bluuebunny/crossref_metadata_2025 huggingface dataset:
Fictive Gill and Lung Ventilation in the Pre- and Postmetamorphic Tadpole Brain Stem
Authors: Torgerson C. S. , Gdovin M. J. , Remmers J. E.
Published: December 2017

Torgerson, C. S., M. J. Gdovin, and J. E. Remmers. Fictive gill and lung ventilation in the pre- and postmetamorphic tadpole brain stem. J. Neurophysiol. 80: 2015–2022, 1998. The pattern of efferent neural activity recorded from the isolated brain stem preparation of the tadpole Rana catesbeiana was examined to characterize fictive gill and lung ventilations during ontogeny. In vitro recordings from cranial nerve (CN) roots V, VII, and X and spinal nerve (SN) root II of premetamorphic tadpoles showed a coordinated sequence of rhythmic bursts occurring in one of two patterns, pattern1, high-frequency, low-amplitude bursts lacking corresponding activity in SN II and pattern 2, low-frequency, high-amplitude bursts with coincident bursts in SN II. These two patterns corresponded to gill and lung ventilatory burst patterns, respectively, recorded from nerve roots of decerebrate, spontaneously breathing tadpoles. Similar patterns were observed in brain stem preparations from postmetamorphic tadpoles except that they showed a greater frequency of lung bursts and they expressed fictive gill ventilation in SN II. The laryngeal branch of the vagus (Xl) displayed efferent bursts in phase with gill and lung activity, suggesting fictive glottal constriction during gill ventilation and glottal dilation during lung ventilation. The fictive gill ventilatory cycle of pre- and postmetamorphic tadpoles was characterized by a rostral to caudal sequence of CN bursts. The fictive lung ventilatory pattern in the premetamorphic animal was initiated by augmenting CN VII discharge followed by synchronous bursts in CN V, X, SN II, and Xl. By contrast, postmetamorphic patterns of fictive lung ventilation were characterized by lung burst activity in SN II that preceded burst onset in CN V and followed the lead burst in CN VII. We conclude that recruitment and timing of pattern 1 and pattern 2 rhythmic bursts recorded in vitro closely resemble that recorded during spontaneous respiratory behavior, indicating that the two patterns are the neural equivalent of gill and lung ventilation, respectively. Further, fictive gill and lung ventilatory patterns in postmetamorphic tadpoles differ in burst onset latency from premetamorphic tadpole patterns and resemble fictive oropharyngeal and pulmonary burst cycles in adult frogs.
Motor Subcircuits Mediating the Control of Movement Velocity: A PET Study
Authors: Turner Robert S. , Grafton Scott T. , Votaw John R. , Delong Mahlon R. , Hoffman John M.
Published: December 2017

Turner, Robert S., Scott T. Grafton, John R. Votaw, Mahlon R. DeLong, and John M. Hoffman. Motor subcircuits mediating the control of movement velocity: a PET study. J. Neurophysiol. 80: 2162–2176, 1998. The influence of changes in the mean velocity of movement on regional cerebral blood flow (rCBF) was studied using positron emission tomography (PET) in nine healthy right-handed adults while they performed a smooth pursuit visuomanual tracking task. Images of relative rCBF were obtained while subjects moved a hand-held joystick to track the movement of a target at three different rates of a sinusoidal displacement (0.1, 0.4, and 0.7 Hz). Significant changes in rCBF between task conditions were detected using analysis of variance and weighted linear contrasts. The kinematics of arm and eye movements indicated that subjects performed tasks in a similar manner, particularly during the faster two tracking conditions. Significant increases in rCBF during arm movement (relative to an eye tracking only control condition) were detected in a widespread network of areas known for their involvement in motor control. The activated areas included primary sensorimotor (M1S1), dorsal and mesial premotor, and dorsal parietal cortices in the left hemisphere and to a lesser extent the sensorimotor and superior parietal cortices in the right hemisphere. Subcortically, activations were found in the left putamen, globus pallidus (GP), and thalamus, in the right basal ganglia, and in the right anterior cerebellum. Within the cerebral volume activated with movement, three areas had changes in rCBF that correlated positively with the rate of movement: left M1S1, left GP, and right anterior cerebellum. No movement-related sites had rCBF that correlated negatively with the rate of movement. Regressions of mean percent change (MPC) in rCBF onto mean hand velocity yielded two nonoverlapping subpopulations of movement-related loci, the three sites with significant rate effects and regression slopes steeper than 0.17 MPC⋅cm−1⋅s−1 and all other sites with nonsignificant rate effects and regression slopes below 0.1 MPC⋅cm−1⋅s−1. Moreover, the effects of movement per se and of movement velocity varied in magnitude independently. These results confirm previous reports that movement-related activations of M1S1 and cerebellum are sensitive to movement frequency or some covarying parameter of movement. The activation of GP with increasing movement velocity, not described in previous functional-imaging studies, supports the hypothesis that the basal ganglia motor circuit may be involved preferentially in controlling or monitoring the scale and/or dynamics of arm movements. The remaining areas that were activated equally for all movement rates may be involved in controlling higher level aspects of motor control that are independent of movement dynamics.
Effects of Focal Inactivation of Dorsal or Ventral Layers of the Lateral Geniculate Nucleus on Cats' Ability to See and Fixate Small Targets
Authors: Tate Andrew K. , Malpeli Joseph G.
Published: December 2017

Tate, Andrew K. and Joseph G. Malpeli. Effects of focal inactivation of dorsal or ventral layers of the lateral geniculate nucleus on cats' ability to see and fixate small targets. J. Neurophysiol. 80: 2206–2209, 1998. To reveal contributions of different subdivisions of the lateral geniculate nucleus (LGN) to visuomotor behavior, segments of either layer A or the C layers were inactivated with microinjections of γ-aminobutyric acid while cats made saccades to retinally stabilized spots of light placed either in affected regions of visual space or mirror-symmetric locations in the opposite hemifield. Inactivating layer A reduced the success rate for saccades to targets presented in affected locations from 82.4 to 26.8% while having no effect on saccades to the control hemifield. Saccades to affected sites had reduced accuracy and longer initiation latency and tended to be hypometric. In contrast, inactivating C layers did not affect performance. Data from all conditions fell along the same saccade velocity/amplitude function (“main sequence”), suggesting that LGN inactivations cause localization deficits, but do not interfere with saccade dynamics. Cerebral cortex is the only target of the A layers, so behavioral decrements caused by inactivating layer A must be related to changes in cortical activity. Inactivating layer A substantially reduces the activity of large subsets of corticotectal cells in areas 17 and 18, whereas few corticotectal cells depend on C layers for visually driven activity. The parallels between these behavioral and electrophysiological data along with the central role of the superior colliculus in saccadic eye movements suggests that the corticotectal pathway is involved in both deficits and remaining capacities resulting from blockade of layer A.
Human Oculomotor System Accounts for 3-D Eye Orientation in the Visual-Motor Transformation for Saccades
Authors: Klier Eliana M. , Crawford J. Douglas
Published: December 2017

Klier, Eliana M. and J. Douglas Crawford. Human oculomotor system accounts for 3-D eye orientation in the visual-motor transformation for saccades. J. Neurophysiol. 80: 2274–2294, 1998. A recent theoretical investigation has demonstrated that three-dimensional (3-D) eye position dependencies in the geometry of retinal stimulation must be accounted for neurally (i.e., in a visuomotor reference frame transformation) if saccades are to be both accurate and obey Listing's law from all initial eye positions. Our goal was to determine whether the human saccade generator correctly implements this eye-to-head reference frame transformation (RFT), or if it approximates this function with a visuomotor look-up table (LT). Six head-fixed subjects participated in three experiments in complete darkness. We recorded 60° horizontal saccades between five parallel pairs of lights, over a vertical range of ±40° ( experiment 1), and 30° radial saccades from a central target, with the head upright or tilted 45° clockwise/counterclockwise to induce torsional ocular counterroll, under both binocular and monocular viewing conditions ( experiments 2 and 3). 3-D eye orientation and oculocentric target direction (i.e., retinal error) were computed from search coil signals in the right eye. Experiment 1: as predicted, retinal error was a nontrivial function of both target displacement in space and 3-D eye orientation (e.g., horizontally displaced targets could induce horizontal or oblique retinal errors, depending on eye position). These data were input to a 3-D visuomotor LT model, which implemented Listing's law, but predicted position-dependent errors in final gaze direction of up to 19.8°. Actual saccades obeyed Listing's law but did not show the predicted pattern of inaccuracies in final gaze direction, i.e., the slope of actual error, as a function of predicted error, was only −0.01 ± 0.14 (compared with 0 for RFT model and 1.0 for LT model), suggesting near-perfect compensation for eye position. Experiments 2 and 3: actual directional errors from initial torsional eye positions were only a fraction of those predicted by the LT model (e.g., 32% for clockwise and 33% for counterclockwise counterroll during binocular viewing). Furthermore, any residual errors were immediately reduced when visual feedback was provided during saccades. Thus, other than sporadic miscalibrations for torsion, saccades were accurate from all 3-D eye positions. We conclude that 1) the hypothesis of a visuomotor look-up table for saccades fails to account even for saccades made directly toward visual targets, but rather, 2) the oculomotor system takes 3-D eye orientation into account in a visuomotor reference frame transformation. This transformation is probably implemented physiologically between retinotopically organized saccade centers (in cortex and superior colliculus) and the brain stem burst generator.
Facilitation of Miniature GABAergic Currents by Ruthenium Red in Neonatal Rat Hippocampal Neurons
Authors: Sciancalepore Marina , Savić Nataša , Györi János , Cherubini Enrico
Published: December 2017

Sciancalepore, Marina, Nataša Savić, János Györi, and Enrico Cherubini. Facilitation of miniature GABAergic currents by ruthenium red in neonatal rat hippocampal neurons. J. Neurophysiol. 80: 2316–2322, 1998. The whole cell configuration of the patch-clamp technique was used to study the modulation γ-aminobutyric acid (GABA)–mediated postsynaptic currents by ruthenium red in CA3 hippocampal neurons in slices obtained from postnatal ( P) days P6–P10 old rats. In the presence of kynurenic acid (1 mM), ruthenium red (100 μM) completely blocked stimulus-elicited GABA-mediated postsynaptic currents and reduced by 50% the amplitude of the spontaneous ones. Ruthenium red (100 μM) increased the frequency but not the amplitude of miniature GABAergic currents recorded in the presence of tetrodotoxin (1 μM) and kynurenic acid (1 mM), an effect that was prevented by heparin (100 μM). Ruthenium red did not modify the kinetics of miniature postsynaptic currents and the currents induced by exogenous application of GABA (10 μM) in the presence of tetrodotoxin, suggesting that its action was presynaptic in origin. The effects of ruthenium red on quantal GABA release was independent of external calcium. In a nominally Ca2+-free solution the potentiating effect induced by this polyvalent cation on miniature postsynaptic currents was still present. Intracellular calcium stores were not involved in ruthenium red action, because this polyvalent cation was able to facilitate miniature currents also in the presence of thapsigargin (10–20 μM). These results indicate that ruthenium red has a dual action on GABA release from GABAergic interneurons: it reduces the amplitude of spontaneous events and increases the frequency of miniature currents. The former effect is calcium-dependent, whereas the latter is calcium independent.
Saccadic Gain Modification: Visual Error Drives Motor Adaptation
Authors: Wallman Josh , Fuchs Albert F.
Published: December 2017

Wallman, Josh and Albert F. Fuchs. Saccadic gain modification: visual error drives motor adaptation. J. Neurophysiol. 80: 2405–2416, 1998. The brain maintains the accuracy of saccadic eye movements by adjusting saccadic amplitude relative to the target distance (i.e., saccade gain) on the basis of the performance of recent saccades. If an experimenter surreptitiously moves the target backward during each saccade, thereby causing the eyes to land beyond their targets, saccades undergo a gradual gain reduction. The error signal driving this conventional saccadic gain adaptation could be either visual (the postsaccadic distance of the target from the fovea) or motoric (the direction and size of the corrective saccade that brings the eye onto the back-stepped target). Similarly, the adaptation itself might be a motor adjustment (change in the size of saccade for a given perceived target distance) or a visual remapping (change in the perceived target distance). We studied these possibilities in experiments both with rhesus macaques and with humans. To test whether the error signal is motoric, we used a paradigm devised by Heiner Deubel. The Deubel paradigm differed from the conventional adaptation paradigm in that the backward step that occurred during the saccade was brief, and the target then returned to its original displaced location. This ploy replaced most of the usual backward corrective saccades with forward ones. Nevertheless, saccadic gain gradually decreased over hundreds of trials. Therefore, we conclude that the direction of saccadic gain adaptation is not determined by the direction of corrective saccades. To test whether gain adaptation is a manifestation of a static visual remapping, we decreased the gain of 10° horizontal saccades by conventional adaptation and then tested the gain to targets appearing at retinal locations unused during adaptation. To make the target appear in such “virgin territory,” we had it jump first vertically and then 10° horizontally; both jumps were completed and the target spot extinguished before saccades were made sequentially to the remembered target locations. Conventional adaptation decreased the gain of the second, horizontal saccade even though the target was in a nonadapted retinal location. In contrast, the horizontal component of oblique saccades made directly to the same virgin location showed much less gain decrease, suggesting that the adaptation is specific to saccade direction rather than to target location. Thus visual remapping cannot account for the entire reduction of saccadic gain. We conclude that saccadic gain adaptation involves an error signal that is primarily visual, not motor, but that the adaptation itself is primarily motor, not visual.
Spatial Receptive Fields of Primary Auditory Cortical Neurons in Quiet and in the Presence of Continuous Background Noise
Authors: Brugge John F. , Reale Richard A. , Hind Joseph E.
Published: December 2017

Brugge, John F., Richard A. Reale, and Joseph E. Hind. Spatial receptive fields of primary auditory cortical neurons in quiet and in the presence of continuous background noise. J. Neurophysiol. 80: 2417–2432, 1998. Spatial receptive fields of primary auditory (AI) neurons were studied by delivering, binaurally, synthesized virtual-space signals via earphones to cats under barbiturate anesthesia. Signals were broadband or narrowband transients presented in quiet anechoic space or in acoustic space filled with uncorrelated continuous broadband noise. In the absence of background noise, AI virtual space receptive fields (VSRFs) are typically large, representing a quadrant or more of acoustic space. Within the receptive field, onset latency and firing strength form functional gradients. We hypothesized earlier that functional gradients in the receptive field provide information about sound-source direction. Previous studies indicated that spatial gradients could remain relatively constant across changes in signal intensity. In the current experiments we tested the hypothesis that directional sensitivity to a transient signal, as reflected in the gradient structure of VSRFs of AI neurons, is also retained in the presence of a continuous background noise. When background noise was introduced three major affects on VSRFs were observed. 1) The size of the VSRF was reduced, accompanied by a reduction of firing strength and lengthening of response latency for signals at an acoustic axis and on-lines of constant azimuth and elevation passing through the acoustic axis. These effects were monotonically related to the intensity of the background noise over a noise intensity range of∼30 dB. 2) The noise intensity-dependent changes in VSRFs were mirrored by the changes that occurred when the signal intensity was changed in signal-alone conditions. Thus adding background noise was equivalent to a shift in the threshold of a directional signal, and this shift was seen across the spatial receptive field. 3) The spatial gradients of response strength and latency remained evident over the range of background noise intensity that reduced spike count and lengthened onset latency. Those gradients along the azimuth that spanned the frontal midline tended to remain constant in slope and position in the face of increasing intensity of background noise. These findings are consistent with our hypothesis that, under background noise conditions, information that underlies directional acuity and accuracy is retained within the spatial receptive fields of an ensemble of AI neurons.
Development of Glycinergic Synaptic Transmission to Rat Brain Stem Motoneurons
Authors: Singer Joshua H. , Talley Edmund M. , Bayliss Douglas A. , Berger Albert J.
Published: December 2017

Singer, Joshua H., Edmund M. Talley, Douglas A. Bayliss, and Albert J. Berger. Development of glycinergic synaptic transmission to rat brain stem motoneurons. J. Neurophysiol. 80: 2608–2620, 1998. Using an in vitro rat brain stem slice preparation, we examined the postnatal changes in glycinergic inhibitory postsynaptic currents (IPSCs) and passive membrane properties that underlie a developmental change in inhibitory postsynaptic potentials (IPSPs) recorded in hypoglossal motoneurons (HMs). Motoneurons were placed in three age groups: neonate (P0–3), intermediate (P5–8), and juvenile (P10–18). During the first two postnatal weeks, the decay time course of both unitary evoked IPSCs [mean decay time constant, τdecay= 17.0 ± 1.6 (SE) ms in neonates and 5.5 ± 0.4 ms in juveniles] and spontaneous miniature IPSCs (τdecay= 14.2 ± 2.4 ms in neonates and 6.3 ± 0.7 ms in juveniles) became faster. As glycine uptake does not influence IPSC time course at any postnatal age, this change most likely results from a developmental alteration in glycine receptor (GlyR) subunit composition. We found that expression of fetal (α2) GlyR subunit mRNA decreased, whereas expression of adult (α1) GlyR subunit mRNA increased postnatally. Single GlyR-channels recorded in outside-out patches excised from neonate motoneurons had longer mean burst durations than those from juveniles (18.3 vs. 11.1 ms). Concurrently, HM input resistance ( RN) and membrane time constant (τm) decreased ( RNfrom 153 ± 12 MΩ to 63 ± 7 MΩ and τmfrom 21.5 ± 2.7 ms to 9.1 ± 1.0 ms, neonates and juveniles, respectively), and the time course of unitary evoked IPSPs also became faster (τdecay= 22.4 ± 1.8 and 7.7 ± 0.9 ms, neonates vs. juveniles, respectively). Simulated synaptic currents were used to probe more closely the interaction between IPSC time course and τm, and these simulations demonstrated that IPSP duration was reduced as a consequence of postnatal changes in both the kinetics of the underlying GlyR channel and the membrane properties that transform the IPSC into a postsynaptic potential. Additionally, gramicidin perforated-patch recordings of glycine-evoked currents reveal a postnatal change in reversal potential, which is shifted from −37 to −73 mV during this same period. Glycinergic PSPs are therefore depolarizing and prolonged in neonate HMs and become faster and hyperpolarizing during the first two postnatal weeks.
Cortical fMRI Activation Produced by Attentive Tracking of Moving Targets
Authors: Culham Jody C. , Brandt Stephan A. , Cavanagh Patrick , Kanwisher Nancy G. , Dale Anders M. , Tootell Roger B. H.
Published: December 2017

Culham, Jody C., Stephan A. Brandt, Patrick Cavanagh, Nancy G. Kanwisher, Anders M. Dale, and Roger B. H. Tootell. Cortical fMRI activation produced by attentive tracking of moving targets. J. Neurophysiol. 80: 2657–2670, 1998. Attention can be used to keep track of moving items, particularly when there are multiple targets of interest that cannot all be followed with eye movements. Functional magnetic resonance imaging (fMRI) was used to investigate cortical regions involved in attentive tracking. Cortical flattening techniques facilitated within-subject comparisons of activation produced by attentive tracking, visual motion, discrete attention shifts, and eye movements. In the main task, subjects viewed a display of nine green “bouncing balls” and used attention to mentally track a subset of them while fixating. At the start of each attentive-tracking condition, several target balls (e.g., 3/9) turned red for 2 s and then reverted to green. Subjects then used attention to keep track of the previously indicated targets, which were otherwise indistinguishable from the nontargets. Attentive-tracking conditions alternated with passive viewing of the same display when no targets had been indicated. Subjects were pretested with an eye-movement monitor to ensure they could perform the task accurately while fixating. For seven subjects, functional activation was superimposed on each individual's cortically unfolded surface. Comparisons between attentive tracking and passive viewing revealed bilateral activation in parietal cortex (intraparietal sulcus, postcentral sulcus, superior parietal lobule, and precuneus), frontal cortex (frontal eye fields and precentral sulcus), and the MT complex (including motion-selective areas MT and MST). Attentional enhancement was absent in early visual areas and weak in the MT complex. However, in parietal and frontal areas, the signal change produced by the moving stimuli was more than doubled when items were tracked attentively. Comparisons between attentive tracking and attention shifting revealed essentially identical activation patterns that differed only in the magnitude of activation. This suggests that parietal cortex is involved not only in discrete shifts of attention between objects at different spatial locations but also in continuous “attentional pursuit” of moving objects. Attentive-tracking activation patterns were also similar, though not identical, to those produced by eye movements. Taken together, these results suggest that attentive tracking is mediated by a network of areas that includes parietal and frontal regions responsible for attention shifts and eye movements and the MT complex, thought to be responsible for motion perception. These results are consistent with theoretical models of attentive tracking as an attentional process that assigns spatial tags to targets and registers changes in their position, generating a high-level percept of apparent motion.
Neurotoxicity Mediated by Aberrant Patterns of Synaptic Activity Between Rat Hippocampal Neurons in Culture
Authors: McLeod John R. , Shen Maoxing , Kim Daniel J. , Thayer Stanley A.
Published: December 2017

McLeod, John R., Jr., Maoxing Shen, Daniel J. Kim, and Stanley A. Thayer. Neurotoxicity mediated by aberrant patterns of synaptic activity between rat hippocampal neurons in culture. J. Neurophysiol. 80: 2688–2698, 1998. Reducing the extracellular Mg2+concentration ([Mg2+]o) to 0.1 mM evoked an aberrant pattern of glutamatergic activity in the synaptic network formed by rat hippocampal neurons grown in primary culture. This treatment resulted in a significant increase in neuronal death when maintained for 20–24 h; 0.1 mM [Mg2+]oelicited a stable and repetitive series of intracellular Ca2+concentration ([Ca2+]i) spikes as indicated by indo-1-based microfluorimetry. Fura-2-based digital imaging experiments found that the [Ca2+]ispikes were synchronized for all the neurons in a given field. Thus electrophysiological recordings from individual cells were reasonable representations of the field as a whole, enabling correlation of electrical activity to viability. Underlying each [Ca2+]ispike was an intense burst of action potentials. Whole cell voltage-clamp experiments showed that a burst was composed of fast action currents superimposed on a slow inward current. The N-methyl-d-aspartate (NMDA) receptor antagonist CGS19755 (10 μM) blocked [Ca2+]ispiking, the slow inward current, and the cell death induced by low [Mg2+]o. The L-type Ca2+channel antagonist nimodipine (10 μM) blocked [Ca2+]ispiking, all synaptic activity, and the cell death induced by low [Mg2+]o. The non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 μM) exerted variable effects on [Ca2+]ispiking and blocked the slow inward current only when the cells were held at a relatively negative holding potential. CNQX did not afford any protection from 0.1 mM [Mg2+]o-induced neurotoxicity. [Ca2+]iimaging experiments showed that CNQX inhibited [Ca2+]ispiking in a subset of neurons within an active network. Thus, the neurons that were insensitive to CNQX appear to be those that were destined to die. We characterized an in vitro model that allowed us to correlate specific electrophysiological components of glutamatergic synaptic activity to the subsequent viability of the network. A slow NMDA receptor-mediated inward current was required to elicit [Ca2+]ispiking and neurotoxicity. Non-NMDA receptors did not contribute to synaptically mediated cell death in this model. An L-type Ca2+channel antagonist was neuroprotective when used at concentrations that blocked synaptic activity, suggesting that dendritic L-type Ca2+channels present a useful target for neuroprotective drugs.
Na+-Dependent Neuritic Spikes Initiate Ca2+-Dependent Somatic Plateau Action Potentials in Insect Dorsal Paired Median Neurons
Authors: Amat Corine , Lapied Bruno , French Andrew S. , Hue Bernard
Published: December 2017

Amat, Corine, Bruno Lapied, Andrew S. French, and Bernard Hue. Na+-dependent neuritic spikes initiate Ca2+-dependent somatic plateau action potentials in insect dorsal paired median neurons J. Neurophysiol. 80: 2718–2726, 1998. The origin of plateau action potentials was studied in short-term cultures of dorsal paired median (DPM) neurons dissociated from the terminal abdominal ganglion of the cockroach, Periplaneta americana. Spontaneous plateau action potentials were recorded by intracellular microelectrodes in cell bodies that had neurite stumps. These action potentials featured a fast initial depolarization followed by a plateau. However, only fast spikes of short duration were observed when the cell was hyperpolarized from the resting membrane potential. These two different components of the action potentials could be separated by applying depolarizing current pulses from a hyperpolarized holding potential. Application of 200 nM tetrodotoxin (TTX) abolished both fast and slow phases, but depolarization to the original resting potential by steady current injection triggered slow monophasic action potentials that could be blocked by 3 mM CoCl2. In contrast, DPM neurons without neurites were not spontaneously active. In these cells, calcium-dependent slow monophasic action potentials were only recorded immediately after impalement or with current pulse stimulation. Immunocytochemical observations showed that dorsal unpaired median (DUM) neuron cell bodies, which are known to exhibit spontaneous sodium-dependent action potentials, reacted with an antibody directed against a synthetic peptide corresponding to the SP19 segment of voltage-activated sodium channels. In contrast, the antibody did not stain DPM neuron cell bodies but gave intense, patchy staining only in the neurite. Whole cell patch-clamp experiments performed on isolated DPM neuron cell bodies without a neurite revealed the presence of an inward current that did not inactivate completly within the duration of the test pulse. This current was insensitive to both 100 nM TTX and sodium-free saline. It was defined as a high-voltage-activated calcium current according to its high threshold of activation (−30 mV) and its sensitivity to 1 mM CdCl2and 100 nM ω-conotoxin GVIA. Our findings demonstrate that spontaneous sodium-dependent spikes arising from the neurite are required to initiate slow somatic calcium-dependent action potentials in DPM neurons.
Representation of Spectral and Temporal Sound Features in Three Cortical Fields of the Cat. Similarities Outweigh Differences
Authors: Eggermont Jos J.
Published: December 2017

Eggermont, Jos J. Representation of spectral and temporal sound features in three cortical fields of the cat. Similarities outweigh differences. J. Neurophysiol. 80: 2743–2764, 1998. This study investigates the degree of similarity of three different auditory cortical areas with respect to the coding of periodic stimuli. Simultaneous single- and multiunit recordings in response to periodic stimuli were made from primary auditory cortex (AI), anterior auditory field (AAF), and secondary auditory cortex (AII) in the cat to addresses the following questions: is there, within each cortical area, a difference in the temporal coding of periodic click trains, amplitude-modulated (AM) noise bursts, and AM tone bursts? Is there a difference in this coding between the three cortical fields? Is the coding based on the temporal modulation transfer function (tMTF) and on the all-order interspike-interval (ISI) histogram the same? Is the perceptual distinction between rhythm and roughness for AM stimuli related to a temporal versus spatial representation of AM frequency in auditory cortex? Are interarea differences in temporal response properties related to differences in frequency tuning? The results showed that: 1) AM stimuli produce much higher best modulation frequencies (BMFs) and limiting rates than periodic click trains. 2) For periodic click trains and AM noise, the BMFs and limiting rates were not significantly different for the three areas. However, for AM tones the BMF and limiting rates were about a factor 2 lower in AAF compared with the other areas. 3) The representation of stimulus periodicity in ISIs resulted in significantly lower mean BMFs and limiting rates compared with those estimated from the tMTFs. The difference was relatively small for periodic click trains but quite large for both AM stimuli, especially in AI and AII. 4) Modulation frequencies <20 Hz were represented in the ISIs, suggesting that rhythm is coded in auditory cortex in temporal fashion. 5) In general only a modest interdependence of spectral- and temporal-response properties in AI and AII was found. The BMFs were correlated positively with characteristic frequency in AAF. The limiting rate was positively correlated with the frequency-tuning curve bandwidth in AI and AII but not in AAF. Only in AAF was a correlation between BMF and minimum latency was found. Thus whereas differences were found in the frequency-tuning curve bandwidth and minimum response latencies among the three areas, the coding of periodic stimuli in these areas was fairly similar with the exception of the very poor representation of AM tones in AII. This suggests a strong parallel processing organization in auditory cortex.
Dynamics and Kinematics of the Angular Vestibulo-Ocular Reflex in Monkey: Effects of Canal Plugging
Authors: Yakushin Sergei B. , Raphan Theodore , Suzuki Jun-Ichi , Arai Yasuko , Cohen Bernard
Published: December 2017

Yakushin, Sergei B., Theodore Raphan, Jun-Ichi Suzuki, Yasuko Arai, and Bernard Cohen. Dynamics and kinematics of the angular vestibulo-ocular reflex in monkey: effects of canal plugging. J. Neurophysiol. 80: 3077–3099, 1998. Horizontal and roll components of the angular vestibulo-ocular reflex (aVOR) were elicited by sinusoidal rotation at frequencies from 0.2 Hz (60°/s) to 4.0 Hz (≈6°/s) in cynomolgus monkeys. Animals had both lateral canals plugged (VC, vertical canals intact), both lateral canals and one pair of the vertical canals plugged (RALP, right anterior and left posterior canals intact; LARP, left anterior and right posterior canal intact), or all six semicircular canal plugged (NC, no canals). In normal animals, horizontal and roll eye velocity was in phase with head velocity and peak horizontal and roll gains were ≈0.8 and 0.6 in upright and 90° pitch, respectively. NC animals had small aVOR gains at 0.2 Hz, and the temporal phases were shifted ≈90° toward acceleration. As the frequency increased to 4 Hz, aVOR temporal gains and phases tended to normalize. Findings were similar for the LARP, RALP, and VC animals when they were rotated in the planes of the plugged canals. That is, they tended to normalize at higher frequencies. A model was developed incorporating the geometric organization of the canals and first order canal-endolymph dynamics. Canal plugging was modeled as an alteration in the low frequency 3-db roll-off and corresponding dominant time constant. The shift in the low-frequency 3-dB roll-off was seen in the temporal responses as a phase lead of the aVOR toward acceleration at higher frequencies. The phase shifted toward stimulus velocity as the frequency increased toward 4.0 Hz. By incorporating a dynamic model of the canals into the three-dimensional canal system, the spatial responses were predicted at all frequencies. Animals were also stimulated with steps of velocity in planes parallel to the plugged lateral canals. This induced a response with a short time constant and low peak velocity in each monkey. Gains were normalized for step rotation with respect to time constant as (steady state eye velocity)/(stimulus acceleration × time constant). Using this procedure, the gains were the same in canal plugged as in normal animals and corresponded to gains obtained in the frequency analysis. The study suggests that canal plugging does not block the afferent response to rotation, it merely shifts the dynamic response to higher frequencies.
Temporal and Intensity Coding of Pain in Human Cortex
Authors: Porro Carlo A. , Cettolo Valentina , Francescato Maria Pia , Baraldi Patrizia
Published: December 2017

Porro, Carlo A., Valentina Cettolo, Maria Pia Francescato, and Patrizia Baraldi. Temporal and intensity coding of pain in human cortex. J. Neurophysiol. 80:3312–3320, 1998. We used a high-resolution functional magnetic resonance imaging (fMRI) technique in healthy right-handed volunteers to demonstrate cortical areas displaying changes of activity significantly related to the time profile of the perceived intensity of experimental somatic pain over the course of several minutes. Twenty-four subjects (ascorbic acid group) received a subcutaneous injection of a dilute ascorbic acid solution into the dorsum of one foot, inducing prolonged burning pain (peak pain intensity on a 0–100 scale: 48 ± 3, mean ± SE; duration: 11.9 ± 0.8 min). fMRI data sets were continuously acquired for ∼20 min, beginning 5 min before and lasting 15 min after the onset of stimulation, from two sagittal planes on the medial hemispheric wall contralateral to the stimulated site, including the cingulate cortex and the putative foot representation area of the primary somatosensory cortex (SI). Neural clusters whose fMRI signal time courses were positively or negatively correlated ( P < 0.0005) with the individual pain intensity curve were identified by cross-correlation statistics in all 24 volunteers. The spatial extent of the identified clusters was linearly related ( P < 0.0001) to peak pain intensity. Regional analyses showed that positively correlated clusters were present in the majority of subjects in SI, cingulate, motor, and premotor cortex. Negative correlations were found predominantly in medial parietal, perigenual cingulate, and medial prefrontal regions. To test whether these neural changes were due to aspecific arousal or emotional reactions, related either to anticipation or presence of pain, fMRI experiments were performed with the same protocol in two additional groups of volunteers, subjected either to subcutaneous saline injection (saline: n = 16), inducing mild short-lasting pain (peak pain intensity 23 ± 4; duration 2.8 ± 0.6 min) or to nonnoxious mechanical stimulation of the skin (controls: n = 16) at the same body site. Subjects did not know in advance which stimulus would occur. The spatial extent of neural clusters whose signal time courses were positively or negatively correlated with the mean pain intensity curve of subjects injected with ascorbic acid was significantly larger ( P < 0.001) in the ascorbic acid group than both saline and controls, suggesting that the observed responses were specifically related to pain intensity and duration. These findings reveal distributed cortical systems, including parietal areas as well as cingulate and frontal regions, involved in dynamic encoding of pain intensity over time, a process of great biological and clinical relevance.
Stimulation of Human Thalamus for Pain Relief: Possible Modulatory Circuits Revealed by Positron Emission Tomography
Authors: Duncan Gary H. , Kupers Ron C. , Marchand Serge , Villemure Jean-Guy , Gybels JAN M. , Bushnell M. Catherine
Published: December 2017

Duncan, Gary H., Ron C. Kupers, Serge Marchand, Jean-Guy Villemure, Jan M. Gybels, and M. Catherine Bushnell. Stimulation of human thalamus for pain relief: possible modulatory circuits revealed by positron emission tomography . J. Neurophysiol. 80: 3326–3330, 1998. Stimulation of the somatosensory thalamus was used for more than 2 decades to treat chronic pain in the human. However, despite clinical reports of successful results, little is known about the actual mechanisms mediating this form of stimulation-produced analgesia. To reveal possible neuronal pathways evoked by thalamic stimulation, we measured regional changes in cerebral blood flow (rCBF) in five patients who received successful long-term relief of chronic pain with somatosensory thalamic stimulation. Positron emission tomography during thalamic stimulation revealed significant activation of the thalamus in the region of the stimulating electrodes as well as activation of the insular cortex ipsilateral to the thalamic electrodes (contralateral to the patients' clinical pain). For these patients, thalamic stimulation also evoked paresthesiae that included thermal sensations in addition to tingling sensations. Results of this study indicate that in some cases somatosensory thalamic stimulation may activate a thalamocortical pain modulation circuit that involves thermal pathways. These results are consistent with other recent reports suggesting that activation of thermal pathways may contribute to modulation of nociceptive information.
Influence of Predictive Information on Responses of Tonically Active Neurons in the Monkey Striatum
Authors: Apicella Paul , Ravel Sabrina , Sardo Pierangelo , Legallet Eric
Published: December 2017

Apicella, Paul, Sabrina Ravel, Pierangelo Sardo, and Eric Legallet. Influence of predictive information on responses of tonically active neurons in the monkey striatum. J. Neurophysiol. 80: 3341–3344, 1998. We investigated how the expectation of a signal of behavioral significance influences the activity of tonically active neurons in the striatum of two monkeys performing a simple reaction time task under two conditions, an uncued condition in which the trigger stimulus occurred randomly in time and a cued condition in which the same trigger was preceded by an instruction stimulus serving as a predictive signal for the forthcoming signal eliciting an immediate behavioral reaction. Both monkeys benefited from the presence of the instruction stimulus to reduce their reaction time, suggesting an increased ability to predict the trigger onset during cued trials compared with uncued trials. A majority of neurons (199/272, 73%) showed a phasic reduction in activity after the onset of the trigger stimulus in the uncued condition, whereas only 38% responded to the same stimulus when it was preceded by the instruction. Furthermore, magnitudes of trigger responses in the uncued condition were significantly higher than in the cued condition. Fifty-seven percent of the neurons responded to the instruction stimulus, and one-half of the neurons losing their response to the trigger in the cued condition responded to the instruction stimulus. These findings suggest that responses of tonic striatal neurons to a trigger stimulus for movement were influenced by predictive information.
Na+-Gated Nonselective Cation Channel From Lobster Olfactory Projection Neurons
Authors: Zhainazarov Aslbek B. , Ache Barry W.
Published: December 2017

Zhainazarov, Aslbek B. and Barry W. Ache. Na+-gated nonselective cation channel from lobster olfactory projection neurons. J. Neurophysiol. 80: 3387–3391, 1998. A nonselective cation channel specifically activated by intracellular Na+ was identified in cell-free patches taken from cultured lobster olfactory projection neurons. Na+ reversibly activates the channel in a concentration-dependent manner, with a “half-effect” Na+ concentration of 76.4 mM at −60 mV. The conductance of the channel is 32 pS. The channel is permeable to both alkali metal (Li+ > Na+ > K+ > Rb+ > Cs+) and divalent (Ca2+ > Mn2+ > Sr2+ > Mg2+ > Ba2+ > Na+) cations. The presence of a channel with the ability to generate plateau potentials suggests that the channel may potentially contribute to oscillatory behavior in these olfactory interneurons.
Task-Dependent Selectivity of Movement-Related Neuronal Activity in the Primate Prefrontal Cortex
Authors: Hoshi Eiji , Shima Keisetsu , Tanji Jun
Published: December 2017

Hoshi, Eiji, Keisetsu Shima, and Jun Tanji. Task-dependent selectivity of movement-related neuronal activity in the primate prefrontal cortex. J. Neurophysiol. 80: 3392–3397, 1998. We studied movement-related neuronal activity in the dorsolateral prefrontal cortex from the perspective of a general role for the prefrontal cortex in controlling motor behavior to achieve a specific goal according to the requirements of a given task. Monkeys were trained to perform two delayed motor tasks. The first task involved reaching for a target that matched the shape of a cue. The second task involved reaching for a target that matched the location of the cue. A majority (54%) of 175 movement-related prefrontal neurons exhibited preference for either the target shape or the type of task requirements. Sixty-four neurons (36%) were selectively active while reaching for a circle or a triangle. On the other hand, the activity of 59 neurons (34%) depended on whether the task required matching the shape or the location. These properties, characterizing the movement-related neuronal activity in the prefrontal cortex, rarely were found in the arm area of the primary motor cortex. Only 1 of 130 movement-related neurons (0.8%) showed task selectivity, and none showed target-shape selectivity.
Norepinephrine Inhibits a Toxin Resistant Ca2+ Current in Carotid Body Glomus Cells: Evidence for a Direct G Protein Mechanism
Authors: Overholt Jeffrey L. , Prabhakar Nanduri R.
Published: December 2017

Overholt, Jeffrey L. and Nanduri R. Prabhakar. Norepinephrine inhibits a toxin resistant Ca2+ current in carotid body glomus cells: evidence for a direct G protein mechanism. J. Neurophysiol. 81: 225–233, 1999. Previous studies have demonstrated that endogenous norepinephrine (NE) inhibits carotid body (CB) sensory discharge, and the cellular actions of NE have been associated with inhibition of Ca2+ current in glomus cells. The purpose of the present study was to elucidate the characteristics and mechanism of NE inhibition of whole cell Ca2+ current isolated from rabbit CB glomus cells and to determine the type(s) of Ca2+ channel involved. NE (10 μM) inhibited 24 ± 2% (SE) of the macroscopic Ca2+ current measured at the end of a 25 ms pulse to 0 mV and slowed activation of the current. The α2 adrenergic receptor antagonist, SK&F 86466, attenuated these effects. Inhibition by NE was fast and voltage-dependent i.e., maximal at −10 mV and then diminished with stronger depolarizations. This is characteristic of G protein βγ subunit interaction with the α1 subunit of certain Ca2+ channels, which can be relieved by depolarizing steps. A depolarizing step (30 ms to +80 mV) significantly increased (14 ± 1%) current in the presence of NE, whereas it had no effect before application of NE (1 ± 1%). To further test for the involvement of G proteins, NE was applied to cells where intracellular GTP was replaced by GDP-βS. NE had little or no effect on Ca2+ current in cells dialyzed with GDP-βS. To determine whether NE was inhibiting N- and/or P/Q-type channels, we applied NE in the presence of ω-conotoxin MVIIC (MVIIC). In the presence of 2.5 μM MVIIC, NE was equally potent at inhibiting the Ca2+ current (23 ± 4% vs. 23 ± 4% in control), suggesting that NE was not exclusively inhibiting N- or P/Q-type channels. NE was also equally potent (30 ± 2% vs. 26 ± 4% in control) at inhibiting the Ca2+ current in the presence of 2 μM nisoldipine, suggesting that NE was not inhibiting L-type channels. Further, NE inhibited a significantly larger proportion (47 ± 6%) of the resistant Ca2+ current remaining in the presence of NISO and MVIIC. These results suggest that NE inhibition of Ca2+ current in rabbit CB glomus cells is mediated in most part by effects on the resistant, non L-, N-, or P/Q-type channel and involves a direct G protein βγ interaction with this channel.
Reduced Voltage-Dependent Ca2+Signaling in CA1 Neurons After Brief Ischemia in Gerbils
Authors: Connor John A. , Razani-Boroujerdi Seddigheh , Greenwood Anders C. , Cormier Robert J. , Petrozzino Jeffrey J. , Lin Rick C. S.
Published: December 2017

Connor, J. A., S. Razani-Boroujerdi, A. C. Greenwood, R. J. Cormier, J. J. Petrozzino, and R.C.S. Lin. Reduced voltage-dependent Ca2+signaling in CA1 neurons after brief ischemia in gerbils. J. Neurophysiol. 81: 299–306, 1999. An initial overload of intracellular Ca2+plays a critical role in the delayed death of hippocampal CA1 neurons that die a few days after transient ischemia. Without direct evidence, the prevailing hypothesis has been that Ca2+overload may recur until cell death. Here, we report the first measurements of intracellular Ca2+in living CA1 neurons within brain slices prepared 1, 2, and 3 days after transient (5 min) ischemia. With no sign of ongoing Ca2+overload, voltage-dependent Ca2+transients were actually reduced after 2–3 days of reperfusion. Resting Ca2+levels and recovery rate after loading were similar to neurons receiving no ischemic insult. The tetrodotoxin-insensitive Ca spike, normally generated by these neurons, was absent at 2 days postischemia, as was a large fraction of Ca2+-dependent spike train adaptation. These surprising findings may lead to a new perspective on delayed neuronal death and intervention.