bluuebunny/crossref_metadata_2025 huggingface dataset:
Mechanisms of Electrical Coupling Between Pyramidal Cells
Authors: Vigmond Edward J. , Velazquez Jose L. Perez , Valiante Taufik A. , Bardakjian BERJ L. , Carlen Peter L.
Published: December 2017

Vigmond, Edward J., Jose L. Perez Velazquez, Taufik A. Valiante, Berj L. Bardakjian, and Peter L. Carlen. Mechanisms of electrical coupling between pyramidal cells. J. Neurophysiol. 78: 3107–3116, 1997. Direct electrical coupling between neurons can be the result of both electrotonic current transfer through gap junctions and extracellular fields. Intracellular recordings from CA1 pyramidal neurons of rat hippocampal slices showed two different types of small-amplitude coupling potentials: short-duration (5 ms) biphasic spikelets, which resembled differentiated action potentials and long-duration (>20 ms) monophasic potentials. A three-dimensional morphological model of a pyramidal cell was employed to determine the extracellular field produced by a neuron and its effect on a nearby neuron resulting from both gap junctional and electric field coupling. Computations were performed with a novel formulation of the boundary element method that employs triangular elements to discretize the soma and cylindrical elements to discretize the dendrites. An analytic formula was derived to aid in computations involving cylindrical elements. Simulation results were compared with biological recordings of intracellular potentials and spikelets. Field effects produced waveforms resembling spikelets although of smaller magnitude than those recorded in vitro. Gap junctional electrotonic connections produced waveforms resembling small-amplitude excitatory postsynaptic potentials. Intracellular electrode measurements were found inadequate for ascertaining membrane events because of externally applied electric fields. The transmembrane voltage induced by the electric field was highly spatially dependent in polarity and wave shape, as well as being an order of magnitude larger than activity measured at the electrode. Membrane voltages because of electrotonic current injection across gap junctions were essentially constant over the cell and were accurately depicted by the electrode. The effects of several parameters were investigated: 1) decreasing the ratio of intra to extracellular conductivity reduced the field effects; 2) the tree structure had a major impact on the intracellular potential; 3) placing the gap junction in the dendrites introduced a time delay in the gap junctional mediated electrotonic potential, as well as deceasing the potential recorded by the somatic electrode; and 4) field effects decayed to one-half of their maximum strength at a cell separation of ∼20 μm. Results indicate that the in vitro measured spikelets are unlikely to be mediated by gap junctions and that a spikelet produced by the electric field of a single source cell has the same waveshape as the measured spikelet but with a much smaller amplitude. It is hypothesized that spikelets are a manifestation of the simultaneous electric field effects from several local cells whose action potential firing is synchronized.
Voltage-Dependent Conductances in Cephalopod Primary Sensory Hair Cells
Authors: Chrachri Abdesslam , Williamson Roddy
Published: December 2017

Chrachri, Abdesslam and Roddy Williamson. Voltage-dependent conductances in primary sensory hair cells. J. Neurophysiol. 78: 3125–3132, 1997. Cephalopods, such as sepia, squid, and octopus, show a well-developed and sophisticated control of balance particularly during prey capture and escape behaviors. There are two separate areas of sensory epithelium in cephalopod statocysts, a macula/statolith system, which detects linear accelerations (gravity), and a crista/cupula system, which detects rotational movements. The aim of this study is to characterize the ionic conductances in the basolateral membrane of primary sensory hair cells. These were studied using a whole cell patch-clamp technique, which allowed us to identify five ionic conductances in the isolated primary hair cells; an inward sodium current, an inward calcium current, and three potassium outward currents. These outward currents were distinguishable on the basis of their voltage-dependence and pharmacological sensitivities. First, a transient outward current ( IA) was elicited by depolarizing voltage steps from a holding potential of −60 mV, was inactivated by holding the cell at −40 mV, and was blocked by 4-aminopyridine. A second, voltage-sensitive, outward current with a sustained time course was identified. This current was not blocked by 4-aminopyridine nor inactivated at a holding potential of −40 mV and hence could be separated from IAusing these protocols. A third outward current that depended on Ca2+entry for its activation was detected, this current was identified by its sensitivity to Ca2+channel blockers such as Co2+and Cd2+and by the N-shaped profile of its current-voltage curve. Inward currents were studied using cesium aspartate solution in the pipette to block the outward currents. Two inward currents were observed in the primary sensory hair cells. A fast transient inward current, which is presumably responsible for spike generation. This inward current appeared as a rapidly activating inward current; this was strongly voltage dependent. Three lines of evidence suggest that this fast transient inward current is a Na+current ( INa). First, it was blocked by tetrodotoxin (TTX); second, it also was blocked by Na+-free saline; and third, it was inactivated when primary hair cells were held at a potential more than −40 mV. The sustained inward current was not affected by TTX and was increased in amplitude 5 min after equimolar Ba2+replaced Ca2+as a charge carrier. This inward current also was blocked after external application of 2 mmol/l Co2+or Cd2+. Furthermore, this current was reduced significantly in a dose-dependent manner by nifedipine, suggesting that it is an L-type Ca2+current ( ICa).
Functional Analysis of the Sensory Motor Pathway of Resistance Reflex in Crayfish. I. Multisensory Coding and Motor Neuron Monosynaptic Responses
Authors: Ray Didier Le , Clarac François , Cattaert Daniel
Published: December 2017

Le Ray, Didier, François Clarac, and Daniel Cattaert. Functional analysis of the sensory motor pathway of resistance reflex in crayfish. I. Multisensory coding and motor neuron monosynaptic responses. J. Neurophysiol. 78: 3133–3143, 1997. An in vitro preparation of the fifth thoracic ganglion of the crayfish was used to study in detail the negative feedback loop involved in the control of passive movements of the leg. Release-sensitive primary afferents of from the coxo-basipodite chordotonal organ (CBCO), a proprioceptor whose strand is released by upward movement of the leg, monosynaptically connect to depressor motor neurons (Dep MNs). Extracellular identification of sensory units from the CBCO neurogram allowed us to determine the global coding of a sine-wave movement, imposed from the most released position of the CBCO strand. Intracellular recordings from sensory terminals (CBTs) and ramp movement stimulations applied to the CBCO strand allowed us to characterize two groups of release-sensitive CBCO fibers. The first group, divided into two subgroups (phasic and phaso-tonic), is characterized by discontinuous firing patterns: phasic CBTs fired exclusively during release movements; phaso-tonic CBTs displayed both a phasic firing and a tonic discharge during the more released plateaus. The second group was continuously firing whatever the movement, with higher frequencies during the release phase of the movement stimulation. All CBTs displayed a marked sensitivity for release movements while only the phaso-tonic ones showed a clear sensitivity to maintained positions. Surprisingly, no pure tonic sensory fibers were encountered. Systematic intracellular recordings from all resistant Dep MNs, performed in high divalent cation saline, allowed us to describe two shapes of monosynaptic resistance reflex responses. A phasic response was characterized by bursts of excitatory postsynaptic potentials (EPSPs) occurring exclusively during CBCO strand release movements. A phaso-tonic response was characterized by a progressive depolarization occurring all along the release phase of the stimulation: during maintained released positions, the amplitude of the sustained depolarization was position dependent; in addition, each release movement produced a phasic burst of EPSPs in the MN. The parallel study of the Dep MN properties failed to point out any correlation between the type of reflex response recorded from the MN and the MN intrinsic properties, which would indicate that the type of MN response is entirely determined by the afferent messages it receives.
Amine Modulation of Glutamate Responses From Pyloric Motor Neurons in Lobster Stomatogastric Ganglion
Authors: Johnson Bruce R. , Harris-Warrick Ronald M.
Published: December 2017

Johnson, Bruce R. and Ronald M. Harris-Warrick. Amine modulation of glutamate responses from pyloric motor neurons in lobster stomatogastric ganglion. J. Neurophysiol. 78: 3210–3221, 1997. The amines dopamine (DA), serotonin (5-HT), and octopamine (Oct) each elicit a distinctive motor pattern from a quiescent pyloric network in the lobster stomatogastric ganglion (STG). We previously have demonstrated that these amines alter the synaptic strength at multiple, distributed sites within the pyloric network that could contribute to the amine-induced motor patterns. Here, we examined the postsynaptic contribution to these changes in synaptic strength by determining how the amines modify responses of pyloric motor neurons to glutamate (Glu), one of the network transmitters, applied iontophoretically into the STG neuropil. Dopamine reduced the Glu responses of the pyloric dilator (PD), ventricular dilator (VD), and inferior cardiac (IC) neurons and enhanced the Glu responses of the lateral pyloric (LP) and pyloric constrictor (PY) neurons. The only effect of 5-HT was to reduce the Glu response of the VD neuron. Oct enhanced the Glu responses of the LP and PY neurons but did not affect the PD, VD, and IC responses. We also examined amine effects on the depolarizing responses to iontophoresed acetylcholine (ACh) in the PD and VD and found that they paralleled the amine effects on Glu responses in these neurons. This suggests that amine modulation of PD and VD responses to Glu and ACh may be explained by general changes in the ionic conductance of these neurons. We compare our results with our earlier work describing amine effects on synaptic strength and input resistance to show that amines act at both pre- and postsynaptic sites to modify graded synaptic transmission in the pyloric network.
Electrophysiological Properties of Rat Pontine Nuclei Neurons In Vitro II. Postsynaptic Potentials
Authors: Möck Martin , Schwarz Cornelius , Thier Peter
Published: December 2017

Möck, Martin, Cornelius Schwarz, and Peter Thier. Electrophysiological properties of rat pontine nuclei neurons in vitro. II. Postsynaptic potentials. J. Neurophysiol. 78: 3338–3350, 1997. We investigated the postsynaptic responses of neurons of the rat pontine nuclei (PN) by performing intracellular recordings in parasagittal slices of the pontine brain stem. Postsynaptic potentials (PSPs) were evoked by brief (0.1 ms) negative current pulses (10–250 μA) applied to either the cerebral peduncle or the pontine tegmentum. First, excitatory postsynaptic potentials (EPSPs) could be evoked readily from peduncular stimulation sites. These EPSPs exhibited short latencies, a nonlinear increment in response to increased stimulation currents, and an unconventional dependency on the somatic membrane potential. Pharmacological blockade of the synaptic transmission using 6,7-dinitroquinoxaline-2,3-dione and d,l-2-amino-5-phosphonovaleric acid, selective antagonists of the α-amino-3-hydroxy-5-methyl-4-isoxazilepropionate- (AMPA) and the N-methyl-d-aspartate (NMDA)-type glutamate receptors, showed that these EPSPs were mediated exclusively by excitatory amino acids via both AMPA and NMDA receptors. Moreover, the pharmacological experiments indicated the existence of voltage-sensitive but NMDA receptor-independent amplification of EPSPs. Second, stimulations at peduncular and tegmental sites also elicited inhibitory postsynaptic potentials (IPSPs) in a substantial proportion of pontine neurons. The short latencies of all IPSPs argued against the participation of inhibitory interneurons. Their sensitivity to bicuculline and reversal potentials around −70 mV suggested that they were mediated by γ-aminobutyric acid-A (GABAA) receptors. In addition to single PSPs, sequences consisting of two to four distinct EPSPs could be recorded after stimulation of the cerebral peduncle. Most remarkably, the onset latencies of the following EPSPs were multiples of the first one indicating the involvement of intercalated synapses. Finally, we used the classic paired-pulse paradigm to study whether the temporal structure of inputs influences the synaptic transmission onto pontine neurons. Pairs of electrical stimuli applied to the cerebral peduncle resulted in a marked enhancement of the amplitude of the second EPSP for interstimulus intervals of 10–100 ms. Delays >200 ms left the EPSP amplitude unaltered. These data provide evidence for a complex synaptic integration and an intrinsic connectivity within the PN too elaborate to support the previous notion that the PN are simply a relay station.
Dopaminergic Modulation of Inhibitory Glutamate Receptors in the Lobster Stomatogastric Ganglion
Authors: Cleland Thomas A. , Selverston Allen I.
Published: December 2017

Cleland, Thomas A. and Allen I. Selverston. Dopaminergic modulation of inhibitory glutamate receptors in the lobster stomatogastric ganglion. J. Neurophysiol. 78: 3450–3452, 1997. The intrinsic rhythmicity of the spiny lobster stomatogastric ganglion (STG) is strongly influenced by the strengths of the graded synapses between identified cells within the neural network. These synaptic strengths can be powerfully influenced by chemical neuromodulators such as dopamine and serotonin. Most of the intraganglionic chemical synapses in the STG are mediated by postsynaptic inhibitory glutamate receptors (IGluRs). To determine whether or not direct effects on these IGluRs contribute to the modulation of synaptic strength, unidentified STG neurons were extracted into primary culture and the effects of these aminergic neuromodulators on the glutamate-evoked membrane current were assessed. Dopamine (100 μM) reliably and significantly reduced the whole cell slope conductance of all IGluRs tested. Serotonin (20 μM) never affected the IGlu response, although it clearly altered other cellular membrane properties. Although all identified STG neurons may not conform to these observations, the data reveal a specific dopamine-activated modulatory pathway within cultured neurons that reduces IGluR slope conductance. The relationship between IGluR modulation and net synaptic modulation in situ contributes to an emerging model in which synaptic strengths can be multiply modulated at different functional sites, yielding a complex, distributed, and state-dependent regulatory structure.
Imaging of Calcium in Drosophila Larval Motor Nerve Terminals
Authors: Karunanithi Shanker , Georgiou John , Charlton Milton P. , Atwood Harold L.
Published: December 2017

Karunanithi, Shanker, John Georgiou, Milton P. Charlton, and Harold L. Atwood. Imaging of calcium in Drosophila larval motor nerve terminals. J. Neurophysiol. 78: 3465–3467, 1997. Calcium measurements in the presynaptic terminal are essential in the investigation of mechanisms underlying neurotransmitter release. To enhance the genetic analysis of secretory mechanisms, we have developed Ca2+ imaging techniques for Drosophila larval motor nerve terminals. We studied Ca2+ signals in “big” (type Ib) and “small” (type Is) boutons that innervate ventral longitudinal muscles 6 and 7 in each abdominal segment of Canton-S (CS)-strain 3rd instar larvae. The indicator fluo-3 in conjunction with confocal microscopy was used to detect stimulus-dependent changes in [Ca2+]i. The Ca2+ signals were reliable and reproducible, and the resting fluorescence remained constant throughout the experiments. The Ca2+ signals increased with stimulus frequency from 5 to 20 Hz for both bouton types. No significant differences in the Ca2+ signals were seen between the two bouton types at 5 and 20 Hz, but there was a difference at 10 Hz. The decay of the Ca2+ signal was more prolonged after 20-Hz stimulation than after 5 and 10 Hz. At the single-synapse level, the secretory efficacy of Is synapses is greater than that of Ib synapses, but our data show that factors other than differences in Ca2+ entry may govern the strength of synaptic transmission.
Loss of Long-Lasting Potentiation Mediated by Group III mGluRs in Amygdala Neurons in Kindling-Induced Epileptogenesis
Authors: Neugebauer Volker , Keele N. Bradley , Shinnick-Gallagher Patricia
Published: December 2017

Neugebauer, Volker, N. Bradley Keele, and Patricia Shinnick-Gallagher. Loss of long-lasting potentiation mediated by group III mGluRs in amygdala neurons in kindling-induced epileptogenesis. J. Neurophysiol. 78: 3475–3478, 1997. Long-lasting modifications of synaptic transmission can be induced in the amygdala by electrical stimulation as done in the long-term potentiation (LTP) model of learning and memory and the kindling model of epilepsy. The present study reports for the first time a long-lasting potentiation (LLP) of synaptic transmission that is induced pharmacologically by the activation of group III metabotropic glutamate receptors (mGluRs) in basolateral amygdala (BLA) neurons. In whole cell voltage-clamp mode, BLA neurons were recorded in brain slices from control rats and rats with amygdala-kindled seizures. The group III mGluR agonist l-2-amino-4-phosphonobutyrate (l-AP4, 10 μM) induced LLP of monosynaptic excitatory postsynaptic currents (EPSCs) evoked by electrical stimulation in the lateral amygdala (maximum 258 ± 50% of predrug control; means ± SE) in control ( n = 7) but not in kindled neurons( n = 6). LLP was measured 15 min after the superfusion of l-AP4, lasted for >45 min, and was not accompanied by postsynaptic membrane changes. l-AP4 induced LLP was prevented by the group III mGluR antagonist (S)-2-methyl-2-amino-4-phosphonobutyrate (MAP4; 100 μM, n = 6) but not the group II mGluR antagonist (2S,3S,4S)-2-methyl-2-carboxycyclopropylglycine (MCCG; 100 μM, n = 3). LLP was not observed after superfusion of the group II mGluR agonist (2S,3S,4S)-2-(carboxycyclopropyl)glycine (l-CCG; 1.0 and 10 μM) in either control ( n = 13) or kindled ( n = 10) neurons. If the underlying mechanisms and the functional significance of pharmacologically induced LLP are similar to those of LTP, the loss of l-AP4 induced LLP in kindled neurons may be a neurobiological correlate of learning and memory deficits in kindled animals and long-term alterations of brain functions in patients with epilepsies.
Corticofugal Amplification of Subcortical Responses to Single Tone Stimuli in the Mustached Bat
Authors: Zhang Yunfeng , Suga Nobuo
Published: December 2017

Zhang, Yunfeng and Nobuo Suga. Corticofugal amplification of subcortical responses to single tone stimuli in the mustached bat. J. Neurophysiol. 78: 3489–3492, 1997. Since 1962, physiological data of corticofugal effects on subcortical auditory neurons have been controversial: inhibitory, excitatory, or both. An inhibitory effect has been much more frequently observed than an excitatory effect. Recent studies performed with an improved experimental design indicate that corticofugal system mediates a highly focused positive feedback to physiologically “matched” subcortical neurons, and widespread lateral inhibition to “unmatched” subcortical neurons, in order to adjust and improve information processing. These results lead to a question: what happens to subcortical auditory responses when the corticofugal system, including matched and unmatched cortical neurons, is functionally eliminated? We temporarily inactivated both matched and unmatched neurons in the primary auditory cortex of the mustached bat with muscimol (an agonist of inhibitory synaptic transmitter) and measured the effect of cortical inactivation on subcortical auditory responses. Cortical inactivation reduced auditory responses in the medial geniculate body and the inferior colliculus. This reduction was larger (60 vs. 34%) and faster (11 vs. 31 min) for thalamic neurons than for collicular neurons. Our data indicate that the corticofugal system amplifies collicular auditory responses by 1.5 times and thalamic responses by 2.5 times on average. The data are consistant with a scheme in which positive feedback from the auditory cortex is modulated by inhibition that may mostly take place in the cortex.
Monkey Posterior Parietal Cortex Neurons Antidromically Activated From Superior Colliculus
Authors: Paré Martin , Wurtz Robert H.
Published: December 2017

Paré, Martin and Robert H. Wurtz. Monkey posterior parietal cortex neurons antidromically activated from superior colliculus. J. Neurophysiol. 78: 3493–3497, 1997. The connection between the posterior parietal cortex (PPC) and the superior colliculus (SC) was investigated by antidromically activating neurons within the lateral intraparietal (LIP) area with single-pulse stimulation delivered to the intermediate layers of the SC. To dissociate visual and saccade-related responses, the discharge properties of the identified efferent neurons were studied in the delayed visually guided saccade task and the memory guided saccade task. We found that the great majority (74%) of the identified LIP efferent neurons have a peripheral visual receptive field, typically with a broad spatial tuning. About two-thirds (64%) exhibited sustained activity during the delay period of the behavioral tasks, during which the monkeys had to withhold eye movements, and 80% of these increased their activity just before the onset of saccades. Both delay and presaccadic discharges in the delayed visually guided saccade task were higher than in the memory guided saccade task. These results establish that the neuronal signal sent by LIP to the SC carries both visual and saccade-related information.
Models of Neuronal Transient Synchrony During Propagation of Activity Through Neocortical Circuitry
Authors: Golomb David
Published: December 2017

Golomb, David. Models of neuronal transient synchrony during propagation of activity through neorcortical circuitry. J. Neurophysiol. 79: 1–12, 1998. Stereotypic paroxysmal discharges that propagate in neocortical tissues after electrical stimulations are used as a probe for studying cortical circuitry. I use modeling to investigate the effects of sparse connectivity, heterogeneity of intrinsic neuronal properties, and synaptic noise on synchronization of evoked propagating neuronal discharges in a network of excitatory, regular spiking neurons with spatially decaying connectivity. The global coherence of the traveling discharge is characterized by the correlation function between spike trains of neurons, averaged over all the pairs of neurons in the system at the same distance. Local coherence of two neurons is characterized by their correlation function averaged over many trials or, for persistent activity, over a long time interval. Spike synchronization between neurons emerges as a result of the transient activity; if activity is persistent, there is no synchrony, and cross-correlation functions are flat. During discharge propagation, system-average cross-correlation between neurons does not depend on their mutual distance except for a time shift. Spike synchronization occurs only when the average number of synapses M a cell receives is large enough. As M increases, there is a cross-over from an asynchronized to a synchronized discharge. Synaptic depression appears to help synchrony; it reduces the M value at the cross-over. The strengths of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) conductances affect synchrony only weakly. Spike synchronization is robust even with large levels of heterogeneity. Synaptic noise reduces synchrony, but strong synchrony is observed at a noise level that cannot evoke spontaneous discharges. System-average spike synchronization is determined by the levels of sparseness, heterogeneity, and noise, whereas trial-average spike synchronization is determined only by the noise level. Therefore, I predict that experiments will reveal local, two-cell spike synchrony, but not global synchrony.
Local Circuit Abnormalities in Chronically Epileptic Rats After Intrahippocampal Tetanus Toxin Injection in Infancy
Authors: Smith Karen L. , Lee Chong L. , Swann John W.
Published: December 2017

Smith, Karen L. Chong L. Lee, and John W. Swann. Local circuit abnormalities in chronically epileptic rats after intrahippocampal tetanus toxin injection in infancy. J. Neurophysiol. 79: 106–116, 1998. In vitro slice experiments were undertaken in adult rats to investigate the physiological origins of a chronic epileptic condition that was initiated in infancy. A unilateral injection of a minute quantity of tetanus toxin into hippocampus on postnatal day 10 produced a severe convulsive syndrome characterized by brief but repeated seizures that lasted for 5–7 days. Hippocampal slices were then taken from these rats in adulthood because at this time previous studies have shown the occurrence of electrographic and behavioral seizures. Dramatic alterations in local circuit functioning were observed. In normal artificial cerebrospinal fluid (ACSF), spontaneous epileptiform network bursts were recorded in a majority (73%) of experimental rats. Network bursts occurred in area CA3of both the injected and contralateral hippocampus. These consisted of intracellular depolarization shifts that were coincident with extracellularly recorded network bursts. Often they occurred at frequencies of 0.05–0.1 Hz and although variable in amplitude and duration, had all-or-none-like qualities. These events appeared to arise largely from local circuits in the CA3Csubfield. Network bursts were rarely recorded in area CA1and were never observed in the dentate gyrus. However in 31% of rats, a novel, higher frequency (2–8 Hz) field potential was recorded in area CA1. This was coincident with rhythmic, intracellularly recorded, inhibitory postsynaptic potentials (IPSPs). These summated IPSPs blocked action potential firing and reversed polarity near −75 mV. To understand the origins of network bursting in area CA3C, comparisons were made of the fundamental neurophysiological properties of pyramidal cells in epileptic and control rats. Of the passive and active membrane properties examined, all appeared normal. Unusually prolonged bursts of action potentials were observed in a small subset of pyramidal cells. However on average the duration of intrinsic bursts were unaltered in the CA3 neurons analyzed from experimental rats. To explore the role that alterations in CA3recurrent excitatory network excitability may play in epileptiform discharges, picrotoxin was bath applied. On blockade of γ-aminobutyric acid (GABAA) receptors, slices from experimental rats underwent prolonged electrographic seizures that were up to 10 s in duration. In contrast, slices from control rats produced only brief 100-ms network bursts. These results suggest that a change in excitability within CA3Crecurrent excitatory networks likely contributes to seizures in chronically epileptic rats. However, at the same time, this hyperexcitability is controlled to an important degree by functional GABAA-mediated synaptic inhibition.
Ventral Intraparietal Area of the Macaque: Congruent Visual and Somatic Response Properties
Authors: Duhamel Jean-René , Colby Carol L. , Goldberg Michael E.
Published: December 2017

Duhamel, Jean-René, Carol L. Colby, and Michael E. Goldberg. Ventral intraparietal area of the macaque: congruent visual and somatic response properties. J. Neurophysiol. 79: 126–136, 1998. In a previous report, we described the visual response properties in the ventral intraparietal area (area VIP) of the awake macaque. Here we describe the somatosensory response properties in area VIP and the patterns of correspondence between the responses of single neurons to independently administered tactile and visual stimulation. VIP neurons responded to visual stimulation only or to visual and tactile stimulation. Of 218 neurons tested, 153 (70%) were bimodal in the sense that they responded to stimuli that were independently applied in either sensory modality. Unimodal visual and bimodal neurons were intermingled within the recording area and could not be distinguished on the basis of their visual response properties alone. Most of the cells with a tactile receptive field (RF) responded well to light touch or air puffs. The distribution of RF locations principally emphasized the head (85%), with approximately equivalent representations of the upper and lower face areas. The tactile and visual RFs were aligned in a congruent manner, with the intersection of the visual vertical and horizontal meridian having its tactile counterpart in the nose/mouth area. Small foveal visual RFs were paired with small tactile RFs on the muzzle, and peripheral visual RFs were associated with tactile RFs on the side of the head or body. Most cells showed a strong sensitivity to moving stimuli, and the preferred directions of visual and tactile motion coincided in 85% of bimodal cells. In some cases, bimodal responses patterns were complementary: cells responding to motion in depth toward the monkey had on responses, whereas cells responding to motion in depth away form the monkey had off responses. Other forms of bimodal response congruence included orientation selectivity, and on, off, and on/off response types. The large proportion of bimodal tactile and visual neurons with congruent response properties in area VIP indicates that there are important functional differences between area VIP and other dorsal stream areas involved in the analysis of motion. We suggest that VIP is involved in the construction of a multisensory, head-centered representation of near extrapersonal space.
Postsynaptic Response Kinetics Are Controlled by a Glutamate Transporter at Cone Photoreceptors
Authors: Gaal Lubor , Roska Botond , Picaud Serge A. , Wu Samuel M. , Marc Robert , Werblin Frank S.
Published: December 2017

Gaal, Lubor, Botond Roska, Serge A. Picaud, Samuel M. Wu, Robert Marc, and Frank S. Werblin. Postsynaptic response kinetics are controlled by a glutamate transporter at cone photoreceptors. J. Neurophysiol. 79: 190–196, 1998. We evaluated the role of the sodium/glutamate transporter at the synaptic terminals of cone photoreceptors in controlling postsynaptic response kinetics. The strategy was to measure the changes in horizontal cell response rate induced by blocking transporter uptake in cones with dihydrokainate (DHK). DHK was chosen as the uptake blocker because, as we show through autoradiographic uptake measurements, DHK specifically blocked uptake in cones without affecting uptake in Mueller cells. Horizontal cells depolarized from about −70 to −20 mV as the exogenous glutamate concentration was increased from ∼1 to 40 μM, so horizontal cells can serve as “glutamate electrodes” during the light response. DHK slowed the rate of hyperpolarization of the horizontal cells in a dose-dependent way, but didn't affect the kinetics of the cone responses. At 300 μM DHK, the rate of the horizontal cell hyperpolarization was slowed to only 17 ± 8.5% (mean ± SD) of control. Translating this to changes in glutamate concentration using the slice dose response curve as calibration in Fig. 2 , DHK reduced the rate of removal of glutamate from ∼0.12 to 0.031 μM/s. The voltage dependence of uptake rate in the transporter alone was capable of modulating glutamate concentration: we blocked vesicular released glutamate with bathed 20 mM Mg2+ and then added 30 μM glutamate to the bath to reestablish a physiological glutamate concentration level at the synapse and thereby depolarize the horizontal cells. Under these conditions, a light flash elicited a 17-mV hyperpolarization in the horizontal cells. When we substituted kainate, which is not transported, for glutamate, horizontal cells were depolarized but light did not elicit any response, indicating that the transporter alone was responsible for the removal of glutamate under these conditions. This suggests that the transporter was both voltage dependent and robust enough to modulate glutamate concentration. The transporter must be at least as effective as diffusion in removing glutamate from the synapse because there is only a very small light response once the transporter is blocked. The transporter, via its voltage dependence on cone membrane potential, appears to contribute significantly to the control of postsynaptic response kinetics.[Figure: see text]
Binocular Cross-Orientation Suppression in the Cat's Striate Cortex
Authors: Walker Gary A. , Ohzawa Izumi , Freeman Ralph D.
Published: December 2017

Walker, Gary A., Izumi Ohzawa, and Ralph D. Freeman. Binocular cross-orientation suppression in the cat's striate cortex. J. Neurophysiol. 79: 227–239, 1998. When a cortical cell is activated by an optimal sinusoidal grating, its response can be attenuated by a superimposed second grating oriented orthogonally to the optimal stimulus. This effect is known as cross-orientation suppression (COS). In previous work, monocular characteristics have been explored and interocular tests have been conducted in an attempt to locate the origin of the suppression. In this study, we have recorded extracellularly from cortical cells to investigate the binocular characteristics of COS. Our hypothesis is that binocular disparity influences the strength of the effect. Our results do not support this supposition. We find that binocular COS is as strong as monocular COS, but disparity changes are of no consequence. We also conducted interocular tests in which the optimal grating and the orthogonal mask were seen by separate eyes. Although most interocular effects were weak, they were present in almost every cell and spanned a wide range of suppression strengths. We also tested the effect of asynchronous presentation of optimal and orthogonal gratings. These temporal offsets did not affect the strength of COS. We conclude that the suppressive mechanism underlying COS is primarily monocular and acts prior to the convergence of the two monocular streams.
Involvement of the Caudal Medulla in Negative Feedback Mechanisms Triggered by Spatial Summation of Nociceptive Inputs
Authors: Gall Olivier , Bouhassira Didier , Chitour Djamel , Le Bars Daniel
Published: December 2017

Gall, Olivier, Didier Bouhassira, Djamel Chitour, and Daniel Le Bars. Involvement of the caudal medulla in negative feedback mechanisms triggered by spatial summation of nociceptive inputs. J. Neurophysiol. 79: 304–311, 1998. In the rat, applying noxious heat stimuli to the excitatory receptive fields and simultaneously to adjacent, much larger, areas of the body results in a surface-related reduction in the responses of lumbar dorsal horn convergent neurons. These inhibitory effects induced by spatial summation of nociceptive inputs have been shown to involve a supraspinally mediated negative feedback loop. The aim of the present study was to determine the anatomic level of integration of these controls and hence to ascertain what relationships they might share with other descending controls modulating the transmission of nociceptive signals. The responses of lumbar convergent neurons to noxious stimulation (15-s immersion in a 48°C water bath) applied to increasing areas of the ipsilateral hindlimb were examined in several anesthetized preparations: sham-operated rats, rats with acute transections performed at various levels of the brain stem, and spinal rats. The effects of heterotopic noxious heat stimulation (tail immersion in a 52°C water bath) on the C-fiber responses of these neurons also were analyzed. The electrophysiological properties of dorsal horn convergent neurons, including their responses to increasing stimulus surface areas, were not different in sham-operated animals and in animals the brain stems of which had been transected completely rostral to a plane −2.8 mm remote from interaural line (200 μm caudal to the caudal end of the rostral ventromedial medulla). In these animals, increasing the stimulated area size from 4.8 to 18 cm2 resulted in a 35–45% reduction in the responses. In contrast, relative to responses elicited by 4.8 cm2 stimuli, responses to 18 cm2 were unchanged or even increased in animals with transections at more caudal level and in spinal animals. Inhibitions of the C-fiber responses elicited by heterotopic noxious heat stimulation were in the 70–80% range during conditioning in sham-operated animals and in animals with rostral brain stem transections. Such effects were reduced significantly (residual inhibitions in the 10–20% range) in animals with transections >500 μm caudal to the caudal end of the rostral ventromedial medulla and in spinal animals. It is concluded that the caudal medulla constitutes a key region for the expression of negative feed-back mechanisms triggered by both spatial summation of noxious inputs and heterotopic noxious inputs.
Participation of GABAA-Mediated Inhibition in Ictallike Discharges in the Rat Entorhinal Cortex
Authors: Lopantsev Valeri , Avoli Massimo
Published: December 2017

Lopantsev, Valeri and Massimo Avoli. Participation of GABAA-mediated inhibition in ictallike discharges in the rat entorhinal cortex. J. Neurophysiol. 79: 352–360, 1998. The spontaneous, synchronous activity induced by 4-aminopyridine (4AP, 50 μM) in the adult rat entorhinal cortex was analyzed with simultaneous field potential and intracellular recordings in an in vitro slice preparation. Four-AP induced isolated negative-going field potentials (interval of occurrence = 27.6 ± 9.9 (SD) s; n = 27 slices) that corresponded to intracellular long-lasting depolarizations (LLDs), and ictallike epileptiform discharges (interval of occurrence = 10.4 ± 5.7 min; n = 27 slices) that were initiated by the negative field potentials. LLDs recorded with K-acetate–filled microelectrodes triggered few action potentials of variable amplitude and had a duration of 1.7 ± 0.8 s ( n = 26 neurons), a peak amplitude of 11.8 ± 5.0 mV ( n = 26 neurons) and a reversal potential of −66.2 ± 3.9 mV ( n = 17 neurons). The ictal discharges studied with K-acetate microelectrodes consisted of prolonged depolarizations (duration = 72.9 ± 44.3 s; peak amplitude = 29.2 ± 11.4 mV; n = 25 neurons) with action-potential firing during both the tonic and the clonic phase. These depolarizations had a reversal potential of −45.3 ± 3.8 mV ( n = 4 neurons). Intracellular Cl−diffusion from KCl-filled microelectrodes made both LLDs and ictal depolarizations increase in amplitude (30.5 ± 8.2 mV, n = 8 and 41.8 ± 9.8 mV, n = 6 neurons, respectively). LLDs recorded with KCl and 2-(trimethyl-amino) N-(2,6-dimethylphenyl)-acetamide (QX-314) microelectrodesreached an amplitude of 36.3 ± 5.2 mV, lasted 12.5 ± 6.5 s, and had a reversal potential of −31.3 ± 2.5 mV ( n = 4 neurons); under these recording procedures the ictal discharge amplitude was 41.5 ± 5.0 mV and the reversal potential −24.0 ± 7.0 mV ( n = 4 neurons). The N-methyl-d-aspartate (NMDA) receptor antagonist 3,3-(2-carboxy-piperazine-4-yl)-pro-pyl-l-phosphonate (10 μM, n = 5 neurons) alone or concomitant with the nonNMDA receptor antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione (10 μM, n = 4 neurons) abolished ictal discharges, without influencing LLDs. LLDs were blocked by the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline methiodide (BMI, 10 μM, n = 6 neurons) or the μ-opioid receptor agonist (d-Ala2-N-Me-Phe, Gly-ol) enkephalin (DAGO, 10 μM, n = 2 neurons). Application of BMI ( n = 4 neurons) or DAGO ( n = 2 neurons) to control the medium abolished LLDs and ictal discharges but disclosed a novel type of epileptiform depolarization that lasted 3.5 ± 1.2 s and occurred every 5.2 ± 2.6 s ( n = 6 neurons). Our data indicate that 4AP induces in the rat entorhinal cortex a synchronous, GABA-mediated potential that is instrumental in initiating NMDA-dependent, ictal discharges. Moreover we present evidence for an active role played by GABAA-mediated potentials in the maintenance and termination of these prolonged epileptiform events.
Contractile Properties of Human Nasal Dilator Motor Units
Authors: Mateika J. H. , Essif E. G. , Dellorusso C. , Fregosi R. F.
Published: December 2017

Mateika, J. H., E. G. Essif, C. DelloRusso, and R. F. Fregosi. Contractile properties of human nasal dilator motor units. J. Neurophysiol. 79: 371–378, 1998. The technique of intramuscular microstimulation was used to activate facial nerve fibers while acquiring simultaneous twitch force measurements to measure the contractile properties and force-frequency responses of human nasal dilator (ND) motor units. Twitch force amplitude (TF), contraction time (CT), half-relaxation time (HRT), and the maximal rate of rise of force normalized to the peak force (maximum contraction rate, MCR) were recorded from 98 ND motor units in 37 subjects. The average CT, HRT, MCR, and TF were 47.9 ± 1.8 ms, 42.6 ± 2.1 ms, 28.6 ± 1.8 s−1, and 1.06 ± 0.1 mN, respectively. Neither CT nor HRT were significantly correlated with TF. The average CT and HRT were similar to values recorded for small muscles of the hand but were faster than the values recorded from human toe extensor motor units. However the lack of an association between twitch force and CT or HRT was similar to the findings obtained for both human hand and foot muscles. Force-frequency curves were recorded from eight ND motor units. The force produced by the eight motor units was recorded in response to stimuli delivered at 1, 5, 10, 15, 20, 25, 30, 35, and 40 Hz to assess force-frequency relationships. The mean twitch force of the eight motor units was 0.91 ± 0.3 mN and the average tetanic force was 8.1 ± 1.8 mN. Therefore the average twitch force was equal to 12.7% of the tetanic force. Fifty percent of the unit tetanic force was achieved at an average frequency of 16.4 ± 1.7 Hz, which is greater than the value recorded for human toe extensor motor units (9.6 Hz). Thus the force produced by the ND motor units was more sensitive to changes in discharge frequency over the range of ∼10–30 Hz and less sensitive to changes in the range of 0–10 Hz because of their fast contractile properties. The mean slope of the regression lines that were fit to the steep portion of each force-frequency curve was 5.15 ± 0.5% change in force/Hz. This value was greater than the slope measured for human toe extensor muscles (4.2% change in force/Hz). These observations suggest that force gradation by ND motor units is more sensitive to changes in stimulation frequency than human toe extensor motor units. We conclude that most ND motor units have fast contractile properties and that rate coding may play a significant role in the gradation of force produced by the ND muscle. Furthermore, the findings of this investigation have demonstrated that contractile speed and TF in a human facial muscle are not correlated. This supports previous findings obtained from human hand and foot muscles and suggests that there may be a fundamental difference in the contractile speed-twitch force relationship between many human muscles and most muscles of other mammals.
Rat group I Metabotropic Glutamate Receptors Inhibit Neuronal Ca2+Channels via Multiple Signal Transduction Pathways in HEK 293 Cells
Authors: McCool Brian A. , Pin Jean-Phillipe , Harpold Michael M. , Brust Paul F. , Stauderman KENNETH A. , Lovinger David M.
Published: December 2017

McCool, Brian A., Jean-Phillipe Pin, Michael M. Harpold, Paul F. Brust, Kenneth A. Stauderman, and David M. Lovinger. Rat group I metabotropic glutamate receptors inhibit neuronal Ca2+channels via multiple signal transduction pathways in HEK 293 cells. J. Neurophysiol. 79: 379–391, 1998. We have shown previously that metabotropic glutamate receptors with group I-like pharmacology couple to N-type and P/Q-type calcium channels in acutely isolated cortical neurons using G proteins most likely belonging to the Gi/Gosubclass. To better understand the potential mechanisms forming the basis for group I mGluR modulation of voltage-gated calcium channels in the CNS, we have examined the ability of specific mGluRs to couple to neuronal N-type (α1B-1/α2δ/β1b) and P/Q-type (α1A-2/α2δ/β1b) voltage-gated calcium channels in an HEK 293 heterologous expression system. Using the whole cell patch-clamp technique where intracellular calcium is buffered to low levels, we have shown that group I receptors inhibit both N-type and P/Q-type calcium channels in a voltage-dependent fashion. Similar to our observations in cortical neurons, this voltage-dependent inhibition is mediated almost entirely by N-ethylmaleimide (NEM)-sensitive heterotrimeric G proteins, strongly suggesting that these receptors can use Gi/Go-like G proteins to couple to N-type and P/Q-type calcium channels. However, inconsistent with the apparent NEM sensitivity of group I modulation of calcium channels, modulation of N-type channels in group I mGluR-expressing cells was only partially sensitive to pertussis toxin (PTX), indicating the potential involvement of both PTX-sensitive and -resistant G proteins. The PTX-resistant modulation was voltage dependent and entirely resistant to NEM and cholera toxin. A time course of treatment with PTX revealed that this toxin caused group I receptors to slowly shift from using a primarily NEM-sensitive G protein to using a NEM-resistant form. The PTX-induced switch from NEM-sensitive to -resistant modulation was also dependent on protein synthesis, indicating some reliance on active cellular processes. In addition to these voltage-dependent pathways, perforated patch recordings on group I mGluR-expressing cells indicate that another slowly developing, calcium-dependent form of modulation for N-type channels may be seen when intracellular calcium is not highly buffered. We conclude that group I mGluRs can modulate neuronal Ca2+channels using a variety of signal transduction pathways and propose that the relative contributions of different pathways may exemplify the diversity of responses mediated by these receptors in the CNS.
Facilitation of L-type Calcium Current in Thalamic Neurons
Authors: Kammermeier Paul J. , Jones Stephen W.
Published: December 2017

Kammermeier, Paul J. and Stephen W. Jones. Facilitation of L-type calcium current in thalamic neurons. J. Neurophysiol. 79: 410–417, 1998. We have studied facilitation of the L-type calcium current in neurons acutely isolated from the ventrobasal nucleus of the rat thalamus. Currents were recorded after pretreatment with 1 μM ω-conotoxin GVIA and 5 μM ω-conotoxin MVIIC, to better isolate L-current. Long, strong depolarizations induced slow tail currents at negative voltages, but did not affect currents at voltages where channels were strongly activated. The initial peak tail current was not measurably increased. The time course of recovery from facilitation paralleled the time course of the tail current, indicating that facilitation does not outlast channel closing. The kinase inhibitors staurosporine and H-7 and the phosphatase inhibitor okadaic acid had no significant effect on L-current facilitation compared with control, but facilitation was greater with H-7 than with okadaic acid. The guanosine 5′-triphosphate (GTP) analogs GTP-γ-S and GDP-β-S did not affect facilitation. We conclude that L-current facilitation in thalamic neurons does not result from Ser/Thr phosphorylation, although phosphorylation may modulate facilitation. This form of facilitation differs kinetically and pharmacologically from facilitation induced by activation of G protein-coupled receptors.