron emission tomography (PET). Subjects observed four types of random dot fields, displayed through a 21° diam aperture: unidirectional motion of a translating dot field, motion in opposing directions of two superimposed translating fields, motion in opposing directions of dots in contiguous spatial regions (motion contrast), producing a square wave grating defined by motion, and luminance variation of stationary dots in contiguous spatial regions, producing a square wave grating defined by luminance. Relative to a static dot field, the unidirectional motion condition activated areas previously described, including areas 17/18, lateral temporal-occipital–parietal cortex (MT/MST), and the superior temporal sulcus. Motion-defined gratings increased the activation of areas 17/18 and MT/MST, but not the superior temporal sulcus, and added more dorsal areas in the cuneus, roughly corresponding to V3/V3a, and ventral areas in the lingual gyrus/collateral sulcus, roughly corresponding to V2/VP. Luminance defined gratings, relative to a static dot field, activated areas 17/18, regions in the dorsal cuneus similar to those activated by motion defined gratings, and a region near the left collateral sulcus, slightly lateral to the motion grating activation. They also activated a region in the right fusiform gyrus that was more weakly activated by the motion grating. These results indicate that adding motion contrast to large moving fields increases activity in areas 17/18 and MT/MST and adds both dorsal and ventral regions that are similar for motion and luminance defined contours.
NMDA Receptor-Mediated Oscillatory Activity in the Neonatal Rat Spinal Cord Is Serotonin Dependent
Authors: Maclean Jason N. , Cowley Kristine C. , Schmidt Brian J.
Published: December 2017

MacLean, Jason N., Kristine C. Cowley, and Brian J. Schmidt. NMDA receptor-mediated oscillatory activity in the neonatal rat spinal cord is serotonin dependent. J. Neurophysiol. 79: 2804–2808, 1998. The effect of serotonin (5-HT) receptor blockade on rhythmic network activity and on N-methyl-d-aspartate (NMDA) receptor-induced membrane voltage oscillations was examined using an in vitro neonatal rat spinal cord preparation. Pharmacologically induced rhythmic hindlimb activity, monitored via flexor and extensor electroneurograms or ventral root recordings, was abolished by 5-HT receptor antagonists. Intrinsic motoneuronal voltage oscillations, induced by NMDA in the presence of tetrodotoxin (TTX), either were abolished completely or transformed to long-lasting voltage shifts by 5-HT receptor antagonists. Conversely, 5-HT application facilitated the expression of NMDA-receptor–mediated rhythmic voltage oscillations. The results suggest that an interplay between 5-HT and NMDA receptor actions may be critical for the production of rhythmic motor behavior in the mammalian spinal cord, both at the network and single cell level.
Change in Motor Plan, Without a Change in the Spatial Locus of Attention, Modulates Activity in Posterior Parietal Cortex
Authors: Snyder Lawrence H. , Batista Aaron P. , Andersen Richard A.
Published: December 2017

Snyder, Lawrence H., Aaron P. Batista, and Richard A. Andersen. Change in motor plan, without a change in the spatial locus of attention, modulates activity in posterior parietal cortex. J. Neurophysiol. 79: 2814–2819, 1998. The lateral intraparietal area (LIP) of macaque monkey, and a parietal reach region (PRR) medial and posterior to LIP, code the intention to make visually guided eye and arm movements, respectively. We studied the effect of changing the motor plan, without changing the locus of attention, on single neurons in these two areas. A central target was fixated while one or two sequential flashes occurred in the periphery. The first appeared either within the response field of the neuron being recorded or else on the opposite side of the fixation point. Animals planned a saccade (red flash) or reach (green flash) to the flash location. In some trials, a second flash 750 ms later could change the motor plan but never shifted attention: second flashes always occurred at the same location as the preceding first flash. Responses in LIP were larger when a saccade was instructed ( n = 20 cells), whereas responses in PRR were larger when a reach was instructed ( n = 17). This motor preference was observed for both first flashes and second flashes. In addition, the response to a second flash depended on whether it affirmed or countermanded the first flash; second flash responses were diminished only in the former case. Control experiments indicated that this differential effect was not due to stimulus novelty. These findings support a role for posterior parietal cortex in coding specific motor intention and are consistent with a possible role in the nonspatial shifting of motor intention.
Localization of CCK Receptors in Thalamic Reticular Neurons: A Modeling Study
Authors: Sohal Vikaas S. , Cox Charles L. , Huguenard John R.
Published: December 2017

Sohal, Vikaas S., Charles L. Cox, and John R. Huguenard. Localization of CCK receptors in thalamic reticular neurons: a modeling study. J. Neurophysiol. 79: 2827–2831, 1998. In an earlier experimental study, intracellular recording suggested that cholecystokinin (CCK) suppresses a K+ conductance in thalamic reticular (RE) neurons, yet the reversal potential of the CCK response, revealed using voltage clamp, was hyperpolarized significantly relative to the K+ equilibrium potential. Here, biophysical models of RE neurons were developed and used to test whether suppression of the K+ conductance, g K, can account for the CCK response observed in vitro and also to determine the likely site of CCK receptors on RE neurons. Suppression of g K in model RE neurons can reproduce the relatively hyperpolarized reversal potential of CCK responses found using voltage clamp if the voltage clamp becomes less effective at hyperpolarized potentials. Three factors would reduce voltage-clamp effectiveness in this model: the nonnegligible series resistance of the voltage-clamp electrode, a hyperpolarization-activated mixed cation current ( I h) in RE neurons, and the dendritic location of CCK-sensitive K+ channels. Although suppression of g K in the dendritic compartments of model RE neurons simulates both the magnitude and reversal potential of the CCK response, suppression of g K in just the somatic compartment of model RE neurons fails to do so. Thus the model predicts that CCK should effectively suppress K+ conductance RE neuron dendrites and thereby regulate burst firing in RE neurons. This may explain the potent effects of CCK on intrathalamic oscillations in vitro.
Phasic Boosting of Medial Perforant Path-Evoked Granule Cell Output Time-Locked to Spontaneous Dentate EEG Spikes in Awake Rats
Authors: Bramham Clive R.
Published: December 2017

Bramham, Clive R. Phasic boosting of medial perforant path-evoked granule cell output time-locked to spontaneous dentate EEG spikes in awake rats. J. Neurophysiol. 79: 2825–2832, 1998. Dentate spikes (DSs) are positive-going field potential transients that occur intermittently in the hilar region of the dentate gyrus during alert wakefulness and slow-wave sleep. The function of dentate spikes is unknown; they have been suggested to be triggered by perforant path input and are associated with firing of hilar interneurons and inhibition of CA3 pyramidal cells. Here we investigated the effect of DSs on medial perforant path (MPP)-granule cell-evoked transmission in freely moving rats. The MPP was stimulated selectively in the angular bundle while evoked field potentials and the EEG were recorded with a vertical multielectrode array in the dentate gyrus. DSs were identified readily on the basis of their characteristic voltage-versus–depth profile, amplitude, duration, and state dependency. Using on-line detection of the DS peak, the timing of MPP stimulation relative to single DSs was controlled. DS-triggered evoked responses were compared with conventional, manually evoked responses in still-alert wakefulness (awake immobility) and, in some cases, slow-wave sleep. Input-output curves were obtained with stimulation on the positive DS peak (0 delay) and at delays of 50, 100, and 500 ms. Stimulation on the peak DS was associated with a significant increase in the population spike amplitude, a reduction in population spike latency, and a decrease in the field excitatory postsynaptic potential (fEPSP) slope, relative to manual stimulation. Granule cell excitability was enhanced markedly during DSs, as indicated by a mean 93% increase in the population spike amplitude and a leftward shift in the fEPSP-spike relation. Maximum effects occurred at the DS peak, and lasted between 50 and 100 ms. Paired-pulse inhibition of the population spike was unaffected, indicating intact recurrent inhibition during DSs. The results demonstrate enhancement of perforant path-evoked granule cell output time-locked to DSs. DSs therefore may function to intermittently boost excitatory transmission in the entorhinal cortex-dentate gyrus-CA3 circuit. Such a mechanism may be important in the natural induction of long-term potentiation in the dentate gyrus and CA3 regions.
AMPA and NMDA Receptors Expressed by DifferentiatingXenopusSpinal Neurons
Authors: Gleason Evanna L. , Spitzer Nicholas C.
Published: December 2017

Gleason, Evanna L. and Nicholas C. Spitzer. AMPA and NMDA receptors expressed by differentiating Xenopus spinal neurons. J. Neurophysiol. 79: 2986–2998, 1998. N-methyl-d-aspartate (NMDA) receptors are often the first ionotropic glutamate receptors expressed at early stages of development and appear to influence neuronal differentiation by mediating Ca2+influx. Although less well studied, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors also can generate Ca2+elevations and may have developmental roles. We document the presence of AMPA and NMDA class receptors and the absence of kainate class receptors with whole cell voltage-clamp recordings from Xenopus embryonic spinal neurons differentiated in vitro. Reversal potential measurements indicate that AMPA receptors are permeable to Ca2+both in differentiated neurons and at the time they first are expressed. The PCa/ Pmonocationof 1.9 is close to that of cloned Ca2+-permeable AMPA receptors expressed in heterologous systems. Ca2+imaging reveals that Ca2+elevations are elicited by AMPA or NMDA in the absence of Mg2+. The amplitudes and durations of these agonist-induced Ca2+elevations are similar to those of spontaneous Ca2+transients known to act as differentiation signals in these cells. Two sources of Ca2+amplify AMPA- and NMDA-induced Ca2+elevations. Activation of voltage-gated Ca2+channels by AMPA- or NMDA-mediated depolarization contributes ∼15 or 30% of cytosolic Ca2+elevations, respectively. Activation of either class of receptor produces elevations of Ca2+that elicit further release of Ca2+from thapsigargin-sensitive but ryanodine-insensitive stores, contributing an additional ∼30% of Ca2+elevations. Voltage-clamp recordings and Ca2+imaging both show that these spinal neurons express functional AMPA receptors soon after neurite initiation and before expression of NMDA receptors. The Ca2+permeability of AMPA receptors, their ability to generate significant elevations of [Ca2+]i, and their appearance before synapse formation position them to play roles in neural development. Spontaneous release of agonists from growth cones is detected with glutamate receptors in outside-out patches, suggesting that spinal neurons are early, nonsynaptic sources of glutamate that can influence neuronal differentiation in vivo.
Changes in Quantal Size Distributions Upon Experimental Variations in the Probability of Release at Striatal Inhibitory Synapses
Authors: Behrends Jan C. , ten Bruggencate Gerrit
Published: December 2017

Behrends, Jan C. and Gerrit ten Bruggencate. Changes in quantal size distributions upon experimental variations in the probability of release at striatal inhibitory synapses. J. Neurophysiol. 79: 2999–3011, 1998. Postsynaptic inhibitory γ-aminobutyric acid-A (GABAA)-receptor–mediated current responses were measured using simultaneous pre- and postsynaptic whole cell recordings in primary cell cultures of rat striatum. Substitution of Sr2+ for extracellular Ca2+ strongly desynchronized the inhibitory postsynaptic currents (IPSCs), resulting in a succession of asynchronous IPSCs (asIPSCs). The rise times and decay time constants of individual evoked asIPSCs were not significantly different from those of miniature IPSCs that are the result of spontaneous vesicular release of GABA. Thus asIPSCs reflect quantal transmission at the individual contacts made by one presynaptic neuron on the recorded postsynaptic cell. Increasing the concentration of Sr2+ from 2 to 10 mM and decreasing that of Mg2+ from 5 to 1 mM produced an increase in the frequency of asIPSCs consistent with an enhancement of the mean probability of release ( P r ). At the same time the amplitude distribution of asIPSCs was shifted toward larger values, whereas responses to exogenously applied GABA on average were slightly decreased in amplitude. Application of the GABAB-receptor agonist baclofen (3–10 μM) strongly reduced the frequency of asIPSC, consistent with a decrease in P r , and led to a shift of the amplitude distribution toward smaller values. Baclofen had no effect on responses to exogenously applied GABA. In summary, our data suggest that at striatal inhibitory connections the weight of single contacts may be controlled presynaptically by variation in the amount of transmitter released.
Single-Neuron Modeling of LSO Unit Responses
Authors: Zacksenhouse Miriam , Johnson Don H. , Williams Jerome , Tsuchitani Chiyeko
Published: December 2017

Zacksenhouse, Miriam, Don H. Johnson, Jerome Williams, and Chiyeko Tsuchitani. Single-neuron modeling of LSO unit responses. J. Neurophysiol. 79: 3098–3110, 1998. We investigated, using a computational model, the biophysical correlates of measured discharge patterns of lateral superior olive (LSO) neuron responses to monaural and binaural stimuli. The model's geometry was based on morphological data, and static electric properties of the model agree with available intracellular responses to hyperpolarizing current pulses. Inhibitory synapses were located on the soma and excitatory ones on the dendrites, which were modeled as passive cables. The active properties of the model were adjusted to agree with statistical measures derived from extracellular recordings. Calcium-dependent potassium channels supplemented the usual Hodgkin-Huxley characterization for the soma to produce observed serial interspike interval dependence characteristics. Intracellular calcium concentration is controlled by voltage- and calcium-dependent potassium channels and by calcium diffusion and homeostatic mechanisms. By adjusting the density of the calcium-dependent potassium channels, we could span the observed range of transient response patterns found in different LSO neurons. Inputs from the two ears were modeled as Poisson processes to describe the responses to tone-burst stimuli. Transient and sustained responses to monaural and binaural tone-burst stimuli over a wide range of stimulus conditions could be well described by varying only the model's inputs. As found in recordings, model responses having similar discharge rates but different binaural stimulus combinations exhibited differences in interval statistics.
A Role for the Dorsal Column in Nociceptive Visceral Input Into the Thalamus of Primates
Authors: Al-Chaer Elie D. , Feng Yi , Willis William D.
Published: December 2017

Al-Chaer, Elie D., Yi Feng, and William D. Willis. A role for the dorsal column in nociceptive visceral input into the thalamus of primates. J. Neurophysiol. 79: 3143–3150, 1998. A possible role of the dorsal column (DC) in the processing of visceral pain has gained attention after studies in the rat have revealed that the DC transmits a major part of the pelvic visceral nociceptive input from the colon into the thalamus. Furthermore, clinical interventions aimed at interrupting ascending DC axons near the midline were successful in relieving the pain suffered by patients with cancer of the pelvic organs. The purpose of this study was to check whether a DC lesion in monkeys would reduce the responses of thalamic neurons to graded colorectal distension (CRD) as in rats. Experiments were done on anesthetized male monkeys ( Macaca fascicularis). Extracellular single cell recordings were made in the ventrolateral complex of the thalamus, mainly the ventral posterolateral (VPL) nucleus, in response to visceral and cutaneous stimulation. Of 80 VPL cells isolated, CRD activated 25, inhibited 25, and had no effect on 30 neurons. The responses of six viscerosensitive VPL neurons were recorded before and after a lesion of the DC at or above the T10 spinal segment. Lesions of other spinal tracts were made after the DC lesion. The results show that the DC lesion significantly reduced the responses of the thalamic neurons tested with CRD by >50%. Lesions of other tracts did not have a consistent effect. These results corroborate findings in the rat and support the proposal that the DC plays an important role in transmitting nociceptive visceral input into the thalamus and subsequently in visceral pain.
Encoding of Shape and Orientation of Objects Indented Into the Monkey Fingerpad by Populations of Slowly and Rapidly Adapting Mechanoreceptors
Authors: Khalsa Partap S. , Friedman Robert M. , Srinivasan Mandayam A. , Lamotte Robert H.
Published: December 2017

Khalsa, Partap S., Robert M. Friedman, Mandayam A. Srinivasan, and Robert H. LaMotte. Encoding of shape and orientation of objects indented into the monkey fingerpad by populations of slowly and rapidly adapting mechanoreceptors. J. Neurophysiol. 79: 3238–3251, 1998. The peripheral neural representation of object shape and orientation was studied by recording the responses of a spatially distributed population of rapidly and slowly adapting type I mechanoreceptors (RAs and SAs, respectively) to objects of different shapes and orientations indented at a fixed location on the fingerpad of the anesthetized monkey. The toroidal objects had a radius of 5 mm on the major axis, and 1, 3, or 5 mm on the minor axis. Each object was indented into the fingerpad for 4 s at orientations of 0, 45, 90, and 135° using a contact force of 15 gwt. Estimations of the population responses (PRs) were constructed by combining the responses of 91 SA and 97 RA single afferents at discrete times during the indentation. The PR was composed of the neural discharge rates ( z coordinate) plotted at x and y coordinates of the most sensitive spot of the receptive field. The shapes of the PRs were related to the shapes of the objects by fitting the PRs with Gaussian surfaces. The orientations of the PRs were determined from weighted principal component analyses. The SA PR encoded both the orientation and shape of the objects, whereas the RA PR did neither. The SA PR orientation was biased toward the long axis of the finger. The RA PR encoded orientation only for the object with the highest curvature but did so ambiguously. Only the SA PR was well fit by a Gaussian surface. The shape of the object was discriminated by the SA PR within the first 500 ms of contact, and the form of the SA PR remained constant during the subsequent 3.5 s. This was manifested by constant widths of the PR along the major and minor axes despite a peak response that decreased from its maximum at 200 ms to an asymptotic value starting at 1 s. Thus the shape and orientation of each object were coded by the shape and orientation of the SA PR.
Trophic and Contact Conditions Modulate Synapse Formation Between Identified Neurons
Authors: Magoski Neil S. , Bulloch Andrew G. M.
Published: December 2017

Magoski, Neil S. and Andrew G. M. Bulloch. Trophic and contact conditions modulate synapse formation between identified neurons. J. Neurophysiol. 79: 3279–3283, 1998. We tested the ability of an identified interneuron from the mollusk, Lymnaea stagnalis, to reestablish appropriate synapses in vitro. In the CNS, the giant dopaminergic neuron, designated as right pedal dorsal one (RPeD1), makes an excitatory, chemical synapse with a pair of essentially identical postsynaptic cells known as visceral dorsal two and three (VD2/3). When the somata of the pre- and postsynaptic neurons were juxtaposed and cultured in vitro in defined medium, i.e., a soma-soma synapse, only an inappropriate electrical synapse was observed. The postsynaptic cell still responded to applied dopamine, the presynaptic transmitter, indicating that the lack of chemical synapse formation was not due to lack of dopamine receptors. When the somata were cultured apart in conditioned medium (medium previously incubated with Lymnaea CNS, thereby deriving trophic factors), the cells exhibited overlapping neurite outgrowth that resulted in an appropriate excitatory, chemical synapse from RPeD1 to VD2/3. On the other hand, when the cell pair was cultured in a soma-soma configuration, but in conditioned medium, a mixed chemical-electrical synapse was observed. Because conditioned medium could partially overcome the limitations of the soma-soma configuration and initiate chemical synapse formation, this data suggests that conditioned medium contains a factor(s) that supports synaptogenesis.
Periodicity of Thalamic Spindle Waves Is Abolished by ZD7288,a Blocker of I h
Authors: Lüthi Anita , Bal Thierry , McCormick David A.
Published: December 2017

Lüthi, Anita, Thierry Bal, and David A. McCormick. Periodicity of thalamic spindle waves is abolished by ZD7288, a blocker of I h. J. Neurophysiol. 79: 3284–3289, 1998. The actions of the novel bradycardiac agent ZD7288 [4-( N-ethyl- N-phenylamino)-1,2-dimethyl-6-(methylamino)pyrimidinium chloride] were investigated on the hyperpolarization-activated cation current I h and on network activity in spontaneously spindling ferret lateral geniculate (LGNd) slices in vitro using intracellular recording techniques. In voltage-clamp recordings, local application of ZD7288 (1 mM in micropipette) resulted in a complete block of I h, whereas in current-clamp recordings, application of this agent resulted in an abolition of the depolarizing sag activated by hyperpolarization and decreased the frequency of intrinsic δ-oscillations for which I h acts as a pacemaker current. In addition, block of I h with ZD7288 resulted in an abolition of the afterdepolarization (ADP) that follows repetitive hyperpolarization and rebound burst firing as well as that occurring in between spindle waves. The block of the ADP was associated with a block of the spindle wave refractory period such that continuous 6- to 10-Hz oscillations were generated throughout the network. These findings give further support to the hypothesis that I h is critically involved in the generation of slow rhythmicity in synchronized thalamic activity.
Pointing Errors Reflect Biases in the Perception of the InitialHand Position
Authors: Vindras Philippe , Desmurget Michel , Prablanc Claude , Viviani Paolo
Published: December 2017

Vindras, Philippe, Michel Desmurget, Claude Prablanc, and Paolo Viviani. Pointing errors reflect biases in the perception of the initial hand position. J. Neurophysiol. 79: 3290–3294, 1998. By comparing the visuomotor performance of 10 adult, normal subjects in three tasks, we investigated whether errors in pointing movements reflect biased estimations of the hand starting position. In a manual pointing task with no visual feedback, subjects aimed at 48 targets spaced regularly around two starting positions. Nine subjects exhibited a similar pattern of systematic errors across targets, i.e., a parallel shift of the end points that accounted, on average, for 49% of the total variability. The direction of the shift depended on the starting location. Systematic errors decreased dramatically in the second condition where subjects were allowed to see their hand before movement onset. The third task was to use a joystick held by the left hand to estimate the location of their (unseen) right hand. The systematic perceptual errors in this condition were found to be highly correlated with the motor errors in the first condition. The results support the following conclusions. 1) Kinesthetic estimation of hand position may be consistently biased. Some of the mechanisms responsible for these biases are always active, irrespective of whether position is estimated overtly (e.g., with a matching paradigm), or covertly as part of the motor planning for aimed movements. 2) Pointing errors reflect to a significant extent the erroneous estimation of initial hand position. This suggests that aimed hand movements are planned vectorially, i.e., in terms of distance and direction, rather than in terms of absolute position in space.
Control of Size and Excitability of Mechanosensory Receptive Fields in Dorsal Column Nuclei by Homolateral Dorsal Horn Neurons
Authors: Dykes Robert W. , Craig A. D.
Published: December 2017

Dykes, Robert W. and A. D. Craig. Control of size and excitability of mechanosensory receptive fields in dorsal column nuclei by homolateral dorsal horn neurons. J. Neurophysiol. 80: 120–129 1998. Both accidental and experimental lesions of the spinal cord suggest that neuronal processes occurring in the spinal cord modify the relay of information through the dorsal column-lemniscal pathway. How such interactions might occur has not been adequately explained. To address this issue, the receptive fields of mechanosensory neurons of the dorsal column nuclei were studied before and after manipulation of the spinal dorsal horn. After either a cervical or lumbar laminectomy and exposure of the dorsal column nuclei in anesthetized cats, the representation of the hindlimb or of the forelimb was defined by multiunit recordings in both the dorsal column nuclei and in the ipsilateral spinal cord. Next, a single cell was isolated in the dorsal column nuclei, and its receptive field carefully defined. Each cell could be activated by light mechanical stimuli from a well-defined cutaneous receptive field. Generally the adequate stimulus was movement of a few hairs or rapid skin indentation. Subsequently a pipette containing either lidocaine or cobalt chloride was lowered into the ipsilateral dorsal horn at the site in the somatosensory representation in the spinal cord corresponding to the receptive field of the neuron isolated in the dorsal column nuclei. Injection of several hundred nanoliters of either lidocaine or cobalt chloride into the dorsal horn produced an enlargement of the receptive field of the neuron being studied in the dorsal column nuclei. The experiment was repeated 16 times, and receptive field enlargements of 147–563% were observed in 15 cases. These data suggest that the dorsal horn exerts a tonic inhibitory control on the mechanosensory signals relayed through the dorsal column-lemniscal pathway. Because published data from other laboratories have shown that receptive field size is controlled by signals arising from the skin, we infer that the control of neuronal excitability, receptive field size and location for lemniscal neurons is determined by tonic afferent activity that is relayed through a synapse in the dorsal horn. This influence of dorsal horn neurons on the relay of mechanosensory information through the lemniscal pathways must modify our traditional views concerning the relative independence of these two systems.
GABAergic Inhibition Influences Auditory Motion-Direction Sensitivity in Barn Owls
Authors: Kautz Dirk , Wagner Hermann
Published: December 2017

Kautz, Dirk and Hermann Wagner. GABAergic inhibition influences auditory motion-direction sensitivity in barn owls. J. Neurophysiol. 80: 172–185, 1998. Many neurons in the barn owl's inferior colliculus (IC) exhibit auditory motion-direction sensitivity (MDS), i.e., they respond more to motion of a sound source in one direction than to motion in the opposite direction. We investigated the cellular mechanisms underlying the phenomenon of auditory MDS by microiontophoretically applying γ-aminobutyric acid (GABA) or the GABA-antagonist bicuculline methiodide (BMI) while recording from neurons in the owl's midbrain. In most cases GABA reduced the overall firing rate, whereas BMI increased it. In addition, 29% of the motion-direction–sensitive cells completely lost their selectivity for the direction of auditory movement during administration of BMI. It had been proposed that auditory MDS in the owl is due to inhibition. The present results show that GABAergic inhibition plays a role in the strengthening of MDS. We discuss the data within the framework of the acoustic motion detector and with respect to microiontophoretic studies on visual motion detection and on inhibitory mechanisms in the inferior colliculus.
Endogenous NMDA-Receptor Activation Regulates Glutamate Release in Cultured Spinal Neurons
Authors: Robert Antoine , Black Joel A. , Waxman Stephen G.
Published: December 2017

Robert, Antoine, Joel A. Black, and Stephen G. Waxman. Endogenous NMDA-receptor activation regulates glutamate release in cultured spinal neurons. J. Neurophysiol. 80: 196–208, 1998. N-methyl-d-aspartate (NMDA) receptor activation plays a fundamental role in the genesis of electrical activity of immature neurons and may participate in activity-dependent aspects of CNS development. A recent study has suggested that NMDA-receptor–mediated glutamatergic neurotransmission might occur in the developing spinal cord via activation of nonsynaptic receptors, but the details of NMDA-receptor activation in the developing CNS are not yet well understood. We describe here a model of cultured spinal neurons that display ongoing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor activity characterized by spontaneous excitatory postsynaptic currents (EPSCs), with NMDA-receptor activity detectable only as single channel events. dl-2-amino-5-phosphonovaleric acid (100 μM) and tetrodotoxin (TTX) 100 nM each reduced the occurrence of spontaneous AMPA EPSCs; quantal analysis showed a decrease in the number of released quanta but no changes in quantal size, indicating that NMDA-receptor activation and Na+channel activity affect the generation of spontaneous AMPA EPSCs, at least in part, via mechanisms that impinge on the presynaptic terminal. Once the Mg2+-block was released, activity of NMDA receptors dramatically increased the release of quantal and multiquantal amounts of glutamate, indicating that the NMDA receptors are physiologically coupled to glutamate release. In Mg2+-free solution, TTX application elicited an increase in the number of quantal AMPA EPSCs and a reduction in the number of multiquantal EPSCs, consistent with an effect of NMDA-receptor activation on presynaptic terminals. Our results suggest that endogenous activity at a small number of NMDA receptors can regulate the release of neurotransmitters at developing AMPA synapses.
Distribution of Effective Synaptic Currents in Cat Triceps Surae Motoneurons. VI. Contralateral Pyramidal Tract
Authors: Binder Marc D. , Robinson Farrel R. , Powers Randall K.
Published: December 2017

Binder, Marc D., Farrel R. Robinson, and Randall K. Powers. Distribution of effective synaptic currents in cat triceps surae motoneurons. VI. Contralateral pyramidal tract. J. Neurophysiol. 80: 241–248, 1998. We measured the effective synaptic currents ( I N) produced by stimulating the contralateral pyramidal tract (PT) in triceps surae motoneurons of the cat. This is an oligosynaptic pathway in the cat that generates both excitation and inhibition in hindlimb motoneurons. We also determined the effect of the PT synaptic input on the discharge rate of some of the motoneurons by inducing repetitive firing with long, injected current pulses during which the PT stimulation was repeated. At resting potential, all but one triceps motoneuron received a net depolarizing effective synaptic current from the PT stimulation. The effective synaptic currents ( I N) were much larger in putative type F motoneurons than in putative type S motoneurons [+4.6 ± 2.9 (SD) nA for type F vs. 0.9 ± 2.4 nA for putative type S]. When the values of I N at the threshold for repetitive firing were estimated, the distribution was markedly altered. More than 60% of the putative type S motoneurons received a net hyperpolarizing effective synaptic current from the pyramidal tract stimulation as did 33% of the putative type F motoneurons. This distribution pattern is very similar to that observed previously for the effective synaptic currents produced by stimulating the contralateral red nucleus. As would be expected from the wide range of I N values at threshold (−4.8 to +8.7 nA), the PT stimulation produced dramatically different effects on the discharge of different triceps motoneurons. The discharge rates of those motoneurons that received depolarizing effective synaptic currents at threshold were accelerated by PT stimulation (+1 to +8 imp/s), whereas the discharge rates of cells that received hyperpolarizing currents were retarded by the PT input (−2 to −7 imp/s). The change in firing rates produced by the PT stimulation was generally approximated by the product of the effective synaptic currents and the slopes of the motoneurons' frequency-current relations. Our findings indicate that the contralateral pyramidal tract may provide a powerful source of synaptic drive to some high-threshold motoneurons while concurrently inhibiting low-threshold cells. Thus this input system, like that from the contralateral red nucleus, can potentially alter the gain of the input-output function of the motoneuron pool as well as disrupt the normal hierarchy of recruitment thresholds.
Carrier-Mediated GABA Release Activates GABA Receptors on Hippocampal Neurons
Authors: Gaspary Heidi L. , Wang Wengang , Richerson George B.
Published: December 2017

Gaspary, Heidi L., Wengang Wang, and George B. Richerson. Carrier-mediated GABA release activates GABA receptors on hippocampal neurons. J. Neurophysiol. 80: 270–281, 1998. γ-Aminobutyric acid (GABA) transporters are electrogenic and sodium-dependent and can operate in reverse when cells are depolarized or when there is reversal of the inward sodium gradient. However, the functional relevance of this phenomenon is unclear. We have examined whether depolarization induced by a physiologically relevant increase in extracellular [K+] leads to sufficient amounts of carrier-mediated GABA release to activate GABAAreceptors on neurons. Patch-clamp recordings were made from rat hippocampal neurons in culture with solutions designed to isolate chloride currents in the recorded neuron. Pressure microejection was used to increase extracellular [K+] from 3 to 12 mM. After blockade of vesicular GABA release by removal of extracellular calcium, this stimulus induced a large conductance increase in hippocampal neurons [18.9 ± 6.8 (SD) nS; n = 16]. This was blocked by the GABAAreceptor antagonists picrotoxin and bicuculline and had a reversal potential that followed the Nernst potential for chloride, indicating that it was mediated by GABAAreceptor activation. Similar responses occurred after block of vesicular neurotransmitter release by tetanus toxin. GABAAreceptors also were activated when an increase in extracellular [K+] (from 3 to 13 mM) was combined with a reduction in extracellular [Na+] or when cells were exposed to a decrease in extracellular [Na+] alone. These results indicate that depolarization and/or reversal of the Na+gradient activated GABA receptors via release of GABA from neighboring cells. We found that the GABA transporter antagonists 1-(4,4-diphenyl-3-butenyl)-3-piperidinecarboxylic acid hydrochloride (SKF89976A; 20–100 μM) and 1-(2-{[(diphenylmethylene)amino]oxy}ethyl) -1, 2, 5, 6 - tetrahydro - 3 - pyridine - carboxylic acid hydrochloride (NO-711; 10 μM) both decreased the responses, indicating that the release of GABA resulted from reversal of the GABA transporter. We propose that carrier-mediated GABA release occurs in vivo during high-frequency neuronal firing and seizures, and dynamically modulates inhibitory tone.