bluuebunny/crossref_metadata_2025 huggingface dataset:
Effects of local oscillator frequency on intersegmental coordination in the lamprey locomotor CPG: theory and experiment
Authors: Sigvardt K. A. , Williams T. L.
Published: December 2017

1. Experiments have been performed on in vitro preparations of lamprey spinal cord bathed in D-glutamate, which induces a pattern of activity recorded from ventral roots that is similar to that seen in the intact animal during swimming. The frequency of fictive swimming increases with increasing D-glutamate concentration, but intersegmental phase lag remains unaffected. 2. The effects on intersegmental phase lags of unequal activation of the rostral and caudal halves of a preparation were determined. Unequal activation was produced by placing a diffusion barrier in the middle of the chamber and perfusing the two halves with different concentrations of D-glutamate. 3. Within the rostral compartment, the phase lag increased from control when the rostral D-glutamate concentration was higher than the caudal concentration, and decreased from control when it was lower. By contrast, the phase lags within the caudal compartment did not depend on the ratio of D-glutamate concentration between the two compartments. 4. The frequency of the ventral root activity during differential activation was not significantly different from that of control experiments that had the same concentration as in the rostral compartment. 5. The results are discussed within the context of the mathematical analysis of chains of coupled oscillators by Kopell and Ermentrout and other current theories about the mechanisms of intersegmental coordination in the lamprey.
Eighth nerve activity regulates intracellular calcium concentration of avian cochlear nucleus neurons via a metabotropic glutamate receptor
Authors: Zirpel L. , Rubel E. W.
Published: December 2017

1. Neurons in the cochlear nucleus, nucleus magnocellularis (NM), of embryonic and neonatal chicks are dependent on eighth nerve activity for their maintenance and survival. Removing this input results in the death of 20–40% of the NM neurons and profound changes in the morphology and metabolism of surviving neurons. 2. One of the first changes in NM neurons after an in vivo cochlea removal is an increase in intracellular calcium concentration ([Ca2+]i). Increased [Ca2+]i has been implicated in a number of neuropathologic conditions. 3. In this study, we orthodromically and antidromically stimulated NM neurons in an in vitro brain stem slice preparation and monitored NM field potentials while simultaneously assessing the [Ca2+]i of NM neurons using fura-2. 4. During continuous orthodromic stimulation, [Ca2+]i of NM neurons remained constant at 80 nM. In the absence of stimulation, NM neuron [Ca2+]i increased steadily to 230 nM by 90 min. Antidromic and contralateral stimulation produced a [Ca2+]i increase in NM neurons that was similar in magnitude but slightly more rapid than that observed in the absence of stimulation. 5. Addition of the metabotropic glutamate receptor (mGluR) antagonists (R,S)-alpha-methyl-4-carboxyphenylglycine or 2-amino-3-phosphonopropionic acid to the superfusate during continued orthodromic stimulation resulted in a dose-dependent, rapid, and dramatic increase in NM neuron [Ca2+]i without affecting the postsynaptic field potentials recorded from NM. 6. The ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione and 2-amino-5-phosphonovalerate eliminated NM field potentials during continued orthodromic stimulation but did not result in an increase in [Ca2+]i. 7. Continuous superfusion of trans-(+/-)-aminocyclopentane dicarboxylate, but not glutamate, prevented the increase in [Ca2+]i in the absence of stimulation. 8. These results suggest that NM neurons rely on eighth nerve activity-dependent activation of a mGluR to maintain physiological [Ca2+]i. Removal of this mGluR activation results in an increase in [Ca2+]i that may contribute to the early stages of degeneration and eventual death of these neurons.
Reduction of rostral dorsal accessory olive responses during reaching
Authors: Horn K. M. , Van Kan P. L. , Gibson A. R.
Published: December 2017

1. Rostral dorsal accessory olive (rDAO) neurons are sensitive to light touch but have little or no discharge during active movement. We hypothesize that sensitivity of the rDAO is reduced during movement. To test this hypothesis, we evaluated sensitivity of rDAO neurons as cats reached out and retrieved a handle. On selected trials, mechanical or electrical perturbations to the forelimb were presented, and responses of rDAO neurons to the disturbances were recorded. 2. All rDAO units were highly sensitive to somatosensory stimuli during periods of stance. The cells responded to stimuli such as touch to hairs or light taps to the platform on which the cat was standing. 3. Discharges of rDAO neurons showed little or no synchronization to any aspect of the reaching task. rDAO neurons failed to fire to mechanical perturbations of the food handle during retrieval or hold phases of the task, even when their receptive fields included the surface of the paw in contact with the handle. 4. Electrical stimulation of the skin produced the greatest evoked response at all rDAO recording sites when the cats were at stance. Stimulation at any time during the reaching task, including periods of holding and licking, produced lower-amplitude evoked responses. The reduction in evoked response could be large and was restricted to the limb performing the task. 5. The data support the hypothesis that the cutaneous sensitivity of the rDAO is reduced during behavior. However, the inhibition does not appear to be tailored to specific times during the task or to neurons with specific receptive field locations on the actively moving limb. The reduction in sensitivity is as likely to be dependent on limb posture as on movement. We conclude that the rDAO discharge provides the cerebellum with information about vibration or contact during stance; it does not provide reliable information about undisturbed or disturbed movement. Climbing fiber input from rDAO might be useful in the preparation to make a movement, but it is probably not useful for correction of movement errors.
Low-frequency rhythms in the thalamus of intact-cortex and decorticated cats
Authors: Timofeev I. , Steriade M.
Published: December 2017

1. The patterns and synchronization of low-frequency, sleeplike rhythms (slow, spindle and delta oscillations) were compared in the intact-cortex and decorticated hemispheres of cats under ketamine-xylazine anesthesia. Intracellular recordings were performed in intact and decorticated hemispheres from 58 rostrolateral thalamic reticular (RE) neurons and from 164 thalamocortical (TC) neurons in the ventrolateral (VL) nucleus. In the decorticated hemisphere, dual intracellular recordings were performed from five RE-VL cell couples and from 12 TC cell couples within the VL nucleus. In addition, field potentials were simultaneously recorded from the neocortex (electroencephalogram) and ipsilateral thalamus [electrothalamogram (EThG)] of the intact (right) hemisphere, while EThG was recorded from the VL nucleus of the decorticated (left) hemisphere. 2. The slow oscillation (< 1 Hz) was absent in all 72 VL cells and in 23 of 25 RE cells from the decorticated hemisphere, as well as in the EThG recorded from the VL nucleus in the decorticated hemisphere, whereas it was simultaneously present in the cortex and thalamus of the intact hemisphere. The remaining two RE neurons (8%) in the decorticated hemisphere oscillated in close time relation with the slow oscillation in the cortex and thalamus of the opposite hemisphere; averaged activities showed that the onset of depolarization in RE cell followed 12 ms after the sharp depth-negative (depolarizing) component in the contralateral cortex. We view this result as the electrophysiological correlate of a disynaptic excitatory pathway consisting of crossed cortical projections, first relayed in contralateral dorsal thalamic nuclei. 3. The patterns of thalamic spindles (7–14 Hz) differed between the two hemispheres. Whereas the decorticated hemisphere displayed prolonged, waxing and waning spindles, the spindles in the intact-cortex hemisphere were short and exclusively waning and followed the depth-negative component of cortical slow oscillation. This result indicates that the synchronized corticothalamic drive associated with the slow oscillation fully entrains thalamic circuits from the onset of spindles, thus preventing further waxing. Similar differences between waxing and waning and waning spindles were obtained by stimulating with different intensities the thalamus in the decorticated hemisphere. 4. Simultaneous intracellular recordings from two VL cells or from RE and VL cells showed nearly simultaneous spindle sequences in the decorticated hemisphere. 5. The hyperpolarization-activated intrinsic delta oscillation (1–4 Hz) of TC cells was asynchronous in the decorticated hemisphere. 6. These results strengthen the idea that the slow oscillation is cortical in origin; demonstrate a full, short-range, intrathalamic synchrony of spindles in the absence of cortex; and indicate that the pattern of spindles, a sleep rhythm that is conventionally regarded as purely thalamic, is shaped by the corticothalamic feedback.
Enhanced NMDAR-dependent epileptiform activity is controlled by oxidizing agents in a chronic model of temporal lobe epilepsy
Authors: Hirsch J. C. , Quesada O. , Esclapez M. , Gozlan H. , Ben-Ari Y. , Bernard C. L.
Published: December 2017

1. Graded N-methyl-D-aspartate receptor (NMDAR)-dependent epileptiform discharges were recorded from ex vivo hippocampal slices obtained from rats injected a week earlier with an intracerebroventricular dose of kainic acid. Intracellular recordings from pyramidal cells of the CA1 area showed that glutamate NMDAR actively participated in synaptic transmission, even at resting membrane potential. When NMDAR were pharmacologically isolated, graded burst discharges could still be evoked. 2. The oxidizing reagent 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB, 200 microM, 15 min) suppressed the late part of the epileptiform burst that did not recover after wash but could be reinstated by the reducing agent tris (2-carboxyethyl) phosphine (TCEP, 200 microM, 15 min) and again abolished with the NMDA antagonist D-2-amino-5-phosphonovaleric acid (D-APV). 3. Pharmacologically isolated NMDAR-mediated responses were decreased by DTNB (56 +/- 10%, mean +/- SD, n = 6), an effect reversed by TCEP. 4. When only the fast glutamateric synaptic component was blocked, NMDA-dependent excitatory postsynaptic potentials (EPSPs) could be evoked despite the presence of underlying fast and slow inhibitory postsynaptic potentials (IPSPs). DTNB decreased EPSPs to 48 +/- 12% (n = 5) of control. 5. Since a decrease of the NMDAR-mediated response by +/- 50% is sufficient to suppress the late part of the burst, we suggest that epileptiform activity can be controlled by manipulation of the redox sites of NMDAR. Our observations raise the possibility of developing new anticonvulsant drugs that would spare alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-R (AMPAR)-mediated synaptic responses and decrease NMDAR-mediated synaptic transmission without blocking it completely.
Spontaneous switching between ortho- and antidromic spiking as the normal mode of firing in the cerebral giant neurons of freely behaving Lymnaea stagnalis
Authors: Jansen R. F. , Pieneman A. W. , ter Maat A.
Published: December 2017

1. Action-potential generation at sites remote from the cell body leads to antidromic firing and occurs in a wide variety of animals and experimental circumstances. Remote sites of spike generation may play a role in the functional subdivision of the axonal branches of a neuron and are also thought to play a role in synaptic integration. 2. Spontaneous ortho- and antidromic firing was investigated by recording the electrical activity of somata and axons of a pair of identified giant neurons [cerebral giant cells (CGCs)] in freely behaving animals. 3. At the soma of each CGC, the shape of the extracellular action potential was not constant but jumped between two well-defined levels. Subsequent recordings of synchronous firing in both cell bodies showed that the shape of the extracellular action potential depended on the firing sequence of the two CGCs. 4. Simultaneous recordings of the cell body and the main axon of a single CGC showed that spontaneous changes in the direction of spike conduction (orthodromic or antidromic) occurred. These changes in the direction of spike conduction coincided with the changes in the shapes of the extracellular action potentials recorded from the somata. 5. These results show that, under physiological conditions, spontaneous switching occurs between ortho- and antidromic spiking in the CGCs, and that action-potential generation at sites remote from the cell body is a physiologically relevant mechanism.
Response Properties of Pretectal Omnidirectional Pause Neurons in the Behaving Primate
Authors: Mustari Michael J. , Fuchs Albert F. , Pong Milton
Published: December 2017

Mustari, Michael J., Albert F. Fuchs, and Milton Pong. Response properties of pretectal omnidirectional pause neurons in the behaving primate. J. Neurophysiol. 77: 116–125, 1997. We have identified a region in the pretectum of rhesus monkeys ( Macaca mulatta) that contains units that evince a complete cessation in firing immediately after saccades. The pause occurs for saccades to target steps and catch up saccades during smooth pursuit, spontaneously in complete darkness or after quick phases of nystagmus. Because the pause in unit firing always follows saccade onset, we call these neurons following omnidirectional pause neurons (FOPNs). Because the pause also occurs with saccades in the dark, it is related to the saccade per se and is not a visually contingent response. The duration of the pause in firing exceeded the duration of all saccades up to 40 deg. For targeting saccades, the start of the pause was locked rather tightly to the beginning of the saccade but began an average of 51 ms after the saccade did. The end of the pause was linked only loosely to either the beginning or end of the saccade. About half (54%) of our 59 FOPNs also discharged a distinct burst of firing that preceded the pause. In different units, the burst preceded saccade onset by from 0 to 20 ms with an average of 11 ms and therefore could signal the occurrence of an impending saccade. The presaccadic burst was not correlated with any parameter of the saccade. Most FOPNs were found 278 μm, on average, dorsal to the direction-selective units characteristic of the pretectal nucleus of the optic tract (NOT) and occasionally slightly beyond the anterior-posterior and medial-lateral borders of the NOT. The FOPN region does not coincide with any known anatomically or functionally delineated pretectal nucleus. Because the characteristics of the FOPN pause are not reflected in the characteristics of the saccade and the FOPN pause occurs well after the saccade is over, it is unlikely that the pause in pretectal FOPNs is involved with saccade generation. On the other hand, the leading burst exhibited by the majority of FOPNs reliably signals that a saccade is occurring but neither its size nor direction. Perhaps this signal indicating the occurrence of all saccades is routed to visual relay neurons to effect saccadic modification of visual pathways. The substantial efferent connections of the FOPN/NOT region to the pregeniculate nucleus and the saccadic discharge of pregeniculate cells are discussed in the context of this suggestion.
Comparison of the Neuronal Activity in the SMA and the Ventral Cingulate Cortex During Prehension in the Monkey
Authors: Cadoret Geneviève , Smith Allan M.
Published: December 2017

Cadoret, Geneviève and Allan M. Smith. Comparison of the neuronal activity in the SMA and the ventral cingulate cortex during prehension in the monkey. J. Neurophysiol. 77: 153–166, 1997. Two monkeys were trained to use the thumb and forefinger to lift and hold an instrumented apparatus within a narrow position window for 1 s. The device was equipped to measure the position and the grip and lifting forces exerted by the animal. On blocks of trials the weight and surface texture could be varied or a force-pulse perturbation could be systematically delivered 750 ms after the object entered the window. If unopposed, the perturbation would displace the hand from the position window, and in preparation for this perturbation the monkeys either increased their grip force before the perturbation or raised the object higher within the position window. Two clearly separated clusters of cells in the medial wall of the frontal lobe were found to be active in relation to the task. One group of cells ( n = 115) was located in the caudal and medial part of area 6, in the supplementary motor area (SMA), and the other ( n = 92) was located in the ventral bank of the cingulate sulcus (CMAv), in area 23c. In each area, neurons were characterized by their sensorimotor features clearly related to the hand in addition to their modulated activity in the task. In the SMA, 71% (42 of 59) of the neurons tested for receptive fields responded to peripheral and mainly proprioceptive stimulation, and 71% of them (30 of 42) received inputs from the hand. In the CMAv, 77% (48 of 62) of the neurons responded to peripheral proprioceptive stimulation, and 77% (37 of 48) exhibited receptive fields originating from the hand. Intracortical microstimulation applied to 43 sites in the SMA evoked discrete hand movements at 12 loci, whereas in the CMAv hand movements were observed at 8 of 27 sites tested with an average threshold of >15 μA. A strong similarity was observed between the SMA and CMAv neurons in their sensorimotor features as well as the modulation of their activity in relation to the prehension task. In both areas the activity was poorly related to grip force and significant correlation with peak grip force was observed for only 9 and 7% of the CMAv and SMA neurons, respectively. In the SMA only five cells exhibited increased activity before the perturbation and in the CMAv no changes in activity were found despite the presence of clear preparatory increases in grip force in anticipation of the perturbation. The perturbation evoked reflexlike excitation of 38% (25 of 65) of the neurons in the CMAv and 28% (20 of 71) of the cells in the SMA; these cells were similar in magnitude and latency (∼50 ms) in both areas. In both the SMA and CMAv, most of the neurons increased their firing rate <200 ms before the grip force onset and the overlap in the distribution of neuronal response times suggests a parallel activation of the SMA and CMAv neurons during the prehension task.
Differential Effects of 4-Aminopyridine, Serotonin, and Phorbol Esters on Facilitation of Sensorimotor Connections inAplysia
Authors: Sugita Shuzo , Baxter Douglas A. , Byrne John H.
Published: December 2017

Sugita, Shuzo, Douglas A. Baxter, and John H. Byrne. Differential effects of 4-aminopyridine, serotonin, and phorbol esters on facilitation of sensorimotor connections in Aplysia. J. Neurophysiol. 77: 177–185, 1997. Serotonergic modulation of sensory neurons in Aplysia and their synaptic connections with follower cells has been used extensively as a model system with which to study mechanisms underlying neuronal plasticity. Serotonin (5-HT)-induced facilitation of sensorimotor connections is due to at least two processes: a process related to the broadening of presynaptic action potentials and a spike-duration-independent (SDI) process that may involve mobilization of transmitter. We have examined the relationship between spike broadening and synaptic facilitation of relatively nondepressed sensorimotor connections in the intact pleural-pedal ganglia. Previously, 5-HT-induced spike broadening in the sensory neuron was shown to be primarily due to the modulation of a voltage-dependent K+current ( IK,V). Low concentrations (20–30 μM) of 4-aminopyridine (4-AP) were used to rather selectively block IK,V. 4-AP increased spike duration in the sensory neuron and the excitatory postsynaptic potential (EPSP) in the motor neuron. The temporal development of 4-AP-induced spike broadening closely paralleled that of synaptic facilitation. Thus spike broadening via the reduction of IK,Vcan directly contribute to synaptic facilitation. The relationship between spike broadening induced by 5-HT (10 μM) and enhancement of the EPSP was also analyzed. We found that components of 5-HT-induced synaptic facilitation preceded the development of 5-HT-induced spike broadening. The comparison between the results of 4-AP and 5-HT revealed that the SDI processes made an important contribution to the rapid development of 5-HT-induced synaptic facilitation and that spike broadening made an important contribution to its maintenance. The SDI process and a slowly developing component of 5-HT-induced spike broadening are mediated, at least in part, by the activation of protein kinase C (PKC). Application of phorbol 12,13-diacetate (PDAc), an activator of PKC, partially mimicked the effects of 5-HT on spike duration and the EPSP.PDAc-induced enhancement of the EPSP preceded the slower development of PDAc-induced spike broadening. Like 5-HT, PDAc enhanced the EPSP via both spike broadening and the SDI processes. In addition, a 15-min exposure to PDAc occluded 5-HT-induced enhancement of the EPSP, suggesting that PKC and 5-HT engage similar or overlapping mechanisms. On the basis of these results and others, we propose a time-dependent hypothesis for the 5-HT-induced synaptic facilitation of nondepressed synapses, in which multiple second-messenger/protein kinase systems mediate the actions of 5-HT via both spike-duration-dependent and SDI processes.
Stimulation Within the Rostral Ventrolateral Medulla Can Evoke Monosynaptic GABAergic IPSPs in Sympathetic Preganglionic Neurons In Vitro
Authors: Deuchars Susan A. , Spyer K. Michael , Gilbey Michael P.
Published: December 2017

Deuchars, Susan A., K. Michael Spyer, and Michael P. Gilbey. Stimulation within the rostral ventrolateral medulla can evoke monosynaptic GABAergic IPSPs in sympathetic preganglionic neurons in vitro. J. Neurophysiol. 77: 229–235, 1997. The inhibitory responses of identified sympathetic preganglionic neurons (SPNs) to stimulation within the rostral ventrolateral medulla (RVLM) were studied to determine their nature and pharmacology. Whole cell patch-clamp recordings were made from 36 SPNs in the upper thoracic segments of the spinal cord in a neonatal rat brain stem-spinal cord preparation. Neurons were identified as SPNs on the basis of their antidromic activation after stimulation of the ipsilateral segmental ventral root and their morphology and location in the intermediolateral cell column and intercalated nucleus. In all SPNs, electrical stimulation of the RVLM evoked fast excitatory postsynaptic potentials (EPSPs) that were mediated by non- N-methyl-d-aspartate (NMDA) and NMDA receptors. These excitatory responses were the most prominent response in control artificial cerebrospinal fluid and have been studied previously. In 22 of the SPNs, RVLM stimulation also elicited fast inhibitory postsynaptic potentials (IPSPs), which increased in amplitude as the membrane was depolarized. Five of these neurons were not studied further as they responded occasionally with IPSPs that had highly variable onset latencies indicating the involvement of a polysynaptic pathway. In the remaining SPNs ( n = 17), the evoked IPSPs persisted in the presence of the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3,-dione and d,l-2-amino-5-phosphonopentanoic acid. In eight of these SPNs, it was necessary to block the EPSPs to reveal the IPSPs. In the 7 SPNs tested, the onset latencies of the IPSPs were not significantly different from the onset latencies of the fast EPSPs. The low sweep-to-sweep fluctuations in onset latency of individual IPSPs (absolute average deviation: 0.4 ms) indicated that the IPSPs were elicited by activation of a monosynaptic pathway. The amplitudes of the IPSPs decreased in amplitude as the membrane was hyperpolarized and reversed in polarity at −70.3 ± 1.7 mV (mean ± SD), which was close to the equilibrium potential for chloride ions. In addition, in seven SPNs, bath applications of 5 μM bicuculline, a γ-aminobuturic acid-A (GABAA) antagonist, abolished or reduced the evoked IPSPs. Five SPNs also were studied that displayed ongoing IPSPs. The amplitudes of these IPSPs increased with membrane depolarization and were blocked by bath applications of 5 μM bicuculline, suggesting that they also were mediated by activation of GABAA receptors. These results demonstrate the existence of a bulbospinal GABAergic pathway impinging directly onto SPNs. This pathway may be tonically active in the neonatal rat brain stem-spinal cord preparation.
Combination of Hand and Gaze Signals During Reaching: Activity in Parietal Area 7m of the Monkey
Authors: Ferraina S. , Johnson P. B. , Garasto M. R. , Battaglia-Mayer A. , Ercolani L. , Bianchi L. , Lacquaniti F. , Caminiti R.
Published: December 2017

Ferraina, S., P. B. Johnson, M. R. Garasto, A. Battaglia-Mayer, L. Ercolani, L. Bianchi, F. Lacquaniti, and R. Caminiti. Combination of hand and gaze signals during reaching: activity in parietal area 7m of the monkey. J. Neurophysiol. 77: 1034–1038, 1997. The role of area 7m has been studied by recording the activity of single neurons of monkeys trained to fixate and reach toward peripheral targets. The target was randomly selected from eight possible locations on a virtual circle, of radius 30° visual angle from a central target. Three tasks were employed to dissociate hand- from eye-related contributions. In the first task, animals looked and reached to the peripheral target. In a second task, the animal reached to the peripheral target while maintaining fixation on the central target. In the third task, the monkey maintained fixation on peripheral targets that were spatially coincident with those of the reaching tasks. The results show that cell activity in area 7m relates, for some cells to eye position, for others to hand position and movement, and for the majority of cells to a combination of visuomanual and oculomotor information. This area, therefore, seems to perform an early combination of information in the processing leading from target localization to movement generation.
Transmitter Release Differs at Snake Twitch and Tonic Endplates During Potassium-Induced Nerve Terminal Depolarization
Authors: Connor Elizabeth A. , Dunaevsky Anna , Griffiths David J. G. , Hardwick Jean C. , Parsons Rodney L.
Published: December 2017

Connor, Elizabeth A., Anna Dunaevsky, David J. G. Griffiths, Jean C. Hardwick, and Rodney L. Parsons. Transmitter release differs at snake twitch and tonic endplates during potassium-induced nerve terminal depolarization. J. Neurophysiol. 77: 749–760, 1997. Twitch and tonic muscle fibers of snake skeletal muscle differ in their synpatic as well as mechanical properties. These experiments were aimed at detemining the basis of the difference in vesicular release properties of nerve terminals at twitch and tonic endplates. Miniature endplate currents (MEPCs) were recorded from voltage-clamped garter snake muscle fibers depolarized by high K+in either a control Ca2+or high-Ca2+solution. MEPC frequency increased at twitch and tonic endplates and remained elevated for 8 h during depolarization in control Ca2+. At twitch endplates depolarized in the presence of high Ca2+, an increase in MEPC frequency was followed by a progressive decline. In contrast, MEPC frequency remained elevated in high Ca2+at tonic endplates. The observed decrease in MEPC freqency at depolarized twitch endplates in high Ca2+was not a function of the level of depolarization or initial MEPC frequency, nor was it due to a reduction in MEPC amplitude and loss of MEPCs in baseline noise. An optical assay of presynaptic function in which the activity-dependent dye FM1-43 was used confired that quantal reslease differs at twitch and tonic endplates. Most twitch nerve terminals were labeled by FM1-43 during prolonged depolarization with control Ca2+or after brief depolarization with high Ca2+. In contrast, the number of twitch nerve terminals and the degree to which they were stained was greatly reduced after prolonged exposure to high K+and high Ca2+, whereas depolarized tonic endplates were well stained by FM1-43 during brief and prolonged exposure to high Ca2+. FM1-43 staining also revealed variable levels of quantal release between individual boutons at twitch endplates after prolonged depolarization in high-Ca2+solution. The observed reduction in presynaptic function at twitch nerve terminals after prolonged depolarization in high-Ca2+solution was reversible and therefore not due to irreversible damage to terminal boutons. MEPC frequency increased at both twitch and tonic endplates when either Sr2+or Ba2+was substituted for high Ca2+during K+-induced depolarization. Over time, in Sr2+or Ba2+solutions, MEPC frequency remained elevated at tonic endplates but declined at twitch endplates with a time course similar to that observed in high Ca2+. MEPC amplitudes at both endplates remained constant. We conclude that the regulation of quantal release differs in nerve terminals innervating twitch and tonic endplates and postulate that differential intraterminal accumulation of Ca2+may underlie the observed difference in presynaptic function.
Characteristics of Saccadic Gain Adaptation in Rhesus Macaques
Authors: Straube Andreas , Fuchs Albert F. , Usher Susan , Robinson Farrel R.
Published: December 2017

Straube, Andreas, Albert F. Fuchs, Susan Usher, and Farrel R. Robinson. Characteristics of saccadic gain adaptation in rhesus macaques. J. Neurophysiol. 77: 874–895, 1997. We adapted the saccadic gain (saccadic amplitude/target step amplitude) by requiring monkeys to track a small spot that stepped to one side by 5, 10, or 15° and then, during the initial targeting saccade, jumped either forward or backward by a fixed percentage of the initial step. Saccadic gain increased or decreased, respectively, as a function of the number of adapting saccades made in that direction. The relation between gain and the number of adapting saccades was fit with an exponential function, yielding an asymptotic gain and a rate constant (the number of saccades to achieve 63% of the total change in gain). Backward intrasaccadic target jumps of 15, 30, and 50% of the initial target step reduced the asymptotic gain by an average of 12.2, 23.1, and 36.4%, respectively, with average rate constants of 163, 368, and 827 saccades, respectively. During 50% backward jumps, some saccades, especially those to larger target steps, became slower and lasted longer. Forward intrasaccadic jumps of 30% increased the asymptotic gain by 23.3% (average rate constant of 1,178 saccades). After we had caused adaptation, we induced recovery of gain toward normal by requiring the animal to track target steps without intrasaccadic jumps. Recovery following forward adaptation required about one third fewer saccades than the preceding gain increase. Recovery following backward adaptation required about the same average number of saccades as the preceding gain decrease. The first saccades of recovery were slightly less adapted than the last saccades of adaptation, suggesting that a small part of adaptation might have been strategic. After 50% backward jumps had reduced saccadic gain, the hypometric primary saccades during recovery were followed by hypometric corrective saccades, suggesting that they too had been adapted. When saccades of only one size underwent gain reduction, saccades to target steps of other amplitudes showed much less adaptation. Also, saccades in the direction opposite to that adapted were not adapted. Gain reductions endured if an adapted animal was placed in complete darkness for 20 h. These data indicate that saccadic gain adaptation is relatively specific to the adapted step and does not produce parametric changes of all saccades. Furthermore, adaptation is not a strategy, but involves enduring neuronal reorganization in the brain. We suggest that this paradigm engages mechanisms that determine saccadic gain in real life and therefore offers a reversible means to study their neuronal substrate.
GABA-Activated Conductance in Cultured Rat Inferior Colliculus Neurons
Authors: Hosomi Hidenobu , Mori Masahiro , Amatsu Mutsuo , Okada Yasuhiro
Published: December 2017

Hosomi, Hidenobu, Masahiro Mori, Mutsuo Amatsu, and Yasuhiro Okada. GABA-activated conductance in cultured rat inferior colliculus neurons. J. Neurophysiol. 77: 994–1002, 1997. With the use of a whole cell voltage-clamp technique and fura-2 fluorescence measurements, the actions of γ-aminobutyric acid (GABA) on cultured neurons from rat inferior colliculus were investigated. GABA (10–1,000 μM) induced currents in neurons held under voltage clamp that were inhibited by bicuculline (20 μM). Muscimol (100 μM) also evoked the currents, whereas baclofen (100 μM) affected neither the holding currents nor K+conductance due to depolarizing pulses. The current density–voltage relation of GABA-induced currents, with equal concentrations of Cl−in the internal and external solutions, reversed near 0 mV. Reduction of the internal Cl−concentration shifted the reversal potential in the negative direction as predicted from the Cl−equilibrium potential. Baclofen did not affect Ca2+conductance due to depolarizing pulses. The extracellular application of 150 mM KCl or 1.0 mM glutamate increased the intracellular Ca2+concentration ([Ca2+]i) of cultured inferior colliculus neurons only when neurons were bathed in a Ca2+-containing external solution. However, GABA (1.0 mM) failed to increase [Ca2+]iat all concentrations of external Ca2+used, indicating that GABA neither depolarized the cultured inferior colliculus neurons sufficiently to activate the voltage-dependent Ca2+conductances nor evoked Ca2+release from intracellular stores. These results suggest that in cultured rat inferior colliculus neurons, GABAAreceptor channels may be predominantly responsible for the membrane conductance evoked by GABA and subsequent hyperpolarization of the neurons.
cAMP-Dependent Protein Kinase Modulates Expiratory Neurons In Vivo
Authors: Lalley Peter M. , Pierrefiche Olivier , Bischoff Anne M. , Richter Diethelm W.
Published: December 2017

Lalley, Peter M., Olivier Pierrefiche, Anne M. Bischoff, and Diethelm W. Richter. cAMP-dependent protein kinase modulates expiratory neurons in vivo. J. Neurophysiol. 77: 1119–1131, 1997. The adenosine 3′,5′-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) second-messenger system influences neuronal excitability by modulating voltage-regulated and transmitter-activated channels. In this study we investigated the influence of the cAMP-PKA system on the excitability of expiratory (E) neurons in the caudal medulla of anesthetized, paralyzed, and artificially ventilated adult cats. We intracellularly injected the PKA inhibitors cAMP-dependent PKA inhibitor 5-22 amide (Walsh inhibitory peptide) and Rp-adenosine 3′,5′-cyclic monophosphothioate triethylamine (Rp-cAMPS), the PKA activator Sp-adenosine 3′,5′-cyclic monophosphothioate triethylamine (Sp-cAMPS), and the adenylyl cyclase activator forskolin and measured membrane potential, neuronal input resistance, and synaptic membrane currents. Inhibition of cAMP-PKA activity by Walsh inhibitory peptide or Rp-cAMPS injections hyperpolarized neurons, decreased input resistance, and depressed spontaneous bursts of action potentials. Action potential duration was shortened and afterhyperpolarizations were increased. Inhibitory synaptic currents increased significantly. Stimulation of cAMP-PKA activity by Sp-cAMPS or forskolin depolarized neurons and increased input resistance. Spontaneous inhibitory synaptic currents were reduced and excitatory synaptic currents were increased. Rp-cAMPS depressed stimulus-evoked excitatory postsynaptic potentials and currents, whereas Sp-cAMPS increased them. Sp-cAMPS also blocked postsynaptic inhibition of E neurons by 8-hydroxy-dipropylaminotetralin, a serotonin-1A (5-HT-1A) receptor agonist that depresses neuronal cAMP-PKA activity. To determine the predominant effect of G protein-mediated neuromodulation of E neurons, we injected guanosine-5′-O-(3-thiotriphosphate) tetralithium salt (GTP-γ-S), an activator of both stimulatory and inhibitory G proteins. GTP-γ-S hyperpolarized E neurons, reduced input resistance, and increased action potential afterhyperpolarization. We conclude that the intracellular cAMP-PKA messenger system plays an important role in the activity-dependent modulation of excitability in E neurons of the caudal medulla. In addition, the cAMP-PKA pathway itself is downregulated during activation of 5-HT-1A receptors.
Serotonergic Modulation of a Voltage-Gated Calcium Current in Parapodial Swim Muscle FromAplysia brasiliana
Authors: Laurienti P. J. , Blankenship J. E.
Published: December 2017

Laurienti, P. J. and J. E. Blankenship. Serotonergic modulation of a voltage-gated calcium current in parapodial swim muscle from Aplysia brasiliana. J. Neurophysiol. 77: 1496–1502, 1997. Here we describe the effects of serotonin (5-HT) on dissociated parapodial muscle fibers from Aplysia brasiliana. 5-HT has previously been implicated as a modulatory transmitter at the parapodial neuromuscular junction. Exogenously applied or endogenously released 5-HT increases the amplitude of motoneuron-induced excitatory junctional potentials and contractions in parapodial muscle. Exogenously applied 5 μM 5-HT increases the amplitude of a voltage-gated inward calcium current in isolated muscle fibers by an average of 42% in response to a voltage step from −70 to −10 mV. The amplitude of the inward current was increased at all voltages tested, with the peak increase occurring between −30 and −20 mV. The dihydropyridine calcium channel antagonist nifedipine (10 μM) blocked this effect of 5-HT. The data indicate that 5-HT increases a previously identified calcium current in parapodial muscle fibers that is similar to the vertebrate L-type current. Although several types of K+channels exist in these fibers, including Ca2+-dependent K+channels, the results suggest that 5-HT has little effect on these currents. Parapodial muscle contractions during swimming behavior occur in response to bursts of motoneuron action potentials that produce graded muscle depolarizations that occur over a 1- to 2-s period rather than being instantaneous or rapid responses as might be produced by one or two action potentials or a brief voltage step. With the use of 1-s voltage ramps, we attempted to mimic physiological depolarization and demonstrate that 5-HT is able to increase the amplitude of the inward calcium current. The data presented in this paper provide evidence that 5-HT increases the Ca2+current, which may be one mechanism by which 5-HT modulates muscle contractions during swim behavior.
Amplification of EPSPs by Low Ni2+- and Amiloride-Sensitive Ca2+ Channels in Apical Dendrites of Rat CA1 Pyramidal Neurons
Authors: Gillessen Thomas , Alzheimer Christian
Published: December 2017

Gillessen, Thomas and Christian Alzheimer. Amplification of EPSPs by low Ni2+- and amiloride-sensitive Ca2+ channels in apical dendrites of rat CA1 pyramidal neurons. J. Neurophysiol. 77: 1639–1643, 1997. Distal synaptic input to hippocampal CA1 pyramidal neurons was evoked by electrical stimulation of afferent fibers in outer stratum radiatum. Whole cell recordings from CA1 cell somata served to monitor excitatory postsynaptic potential (EPSP) envelopes after dendritic processing. To probe a functional role of low-voltage-activated Ca2+ current [or T current ( I T)] in the apical dendrite, EPSP recordings were combined with local application of antagonists of I T. Dendritic application of low concentrations of Ni2+ (5 μM) and amiloride (50 μM) reduced EPSP amplitude measured at the soma (resting membrane potential −70 mV) by 33.0 ± 2.9% (mean ± SE, n = 27) and 27.0 ± 2.1%( n = 26), respectively. No appreciable effect on EPSP time course was observed. As expected from the voltage dependence of I T activation, the inhibitory effect of both antagonists was strongly attenuated when EPSPs were recorded at hyperpolarized membrane potential (−90 mV). In contrast to dendritic application, somatic application of Ni2+ or amiloride produced only weak reduction of EPSP amplitude. Our data indicate that dendritic low Ni2+- and amiloride-sensitive Ca2+ channels giving rise predominantly to I T can produce substantial amplification of synaptic input. We thus propose that these channels represent an important component of subthreshold signal integration in apical dendrites of CA1 pyramidal cells.
Constrained and Unconstrained Movements Involve Different Control Strategies
Authors: Desmurget Michel , Jordan Michael , Prablanc Claude , Jeannerod Marc
Published: December 2017

Desmurget, Michel, Michael Jordan, Claude Prablanc, and Marc Jeannerod. Constrained and unconstrained movements involve different control strategies. J. Neurophysiol. 77: 1644–1650, 1997. This experiment was carried out to test whether or not the rules governing the execution of compliant and unconstrained movements are different (a compliant motion is defined as a motion constrained by external contact). To answer this question we examined the characteristics of visually directed movements performed with either the index fingertip (unconstrained) or a hand-held cursor (compliant). For each of these categories of movements, two experimental conditions were investigated: no instruction about hand path, and instruction to move the fingertip along a straight-line path. The results of the experiment were as follows. 1) The spatiotemporal characteristics of the compliant and unconstrained movements were fundamentally different when the subjects were not required to follow a specific hand path. 2) The instruction to perform straight movements modified the characteristics of the unconstrained movements, but not those of the compliant movements. 3) The target eccentricity influenced selectively the curvature of the “unconstrained–no path instruction” movements. Taken together, these results suggest that compliant and unconstrained movements involve different control strategies. Our data support the hypothesis that unconstrained motions are, unlike compliant motions, not programmed to follow a straight-line path in the task space. These observations provide a theoretical reference frame within which some apparently contradictory results reported in the movement generation literature may be explained.
Neuronal Encoding of Texture Changes in the Primary and the Secondary Somatosensory Cortical Areas of Monkeys During Passive Texture Discrimination
Authors: Jiang Wan , Tremblay François , Chapman C. Elaine
Published: December 2017

Jiang, Wan, François Tremblay, and C. Elaine Chapman. Neuronal encoding of texture changes in the primary and the secondary somatosensory cortical areas of monkeys during passive texture discrimination. J. Neurophysiol. 77: 1656–1662, 1997. Two rhesus monkeys were trained to discriminate, with the use of passive touch, a standard surface [rectangular arrays of raised dots with a spatial period (SP) of 2 mm across the rows and columns] from three modified surfaces in which the SP between rows was increased to 3, 4, or 5 mm over the second half of the surface. After the surface presentation (to digit tips 3 and 4 of one hand) the monkeys indicated the presence or absence of a change in texture by pulling or pushing a lever, respectively, with the opposite hand. Of 193 neurons recorded from primary somatosensory cortex (SI, 3 hemispheres) and 94 neurons from secondary somatosensory cortex (SII, 1 hemisphere), all contralateral to the stimulated hand, the discharge of 51 SI and 19 SII neurons was classified as texture related. Two types of texture-related responses were obtained. Graded neurons showed a linear relationship between mean discharge frequency and SP; nongraded neurons showed a significant change in discharge over the modified half of the surfaces but the discharge did not distinguish between the three modified surfaces. The distribution of these texture responses was significantly different in SI and SII: whereas most of the texture-related neurons in SI (44 of 51, 86%) were graded, the majority of those in SII (12 of 19, 63%) were nongraded. The results were interpreted as suggesting that the nongraded responses reflect feature extraction in SII, signaling the presence of a change in texture but not its magnitude, and so support the notion that texture signals are processed sequentially, first in SI and then in SII.
Association Between Dendritic Lamellar Bodies and Complex Spike Synchrony in the Olivocerebellar System
Authors: De Zeeuw C. I. , Koekkoek S.K.E. , Wylie D.R.W. , Simpson J. I.
Published: December 2017

De Zeeuw, C. I., S.K.E. Koekkoek, D.R.W. Wylie, and J. I. Simpson. Association between dendritic lamellar bodies and complex spike synchrony in the olivocerebellar system. J. Neurophysiol. 77: 1747–1758, 1997. Dendritic lamellar bodies have been reported to be associated with dendrodendritic gap junctions. In the present study we investigated this association at both the morphological and electrophysiological level in the olivocerebellar system. Because cerebellar GABAergic terminals are apposed to olivary dendrites coupled by gap junctions, and because lesions of cerebellar nuclei influence the coupling between neurons in the inferior olive, we postulated that if lamellar bodies and gap junctions are related, then the densities of both structures will change together when the cerebellar input is removed. Lesions of the cerebellar nuclei in rats and rabbits resulted in a reduction of the density of lamellar bodies, the number of lamellae per lamellar body, and the density of gap junctions in the inferior olive, whereas the number of olivary neurons was not significantly reduced. The association between lamellar bodies and electrotonic coupling was evaluated electrophysiologically in alert rabbits by comparing the occurrence of complex spike synchrony in different Purkinje cell zones of the flocculus that receive their climbing fibers from olivary subnuclei with different densities of lamellar bodies. The complex spike synchrony of Purkinje cell pairs, that receive their climbing fibers from an olivary subnucleus with a high density of lamellar bodies, was significantly higher than that of Purkinje cells, that receive their climbing fibers from a subnucleus with a low density of lamellar bodies. To investigate whether the complex spike synchrony is related to a possible synchrony between simple spikes, we recorded simultaneously the complex spike and simple spike responses of Purkinje cell pairs during natural visual stimulation. Synchronous simple spike responses did occur, and this synchrony tended to increase as the synchrony between the complex spikes increased. This relation raises the possibility that synchronously activated climbing fibers evoke their effects in part via the simple spike response of Purkinje cells. The present results indicate that dendritic lamellar bodies and dendrodendritic gap junctions can be downregulated concomitantly, and that the density of lamellar bodies in different olivary subdivisions is correlated with the degree of synchrony of their climbing fiber activity. Therefore these data support the hypothesis that dendritic lamellar bodies can be associated with dendrodendritic gap junctions. Considering that the density of dedritic lamellar bodies in the inferior olive is higher than in any other area of the brain, this conclusion implies that electrotonic coupling is important for the function of the olivocerebellar system.