bluuebunny/crossref_metadata_2025 huggingface dataset:
Relation Between Axon Morphology in C1Spinal Cord and Spatial Properties of Medial Vestibulospinal Tract Neurons in the Cat
Authors: Perlmutter S. I. , Iwamoto Y. , Barke L. F. , Baker J. F. , Peterson B. W.
Published: December 2017

Perlmutter, S. I., Y. Iwamoto, L. F. Barke, J. F. Baker, and B. W. Peterson. Relation between axon morphology in C1spinal cord and spatial properties of medial vestibulospinal tract neurons in the cat. J. Neurophysiol. 79: 285–303, 1998. Twenty-one secondary medial vestibulospinal tract neurons were recorded intraaxonally in the ventromedial funiculi of the C1spinal cord in decerebrate, paralyzed cats. Antidromic stimulation in C6and the oculomotor nucleus identified the projection pattern of each neuron. Responses to sinusoidal, whole-body rotations in many planes in three-dimensional space were characterized before injection of horseradish peroxidase or Neurobiotin. The spatial response properties of 19 neurons were described by a maximum activation direction vector (MAD), which defines the axis and direction of rotation that maximally excites the neuron. The other two neurons had spatio-temporal convergent behavior and no MAD was calculated. Collateral morphologies were reconstructed from serial frontal sections to reveal terminal fields in the C1gray matter. Axons gave off multiple collaterals that terminated ipsilaterally to the stem axon. Collaterals of individual axons rarely overlapped longitudinally but projected to similar regions in the ventral horn when viewed in transverse sections. The number of primary collaterals in C1was different for vestibulo-collic, vestibulo-oculo-collic, and C6-projecting neurons: on average one every 1.34, 1.72, and 4.25 mm, respectively. The heaviest arborization and most terminal boutons were seen in the ventral horn, in laminae VIII and IX. Varicosities on terminal branches in lamina IX were observed adjacent to large cell bodies—putative neck motoneurons—in counterstained tissue. Some collaterals had branches that extended dorsally to lamina VII. Neurons with different spatial properties had terminal fields in different regions of the ventral horn. Axons with type I responses and MADs near those of a semicircular canal pair had widely distributed collateral branches and numerous terminations in the dorsomedial, ventromedial, and spinal accessory nuclei and in lamina VIII. Axons with type I responses that suggested convergent canal pair input, with type II responses, and with spatio-temporal convergent behavior had smaller terminal fields. Some neurons with these more complex spatial properties projected to the dorsomedial and spinal accessory but not to the ventromedial nuclei. Others had focused projections to dorsolateral regions of the ventral horn with few branches in the motor nuclei.
Aging Differentially Alters Forms of Long-Term Potentiation in Rat Hippocampal Area CA1
Authors: Shankar Subbakrishna , Teyler Timothy J. , Robbins Norman
Published: December 2017

Shankar, Subbakrishna, Timothy J. Teyler, and Norman Robbins. Aging differentially alters forms of long-term potentiation in rat hippocampal area CA1. J. Neurophysiol. 79: 334–341, 1998. Long-term potentiation (LTP) of the Schaffer collateral/commissural inputs to CA1 in the hippocampus was shown to consist of N-methyl-d-aspartate receptor (NMDAR) and voltage-dependent calcium channel (VDCC) dependent forms. In this study, the relative contributions of these two forms of LTP in in vitro hippocampal slices from young (2 mo) and old (24 mo) Fischer 344 rats were examined. Excitatory postsynaptic potentials (EPSP) were recorded extracellularly from stratum radiatum before and after a tetanic stimulus consisting of four 200-Hz, 0.5-s trains given 5 s apart. Under control conditions, a compound LTP consisting of both forms was induced and was similar, in both time course and magnitude, in young and old animals. NMDAR-dependent LTP (nmdaLTP), isolated by the application of 10 μM nifedipine (a voltage-dependent calcium channel blocker), was significantly reduced in magnitude in aged animals. The VDCC dependent form (vdccLTP), isolated by the application of 50 μM d,l-2-amino-5-phosphonvalerate (APV), was significantly larger in aged animals. Although both LTP forms reached stable values 40–60 min posttetanus in young animals, in aged animals vdccLTP increased and nmdaLTP decreased during this time. In both young and old animals, the sum of the two isolated LTP forms approximated the magnitude of the compound LTP, and application of APV and nifedipine or genestein (a tyrosine kinase inhibitor) together blocked potentiation. These results suggest that aging causes a shift in synaptic plasticity from NMDAR-dependent mechanisms to VDCC-dependent mechanisms. The data are consistent with previous findings of increased L-type calcium current and decreased NMDAR number in aged CA1 cells and may help explain age-related deficits in learning and memory.
Closely Spaced, Fast Dynamic Movements in Disparity Vergence
Authors: Alvarez Tara L. , Semmlow John L. , Yuan Weihong
Published: December 2017

Alvarez, Tara L., John L. Semmlow, and Weihong Yuan. Closely spaced, fast dynamic movements in disparity vergence. J. Neurophysiol. 79: 37–44, 1998. Conflicting theories exist describing how symmetrical vergence responses, the inward or outward turning of the eyes, are mediated. Classical theories describe vergence control as mediated by visual feedback. Extensive experimental evidence indicates that two distinct control components comprise the vergence response, and a recent theory supports the concept that one of these components is not visually guided. Occasionally, saccadic eye movements will respond to a single step stimulus with two closely spaced saccades, a behavior that is indicative of its switching control structure. If a portion of the vergence response is controlled in a manner analogous to saccades, then occasional double fast dynamic components might be expected. During this study, eye movements were recorded in response to symmetrical vergence stimuli of 2, 4, 6, 8, and 10° steps. The left and right eye movements were subtracted to yield a net vergence response, and only convergent responses were investigated. Double fast dynamic components associated with high-velocity movements were observed in all four subjects studied. In double high-velocity component responses, the average peak velocity of both fast dynamic movements was always considerably less than the average peak velocity found when the response to the same stimulus was made with only a single component. Response amplitudes of single and double movements showed that if the primary component of a double response did not reach ≥80% of the stimulus amplitude, a secondary component would be generated to aid the movement. Plots of peak velocity as a function of response amplitude for both double and single movements followed the main sequence for vergence eye movements demonstrating that the first-order dynamic characteristics of all high-velocity components were the same. The time at which maximum velocity occurred (relative to stimulus onset) was also the same for both single component responses and the first component of double responses. The similarity in dynamics and timing implies that the high-velocity components were processed by the same controller mechanism. The existence of double high-velocity movements is indicative of an internal, switching mechanism similar to that found in saccades and is difficult to explain with theories that rely on visual feedback control alone.
NMDA Receptor-Mediated Differential Laminar Susceptibility to the Intracellular Ca2+ Accumulation Induced by Oxygen-Glucose Deprivation in Rat Neocortical Slices
Authors: Fukuda Atsuo , Muramatsu Kanji , Okabe Akihito , Shimano Yasunobu , Hida Hideki , Fujimoto Ichiro , Nishino Hitoo
Published: December 2017

Fukuda, Atsuo, Kanji Muramatsu, Akihito Okabe, Yasunobu Shimano, Hideki Hida, Ichiro Fujimoto, and Hitoo Nishino. NMDA receptor-mediated differential laminar susceptibility to the intracellular Ca2+ accumulation induced by oxygen-glucose deprivation in rat neocortical slices. J. Neurophysiol. 79: 430–438, 1998. Slices of somatosensory cortex taken from immature rats on postnatal day (P)7–14 were labeled with fura-2. Intracellular Ca2+ concentration ([Ca2+]i) was monitored in identified pyramidal cells as the ratio of fluorescence intensities (RF340/F380) during oxygen-glucose deprivation. The RF340/F380 ([Ca2+]i) of individual pyramidal cells was monitored in each of the cortical layers II–VI simultaneously. Neurons in all neocortical layers exhibited significant increases in [Ca2+]i that varied with the duration of oxygen-glucose deprivation. Individual neurons responded to oxygen-glucose deprivation with abrupt increases in [Ca2+]i after various latencies. The ceiling level of the [Ca2+]i increase differed from cell to cell. Neurons in layer II/III showed significantly greater increases in [Ca2+]i than those in layers IV, V, or VI. Kynurenic acid, a nonselective glutamate receptor antagonist, and bicuculline, a selective γ-aminobutyric acid (GABA)A receptor antagonist, suppressed the intracellular Ca2+ accumulation induced by oxygen-glucose deprivation in all neocortical layers examined. After kynurenic acid, but not after bicuculline, there was no longer a differential [Ca2+]i increases in layer II/III. Both 2-amino-5-phosphonopentanoic acid (AP5), a selective N-methyl-d-aspartate (NMDA) receptor antagonist, and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a non-NMDA receptor antagonist, strongly suppressed the intracellular Ca2+ accumulation induced by oxygen-glucose deprivation in all layers. The laminar difference in terms of the [Ca2+]i increases was abolished by AP5, but not by CNQX. These results indicate that layer II/III cells are the most prone to oxygen-glucose deprivation-induced intracellular Ca2+ accumulation, and that this is primarily mediated by NMDA receptors. Thus, layer II/III neurons would be more likely to suffer cellular Ca2+ overload and excitotoxicity during ischemia than layer IV–VI cells. Such a differential laminar vulnerability might play an important role in determining the pathological characteristics of the immature cortex and its sequelae later in life.
Focal Stimulation of the Thalamic Reticular Nucleus Induces Focal Gamma Waves in Cortex
Authors: Macdonald Kurt D. , Fifkova Eva , Jones Michael S. , Barth Daniel S.
Published: December 2017

MacDonald, Kurt D., Eva Fifkova, Michael S. Jones, and Daniel S. Barth. Focal stimulation of the thalamic reticular nucleus induces focal gamma waves in cortex. J. Neurophysiol. 79: 474–477, 1998. Electrical stimulation of the thalamic reticular nucleus (TRN; 0.5-s trains of 500-Hz 0.5-ms pulses at 5–10 μA) evokes focal oscillations of cortical electrical potentials in the gamma frequency band (∼35–55 Hz). These evoked oscillations are specific to either the somatosensory or auditory cortex and to subregions of the cortical receptotopic map, depending on what part of the TRN is stimulated. Focal stimulation of the internal capsule, however, evokes focal slow potentials, without gamma activity. Our results suggest that the TRN's role extends beyond that of general cortical arousal to include specific modality and submodality activation of the forebrain.
Protein Kinase C Activation Decreases Activity-Dependent Attenuation of Dendritic Na+ Current in Hippocampal CA1 Pyramidal Neurons
Authors: Colbert Costa M. , Johnston Daniel
Published: December 2017

Colbert, Costa M. and Daniel Johnston. Protein kinase C activation decreases activity-dependent attenuation of dendritic Na+ current in hippocampal CA1 pyramidal neurons. J. Neurophysiol. 79: 491–495, 1998. Action potentials recorded from the soma of CA1 pyramidal neurons remain relatively uniform in amplitude during repetitive firing. In contrast, the amplitudes of back-propagating action potentials in dendrites decrease progressively during a spike train. This activity-dependent decrease in amplitude is dependent on the frequency of firing during the train and distance from the soma. Previously, we described a property of Na+ channels that provides a plausible mechanism for the activity dependence of the amplitude of the dendritic action potentials: available Na+ current decreases during trains of action potentials through an inactivation, distinct from fast inactivation, that appears rapid in onset, but slow and voltage-dependent in its recovery. In this study we found that activation of protein kinase C by phorbol esters decreased this activity-dependent inactivation of pharmacologically isolated Na+ current in cell-attached dendritic, but not somatic, patches. Similarly in whole cell recordings phorbol esters decreased the attenuation of back-propagating dendritic action potentials during trains. These results indicate a novel effect of protein kinase C on the dendritic Na+ channel and further support the hypothesis that the activity dependence of the dendritic action potentials is derived from the inactivation properties of Na+ channels.
Synaptic Inputs to Stellate Cells in the Ventral Cochlear Nucleus
Authors: Ferragamo Michael J. , Golding Nace L. , Oertel Donata
Published: December 2017

Ferragamo, Michael J., Nace L Golding, and Donata Oertel. Synaptic inputs to stellate cells in the ventral cochlear nucleus. J. Neurophysiol. 79: 51–63, 1998. Auditory information is carried from the cochlear nuclei to the inferior colliculi through six parallel ascending pathways, one of which is through stellate cells of the ventral cochlear nuclei (VCN) through the trapezoid body. To characterize and identify the synaptic influences on T stellate cells, intracellular recordings were made from anatomically identified stellate cells in parasagittal slices of murine cochlear nuclei. Shocks to the auditory nerve consistently evoked five types of synaptic responses in T stellate cells, which reflect sources intrinsic to the cochlear nuclear complex. 1) Monosynaptic excitatory postsynaptic potentials (EPSPs) that were blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX), an antagonist of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, probably reflected activation by auditory nerve fibers. Electrophysiological estimates indicate that about five auditory nerve fibers converge on one T stellate cell. 2) Disynaptic, glycinergic inhibitory postsynaptic potentials (IPSPs) arise through inhibitory interneurons in the VCN or in the dorsal cochlear nucleus (DCN). 3) Slow depolarizations, the source of which has not been identified, that lasted between 0.2 and 1 s and were blocked by dl-2-amino-5-phosphonovaleric acid (APV), the N-methyl-d-aspartate (NMDA) receptor antagonist. 4) Rapid, late glutamatergic EPSPs are polysynaptic and may arise from other T stellate cells. 5) Trains of late glycinergic IPSPs after single or repetitive shocks match the responses of D stellate cells, showing that D stellate cells are one source of glycinergic inhibition to T stellate cells. The source of late, polysynaptic EPSPs and IPSPs was assessed electrophysiologically and pharmacologically. Late synaptic responses in T stellate cells were enhanced by repetitive stimulation, indicating that the interneurons from which they arose should fire trains of action potentials in responses to trains of shocks. Late EPSPs and late IPSPs were blocked by APV and enhanced by the removal of Mg2+, indicating that the interneurons were driven at least in part through NMDA receptors. Bicuculline, a γ-aminobutyric acid-A (GABAA) receptor antagonist, enhanced the late PSPs, indicating that GABAergic inhibition suppresses both the glycinergic interneurons responsible for the trains of IPSPs in T-stellate cells and the interneuron responsible for late EPSPs in T stellate cells. The glycinergic interneurons that mediate the series of IPSPs are intrinsic to the ventral cochlear nucleus because long series of IPSPs were recorded from T stellate cells in slices in which the DCN was removed. These experiments indicate that T stellate cells are a potential source of late EPSPs and that D stellate cells are a potential source for trains of late IPSPs.
Interpreting Neuronal Population Activity by Reconstruction: Unified Framework With Application to Hippocampal Place Cells
Authors: Zhang Kechen , Ginzburg Iris , McNaughton Bruce L. , Sejnowski Terrence J.
Published: December 2017

Zhang, Kechen, Iris Ginzburg, Bruce L. McNaughton, and Terrence J. Sejnowski. Interpreting neuronal population activity by reconstruction: unified framework with application to hippocampal place cells. J. Neurophysiol. 79: 1017–1044, 1998. Physical variables such as the orientation of a line in the visual field or the location of the body in space are coded as activity levels in populations of neurons. Reconstruction or decoding is an inverse problem in which the physical variables are estimated from observed neural activity. Reconstruction is useful first in quantifying how much information about the physical variables is present in the population and, second, in providing insight into how the brain might use distributed representations in solving related computational problems such as visual object recognition and spatial navigation. Two classes of reconstruction methods, namely, probabilistic or Bayesian methods and basis function methods, are discussed. They include important existing methods as special cases, such as population vector coding, optimal linear estimation, and template matching. As a representative example for the reconstruction problem, different methods were applied to multi-electrode spike train data from hippocampal place cells in freely moving rats. The reconstruction accuracy of the trajectories of the rats was compared for the different methods. Bayesian methods were especially accurate when a continuity constraint was enforced, and the best errors were within a factor of two of the information-theoretic limit on how accurate any reconstruction can be and were comparable with the intrinsic experimental errors in position tracking. In addition, the reconstruction analysis uncovered some interesting aspects of place cell activity, such as the tendency for erratic jumps of the reconstructed trajectory when the animal stopped running. In general, the theoretical values of the minimal achievable reconstruction errors quantify how accurately a physical variable is encoded in the neuronal population in the sense of mean square error, regardless of the method used for reading out the information. One related result is that the theoretical accuracy is independent of the width of the Gaussian tuning function only in two dimensions. Finally, all the reconstruction methods considered in this paper can be implemented by a unified neural network architecture, which the brain feasibly could use to solve related problems.
Dose-Dependent Reduction of Cerebral Blood Flow During Rapid-Rate Transcranial Magnetic Stimulation of the Human Sensorimotor Cortex
Authors: Paus Tomáš , Jech Robert , Thompson Christopher J. , Comeau Roch , Peters Terry , Evans Alan C.
Published: December 2017

Paus, Tomáš, Robert Jech, Christopher J. Thompson, Roch Comeau, Terry Peters, and Alan C. Evans. Dose-dependent reduction of cerebral blood flow during rapid-rate transcranial magnetic stimulation of the human sensorimotor cortex. J. Neurophysiol. 79: 1102–1107, 1998. Rapid-rate transcranial magnetic stimulation (rTMS) was used to stimulate the primary sensorimotor cortex in six healthy volunteers while regional changes in cerebral blood flow (CBF) were simultaneously measured by means of positron emission tomography. A figure-eight TMS coil (Cadwell Corticoil) was positioned, using frameless stereotaxy, over the probabilistic location of the left primary sensorimotor cortex, and a series of brief 10-Hz trains of TMS was delivered at subthreshold intensity during each of six 60-s scans. The scans differed in the number of trains delivered, namely 5, 10, 15, 20, 25, and 30 trains/scan, respectively. In the left primary sensorimotor cortex, CBF covaried significantly and negatively with the number of stimulus trains. These CBF decreases may reflect TMS–induced activation of local inhibitory mechanisms known to play a role in TMS–related phenomena, such as the electromyographic silent period.
Enhancement of Synaptic Excitation by GABAA Receptor Antagonists in Rat Embryonic Midbrain Culture
Authors: Rohrbacher Jutta , Sauer Katja , Lewen Andrea , Misgeld Ulrich
Published: December 2017

Rohrbacher, Jutta, Katja Sauer, Andrea Lewen, and Ulrich Misgeld. Enhancement of synaptic excitation by GABAA receptor antagonists in rat embryonic midbrain culture. J. Neurophysiol. 79: 1113–1116, 1998. Alterations of synaptic excitation induced by exposure to γ-aminobutyric acid-A (GABAA) receptor antagonists were investigated employing tight-seal whole cell recording from single neurons or pairs of neurons in rat embryonic midbrain culture. Application of GABAA receptor antagonists led to sustained depolarizations followed by synchronous paroxysmal depolarization shifts (PDSs). PDSs induced a transient increase in miniature excitatory postsynaptic currents in the presence as well as in the absence of a N-methyl-d-aspartate receptor antagonist. The increase in glutamate release supports the excitatory drive required to reinitiate PDSs from the quiescent interburst intervals. After washout of GABAA receptor antagonists, synaptic activity remained grouped, regardless of the presence or absence of PDS blockade by tetrodotoxin (TTX). Impediment of action potential-triggered transmitter release by Cd2+ or TTX also induced grouped activity. We conclude that changes in synaptic excitation are produced by the impaired GABAA inhibition per se and by the initiation of PDSs.
Example of 2:1 Interlimb Coordination During Fictive Rostral Scratching in a Spinal Turtle
Authors: Stein Paul S. G. , McCullough Margaret L.
Published: December 2017

Stein, Paul S. G. and Margaret L. McCullough. Example of 2:1 interlimb coordination during fictive rostral scratching in a spinal turtle. J. Neurophysiol. 79: 1132–1134, 1998. The usual interlimb coordination pattern during fictive rostral scratching in turtles is 1:1 coordination. We describe an example in a turtle of 2:1 coordination during fictive rostral scratching in which there were two cycles of ipsilateral hip flexor activity during each cycle of contralateral hip extensor activity. During 2:1 coordination, there were fluctuations in the ipsilateral hip flexor cycle period such that a larger ipsilateral hip flexor normalized period, which was associated with the onset of a contralateral hip extensor burst, alternated with a smaller ipsilateral hip flexor normalized period, which was associated with the absence of the onset of a contralateral hip extensor burst. These observations support the concept that contralateral circuitry modulates the timing of ipsilateral motor rhythms and therefore contributes to the production of the ipsilateral motor pattern for rostral scratching.
Comparison of the Discharge Characteristics of Brain Stem Omnipause Neurons and Superior Colliculus Fixation Neurons in Monkey: Implications for Control of Fixation and Saccade Behavior
Authors: Everling Stefan , Paré Martin , Dorris Michael C. , Munoz Douglas P.
Published: December 2017

Everling, Stefan, Martin Paré, Michael C. Dorris, and Douglas P. Munoz. Comparison of the discharge characteristics of brain stem omnipause neurons and superior colliculus fixation neurons in monkey: implications for control of fixation and saccade behavior. J. Neurophysiol. 79: 511–528, 1998. Fixation neurons (SCFNs) in the rostral pole of the superior colliculus (SC) and omnipause neurons (OPNs) in the nucleus raphe interpositus (rip) in the pons share similar discharge properties. Both types of neurons discharge tonically during periods of visual fixation and pause for saccadic eye movements, and their activation by electrical stimulation suppresses saccade generation. On the basis of these similarities and the projection from the rostral SC to the rip, it was hypothesized that SCFNs provide a major excitatory input to OPNs. We investigated the role and relationship of SCFNs and OPNs with respect to both fixation behavior and saccade generation by comparing their activity recorded in the same monkeys performing a gap saccade task. In this task, the central fixation point was extinguished 200 ms before the presentation of an eccentric saccadic target, and the discharges of OPNs and SCFNs were contrasted during visual fixation, nonvisual (gap) fixation, and saccade generation. During visual fixation, the mean discharge rate of OPNs was higher and more regular than that of SCFNs. During the gap period, SCFNs decreased their discharge rate before target appearance, whereas no change in discharge rate was observed in OPNs. For both SCFNs and OPNs, the activity level before target appearance was not correlated to saccadic reaction time. In contrast to SCFNs, several OPNs responded with a transient phasic increase in discharge immediately after the target presentation. Before their saccade-related pause, there was a gradual reduction in the activity of SCFNs, whereas OPNs had an abrupt cessation of discharge. SCFNs paused earlier than OPNs, but the OPN pause onset was better synchronized to saccade onset than the SCFN pause onset. OPNs resumed firing after their pause in activity earlier than SCFNs, and the OPN pause end was better synchronized to saccade end than the SCFN pause end. These physiological data reveal differences in the discharge properties of SCFNs and OPNs that are irreconcilable with the hypothesis that the discharge pattern of OPNs reflects simply the excitatory input from SCFNs. It is most likely that additional inputs to OPNs compensate for the reduction in discharge of SCFNs during these periods.
Identification and Characterization of Catecholaminergic Neuron B65, Which Initiates and Modifies Patterned Activity in the Buccal Ganglia of Aplysia
Authors: Kabotyanski E. A. , Baxter D. A. , Byrne J. H.
Published: December 2017

Kabotyanski, E. A., D. A. Baxter, and J. H. Byrne. Identification and characterization of catecholaminergic neuron B65, which initiates and modifies patterned activity in the buccal ganglia of Aplysia. J. Neurophysiol. 79: 605–621, 1998. Catecholamines are believed to play an important role in regulating the properties and functional organization of the neural circuitry mediating consummatory feeding behaviors in Aplysia. In the present study, we morphologically and electrophysiologically identified a pair of catecholaminergic interneurons, referred to as B65, in the buccal ganglia. Their processes innervate both the ipsi- and contralateral neuropil, and separate branches of B65 appeared to innervate the somata of both ipsi- and contralateral B4/5 neurons. B65 exhibited patterned burst(s) of activity during spontaneous cycles of fictive feeding. Patterned activity in B65 also was elicited by stimulation of the radula nerve, by depolarization of the pattern initiating neurons B31/32 or B63, and by bath application of l-3,4-dihydroxyphenylalanine (DOPA). B65 appeared to be a member of the protraction group of neurons. Action potentials in B65 elicited fast one-for-one excitatory postsynaptic potentials (EPSPs) in neurons B4/5, B8A/B, B31/32, B63, and B64. In turn, B31/32 and B63 excited B65 and B64 inhibited B65. Some of the synaptic connections of B65 were plastic. For example, the fast EPSPs elicited in B4/5 and B64 decremented, whereas those in B31/32 andB8A/B facilitated. In addition to fast EPSPs, B65 elicited slow postsynaptic potentials in some of its follower cells. Depolarization of B65 elicited cycles of patterned activity indicative of fictive feeding in buccal neurons, including B65 itself. During series of B65-induced patterns, the properties of the buccal motor programs appeared to change. In particular, the activity of radula closure motor neurons B8A/B, which initially coincided mainly with the protraction phase of a cycle, gradually extended to overlap mostly with the retraction phase. This observation suggests that prolonged activity in B65 may play a role in transitioning from rejection-like to ingestion-like fictive feeding. The phase shift of the activity of B8A/B appears due, at least in part, to a decrease in activity of B4/5, and thus a reduction in inhibition from B4/5 onto B8A/B, during the retraction phase. The functional properties and synaptic connections of B65 suggest that it may play an important role in determining features of patterned neural activity in the buccal ganglia.
GABA-Dependent Firing of Glutamate-Evoked Action Potentials at AMPA/Kainate Receptors in Developing Hypothalamic Neurons
Authors: Gao Xiao-Bing , Chen Gong , van den Pol Anthony N.
Published: December 2017

Gao, Xiao-Bing, Gong Chen, and Anthony N. van den Pol. GABA-dependent firing of glutamate-evoked action potentials at AMPA/kainate receptors in developing hypothalamic neurons. J. Neurophysiol. 79: 716–726, 1998. Although it plays a major inhibitory role in the adult mammalian CNS, γ-aminobutyric acid (GABA) may have an excitatory function in developing neurons. The present study focuses on the dependence of glutamate on GABA to generate action potentials in developing hypothalamic neurons. Under conditions where glutamate by itself could not evoke an action potential, GABA facilitated glutamate-mediated depolarization to fire action potentials. This facilitation had a broad time window during the decaying phase of the GABA-mediated depolarization in developing neurons in culture. The glutamate-mediated depolarization was shunted only during the peak of GABA-mediated depolarization, but was facilitated after that.Similar results were obtained in the presence of 2-amino-5-phosphonopentanoic acid (AP5), indicating that GABA can facilitate glutamate responses independent of relief of the Mg2+ block of the N-methyl-d-aspartate (NMDA) receptor. This novel interaction between GABA- and glutamate-mediated excitation could play a role in strengthening neuronal circuits during early development and would exert a maximal effect if GABA and glutamate receptors were activated after a slight temporal delay.
Synaptic Current at the Rat Ganglionic Synapse and Its Interactions With the Neuronal Voltage-Dependent Currents
Authors: Sacchi Oscar , Rossi Maria Lisa , Canella Rita , Fesce Riccardo
Published: December 2017

Sacchi, Oscar, Maria Lisa Rossi, Rita Canella, and Riccardo Fesce. Synaptic current at the rat ganglionic synapse and its interactions with the neuronal voltage-dependent currents. J. Neurophysiol. 79: 727–742, 1998. The membrane current activated by fast nicotinic excitation of intact and mature rat sympathetic neurons was studied at 37°C, by using the two-microelectrode voltage-clamp technique. The excitatory postsynaptic current (EPSC) was modeled as the difference between two exponentials. A fast time constant (τ2; mean value 0.57 ms), which proves to be virtually voltage-independent, governs the current rise phase and a longer time constant (τ1; range 5.2–6.8 ms in 2 mM Ca2+) describes the current decay and shows a small negative voltage dependence. A mean peak synaptic conductance of 0.58 μS per neuron is measured after activation of the whole presynaptic input in 5 mM Ca2+ external solution (0.40 μS in 2 mM Ca2+). The miniature EPSCs also rise and decay with exponential time constants very similar to those of the compound EPSC recorded at the same voltage. A mean peak conductance of 4.04 nS is estimated for the unitary event. Deconvolution procedures were employed to decompose evoked macrocurrents. It is shown that under appropriate conditions the duration of the driving function describing quantal secretion can be reduced to <1 ms. The shape of the EPSC is accurately mimicked by a complete mathematical model of the sympathetic neuron incorporating the kinetic properties of five different voltage-dependent current types, which were characterized in a previous work. We show that I A channels are opened by depolarizing voltage steps or by synaptic potentials in the subthreshold voltage range, provided that the starting holding voltage is sufficiently negative to remove I A steady-state inactivation (less than −50 mV) and the voltage trajectories are sufficiently large to enter the I A activation range (greater than −65 mV). Under current-clamp conditions, this gives rise to an additional fast component in the early phase of membrane repolarization—in response to voltage pulses—and to a consistent distortion of the excitatory postsynaptic potential (EPSP) time course around its peak—in response to the synaptic signal. When the stimulation initiates an action potential, I A is shown to significantly increase the synaptic threshold conductance (up to a factor of 2 when I A is fully deinactivated), compared with that required when I A is omitted. The voltage dependence of this effect is consistent with the I A steady-state inactivation curve. It is concluded that I A, in addition to speeding up the spike repolarization process, also shunts the excitatory drive and delays or prevents the firing of the neuron action potential.
Synaptic Differentiation of Single Descending Fibers Studied by Triple Intracellular Recording in the Frog Spinal Cord
Authors: Dityatev Alexander E. , Clamann H. Peter
Published: December 2017

Dityatev, Alexander E. and H. Peter Clamann. Synaptic differentiation of single descending fibers studied by triple intracellular recording in the frog spinal cord. J. Neurophysiol. 79: 763–768, 1998. Evoked excitatory postsynaptic potentials (EPSPs) were simultaneously intracellularly recorded in two lumbar motoneurons located in spinal segments 8–10 in response to intraaxonal stimulation of a descending fiber. Their mean amplitudes, paired-pulse facilitation, and short- and long-term posttetanic potentiation were compared to reveal possible functional differences among synapses formed by one axon on different postsynaptic targets. The mean amplitudes of EPSPs recorded in two motoneurons were significantly different in most experiments. This amplitude difference was related to the location of motoneurons in that it was twofold larger in motoneurons separated by >1 mm than in motoneurons located within 200 μm of one another and also that the amplitude of EPSPs recorded in motoneurons located in the tenth segment was regularly smaller than the amplitude recorded in the ninth segment. The estimation of binomial model parameters suggests that the difference in mean EPSP amplitude was due mostly to differences in the maximal number of quanta prepared for release (binomial parameter N) and in mean release probability rather than to differences in quantal size. The ability of connections formed by a single axon on different motoneurons to undergo use-dependent synaptic modulations was different on scales of milliseconds, seconds, and tens of minutes as revealed by the measurements of effects of paired-pulse and tetanic stimulation. The difference in magnitude of short-term posttetanic potentiation in connections formed by a single descending axon was significantly correlated with the difference in mean probability of release in these connections. Thus our data revealed a functional nonuniformity of synapses formed by individual descending fibers on widely separated motoneurons, most likely innervating different muscles. This process can be one of the mechanisms by which a fine descending control of recruitment of motoneuronal populations is achieved.
Visually Induced Adaptation in Three-Dimensional Organization of Primate Vestibuloocular Reflex
Authors: Angelaki Dora E. , Hess Bernhard J. M.
Published: December 2017

Angelaki, Dora E. and Bernhard J. M. Hess. Visually induced adaptation in three-dimensional organization of primate vestibulo-ocular reflex. J. Neurophysiol. 79: 791–807, 1998. The adaptive plasticity of the spatial organization of the vestibuloocular reflex (VOR) has been investigated in intact and canal-plugged primates using 2-h exposure to conflicting visual (optokinetic, OKN) and vestibular rotational stimuli about mutually orthogonal axes (generating torsional VOR + vertical OKN, torsional VOR + horizontal OKN, vertical VOR + horizontal OKN, and horizontal VOR + vertical OKN). Adaptation protocols with 0.5-Hz (±18°) head movements about either an earth-vertical or an earth-horizontal axis induced orthogonal response components as high as 40–70% of those required for ideal adaptation. Orthogonal response gains were highest at the adapting frequency with phase leads present at lower and phase lags present at higher frequencies. Furthermore, the time course of adaptation, as well as orthogonal response dynamics were similar and relatively independent of the particular visual/vestibular stimulus combination. Low-frequency (0.05 Hz, vestibular stimulus: ±60°; optokinetic stimulus: ±180°) adaptation protocols with head movements about an earth-vertical axis induced smaller orthogonal response components that did not exceed 20–40% of the head velocity stimulus (i.e., ∼10% of that required for ideal adaptation). At the same frequency, adaptation with head movements about an earth-horizontal axis generated large orthogonal responses that reached values as high as 100–120% of head velocity after 2 h of adaptation (i.e., ∼40% of ideal adaptation gains). The particular spatial and temporal response characteristics after low-frequency, earth-horizontal axis adaptation in both intact and canal-plugged animals strongly suggests that the orienting (and perhaps translational) but not inertial (velocity storage) components of the primate otolith-ocular system exhibit spatial adaptability. Due to the particular nested arrangement of the visual and vestibular stimuli, the optic flow pattern exhibited a significant component about the third spatial axis (i.e., orthogonal to the axes of rotation of the head and visual surround) at twice the oscillation frequency. Accordingly, the adapted VOR was characterized consistently by a third response component (orthogonal to both the axes of head and optokinetic drum rotation) at twice the oscillation frequency after earth-horizontal but not after earth-vertical axis 0.05-Hz adaptation. This suggests that the otolith-ocular (but not the semicircular canal-ocular) system can adaptively change its spatial organization at frequencies different from those of the head movement.
Low-Voltage Activated T-Type Calcium Currents Are Differently Expressed in Superficial and Deep Layers of Guinea PigPiriform Cortex
Authors: Magistretti Jacopo , de Curtis Marco
Published: December 2017

Magistretti, Jacopo and Marco de Curtis. Low-voltage activated T-type calcium currents are differently expressed in superficial and deep layers of guinea pig piriform cortex. J. Neurophysiol. 79: 808–816, 1998. A variety of voltage-dependent calcium conductances are known to control neuronal excitability by boosting peripheral synaptic potentials and by shaping neuronal firing patterns. The existence and functional significance of a differential expression of low- and high-voltage activated (LVA and HVA, respectively) calcium currents in subpopulations of neurons, acutely isolated from different layers of the guinea pig piriform cortex, were investigated with the whole cell variant of the patch-clamp technique. Calcium currents were recorded from pyramidal and multipolar neurons dissociated from layers II, III, and IV. Average membrane capacitance was larger in layer IV cells [13.1 ± 6.2 (SD) pF] than in neurons from layers II and III (8.6 ± 2.8 and 7.9 ± 3.1 pF, respectively). Neurons from all layers showed HVA calcium currents with an activation voltage range positive to −40 mV. Neurons dissociated from layers III and IV showed an LVA calcium current with the biophysical properties of a T-type conductance. Such a current displayed the following characteristics: 1) showed maximal amplitude of 11–16 pA/pF at −30 mV, 2) inactivated rapidly with a time constant of ∼22 ms at −30 mV, and 3) was completely steady-state inactivated at −60 mV. Only a subpopulation of layer II neurons (group 2 cells; circa 18%) displayed an LVA calcium current similar to that observed in deep layers. The general properties of layer II-group 2 cells were otherwise identical to those of group 1 neurons. The present study demonstrates that LVA calcium currents are differentially expressed in neurons acutely dissociated from distinct layers of the guinea pig piriform cortex.
Neural Constraints on Eye Motion in Human Eye-Head Saccades
Authors: Misslisch H. , Tweed D. , Vilis T.
Published: December 2017

Misslisch, H., D. Tweed, and T. Vilis. Neural constraints on eye motion in human eye-head saccades. J. Neurophysiol. 79: 859–869, 1998. We examined two ways in which the neural control system for eye-head saccades constrains the motion of the eye in the head. The first constraint involves Listing's law, which holds ocular torsion at zero during head-fixed saccades. During eye-head saccades, does this law govern the eye's motion in space or in the head? Our subjects, instructed to saccade between space-fixed targets with the head held still in different positions, systematically violated Listing's law of the eye in space in a way that approximately, but not perfectly, preserved Listing's law of the eye in head. This finding implies that the brain does not compute desired eye position based on the desired gaze direction alone but also considers head position. The second constraint we studied was saturation, the process where desired-eye–position commands in the brain are “clipped” to keep them within an effective oculomotor range (EOMR), which is smaller than the mechanical range of eye motion. We studied the adaptability of the EOMR by asking subjects to make head-only saccades. As predicted by current eye-head models, subjects failed to hold their eyes still in their orbits. Unexpectedly, though, the range of eye-in-head motion in the horizontal-vertical plane was on average 31% smaller in area than during normal eye-head saccades, suggesting that the EOMR had been reduced by effort of will. Larger reductions were possible with altered visual input: when subjects donned pinhole glasses, the EOMR immediately shrank by 80%. But even with its reduced EOMR, the eye still moved into the “blind” region beyond the pinhole aperture during eye-head saccades. Then, as the head movement brought the saccade target toward the pinhole, the eyes reversed their motion, anticipating or roughly matching the target's motion even though it was still outside the pinhole and therefore invisible. This finding shows that the backward rotation of the eye is timed by internal computations, not by vision. When subjects wore slit glasses, their EOMRs shrank mostly in the direction perpendicular to the slit, showing that altered vision can change the shape as well as the size of the EOMR. A recent, three-dimensional model of eye-head coordination can explain all these findings if we add to it a mechanism for adjusting the EOMR.
Modulation of Nicotinic AChR Channels by Prostaglandin E2in Chick Sympathetic Ganglion Neurons
Authors: Tan Wen , Du Chuang , Siegelbaum Steven A. , Role Lorna W.
Published: December 2017

Tan, Wen, Chuang Du, Steven A. Siegelbaum, and Lorna W. Role. Modulation of nicotinic AChR channels by prostaglandin E2in chick sympathetic ganglion neurons. J. Neurophysiol. 79: 870–879, 1998. The effects of prostaglandin E2(PGE2), an important metabolite of arachidonic acid, were studied on the activity of nicotinic AChR channels in cultured chick sympathetic ganglion neurons. In whole cell recordings, PGE2(25 nM) inhibited significantly the ACh-evoked macroscopic current. In cell-attached patch recordings, PGE2significantly inhibited single AChR channel currents as a result of a decrease in the frequency of channel opening, with no change in open time and conductance. PGE2did not alter the extent or rate of agonist-induced desensitization of the AChR channels. These effects are specific since the related compound PGD2had no effect on AChR channel function. Because there is an abundant endogenous production of PGE2within sympathetic ganglia in response to certain stimuli, the inhibition of AChR channel function by PGE2could serve an important role to modulate synaptic transmission in the sympathetic nervous system.
Interactions Between Natural and Electrically Evoked Saccades.III. Is the Nonstationarity the Result of an Integrator Not Instantaneously Reset?
Authors: Schlag John , Pouget Alexandre , Sadeghpour Safa , Schlag-Rey Madeleine
Published: December 2017

Schlag, John, Alexandre Pouget, Safa Sadeghpour, and Madeleine Schlag-Rey. Interactions between natural and electrically evoked saccades. III. Is the nonstationarity the result of an integrator not instantaneously reset? J Neurophysiol. 79: 903–910, 1998. In the monkey, fixed-vector saccades evoked by superior colliculus (SC) stimulation when the animal fixates can be dramatically modified if the stimulation is applied during or immediately after an initial natural saccade. The vector is then deviated in the direction opposite to the displacement just accomplished as if it were compensating for part of the preceding trajectory. Recently, it was suggested that the amplitude of the compensatory deviation is related to the amplitude of the initial saccade linearly, and that the ratio between the two decreases exponentially as stimulation is applied later. These two findings (spatial linearity and temporal nonstationarity) were invoked as evidence for the noninstantaneous resetting of a feedback integrator. Such an integrator is included in most models of saccade generation for the specific purpose of terminating a saccade when it has reached its intended goal. However, the hypothesis of a feedback integrator in the process of being reset implies that the exponential decay of the compensatory deviation is temporally linked to the end of the initial saccade. We analyzed the time course of this decay in stimulation experiments performed at 24 SC sites in two monkeys. The results show that if the start of the exponential decay of compensation is assumed to be linked to the end of the initial saccade, then the relation between the amount of compensatory deviation and the amplitude of the initial saccade is not linear. On the other hand, it is possible to show a linear relation if the measurements of compensatory deviation are made in terms of delay of stimulation from the saccade beginning. We conclude that stimulating the SC just after a visually guided saccade does not seem to test the properties of a feedback integrator. Whether such an integrator is or is not resettable is not likely to be decided by this approach. Conversely, as the nonstationarity of compensation is linked to the beginning of the saccade, the nonstationarity seems to represent a property of an event occurring at saccade onset. We suggest that this event, close to the input of the oculomotor apparatus, is the summation of the visual signal with a damped signal of eye position or displacement.