Intracellular Recordings from Interneurones and Motoneurones During Bilateral Kicks in the Locust: Implications for Mechanisms Controlling the Jump

Intracellular recordings were made from the neuropile processes of thoracic neurones of Locusta migratoria during bilateral kicks of the hindlegs. Electromyographic (EMG) recordings showed that the pattern of flexor and extensor tibiae muscle activity during kicks in this extensively dissected preparation was similar to that seen during a jump. Intracellular recordings from hindleg flexor and extensor motoneurones and from 13 identified interneurones revealed additional features of the motor programme for jumping and kicking and of the mechanism which triggers these events. There was a discrete burst of activity in the fast extensor tibiae (FETi) motoneurone at the end of the co-contraction phase, generated by a system that appeared to be separate from that triggering the kick. The excitatory connection from FETi to flexors was not responsible for initiating flexor activity and was of little functional importance in maintaining this activity during the co-contraction phase. The initial flexor excitation came from another, unidentified, central source. A pair of identified interneurones, the M-neurones, discharged with a high frequency burst just prior to the kick. Since these neurones inhibit hindleg flexor tibiae motoneurones, this observation provides further support for their proposed role as the neurones responsible for triggering kicks and jumps. Our data do not support the proposal that the activation of the M-neurones depends on them receiving progressively increasing proprioceptive input during the co-contraction phase. Throughout co-contraction, the M-neurones were hyperpolarized. Their activation was rapid and strong enough to cause them to discharge at rates as high as 400 spikes s−1. We suggest that the pulse-like activation of the M-neurones is produced centrally by a higher order system of interneurones. Another pair of previously identified interneurones, the C-neurones, were not necessary for the generation of the co-contraction phase of the motor programme. Their pattern of activity and their known connections indicated that they provide additional excitation to the flexors and extensors towards the end of co-contraction. Many other interneurones discharged either during co-contraction or when a kick was triggered. We conclude that the system generating the motor programme for a kick (jump) is more complex than proposed in previous studies.

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Flight-initiating interneurons in the locust

Journal of Neurophysiology ◽

10.1152/jn.1985.53.4.910 ◽

1985 ◽

Vol 53 (4) ◽

pp. 910-925 ◽

Cited By ~ 33

Author(s):

K. G. Pearson ◽

D. N. Reye ◽

D. W. Parsons ◽

G. Bicker

Keyword(s):

High Frequency ◽

Discharge Rate ◽

Locusta Migratoria ◽

Motor Program ◽

Flight Activity ◽

Neuronal System ◽

Cellular Mechanisms ◽

Closely Related Species ◽

Staining Techniques ◽

Frequency Burst

We have used intracellular recording and staining techniques to investigate the cellular mechanisms for the initiation and maintenance of flight in the locust, Locusta migratoria. In particular, we examined the properties of a small group of interneurons in the mesothoracic ganglion. We refer to these interneurons as 404 neurons. Their structure has been described, in a closely related species, by Watson and Burrows (21). Using a preparation in which intracellular recordings could be made from the main neurite of a 404 neuron during the generation of flight activity, we observed that the 404 neurons discharged tonically throughout flight episodes elicited by a constant wind stimulus on the head and by a sudden dimming of the lights. Their discharge rate was linearly related to the frequency of the flight activity. Depolarization of individual 404 neurons often initiated flight activity in quiescent preparations, and the application of hyperpolarizing currents during a flight episode either slowed or stopped flight activity. Hyperpolarizing currents also prevented the initiation of flight activity in some preparations. Individual 404 neurons were not always necessary for the generation of flight activity, since flight activity sometimes persisted when all spiking in a 404 neuron was prevented by the application of a hyperpolarizing current. We conclude that the 404 neurons function to initiate and maintain flight activity in response to wind stimulation of the head, but we have not yet established that they are the only thoracic neurons with this function. The 404 neurons discharged with a high-frequency burst at the time of triggering of a kick. Since the motor program for a jump is similar to that for a kick, the 404 neurons may also be involved in linking the initiation of flight activity to the jump. None of our data indicate that the 404 neurons receive input from the central rhythm generator. Thus the neuronal circuitry for flight appears to be hierarchically organized with at least one distinct neuronal system providing a tonic drive to initiate and maintain activity in the system that patterns activity in flight motoneurons.

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Measurement of Leaked High-Frequency Burst Electric Field and EMI Evaluation for Cardiac Pacemaker in Fusion Facility

IEEJ Transactions on Fundamentals and Materials ◽

10.1541/ieejfms.132.356 ◽

2012 ◽

Vol 132 (5) ◽

pp. 356-361

Author(s):

Yukio Yamanaka ◽

Jianqing Wang ◽

Osamu Fujiwara ◽

Tatsuhiko Uda

Keyword(s):

Electric Field ◽

High Frequency ◽

Cardiac Pacemaker ◽

Frequency Burst

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High-fidelity transmission of high-frequency burst stimuli from peripheral nerve to thalamic nuclei in children with dystonia

Scientific Reports ◽

10.1038/s41598-021-88114-w ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Estefanía Hernandez-Martin ◽

Enrique Arguelles ◽

Yifei Zheng ◽

Ruta Deshpande ◽

Terence D. Sanger

Keyword(s):

Deep Brain Stimulation ◽

Peripheral Nerve ◽

Brain Stimulation ◽

High Frequency ◽

Sensory Information ◽

Brain Structures ◽

High Fidelity ◽

Thalamic Nuclei ◽

Frequency Burst ◽

Deep Brain

AbstractHigh-frequency peripheral nerve stimulation has emerged as a noninvasive alternative to thalamic deep brain stimulation for some patients with essential tremor. It is not known whether such techniques might be effective for movement disorders in children, nor is the mechanism and transmission of the peripheral stimuli to central brain structures understood. This study was designed to investigate the fidelity of transmission from peripheral nerves to thalamic nuclei in children with dystonia undergoing deep brain stimulation surgery. The ventralis intermediate (VIM) thalamus nuclei showed a robust evoked response to peripheral high-frequency burst stimulation, with a greatest response magnitude to intra-burst frequencies between 50 and 100 Hz, and reliable but smaller responses up to 170 Hz. The earliest response occurred at 12–15 ms following stimulation onset, suggesting rapid high-fidelity transmission between peripheral nerve and thalamic nuclei. A high-bandwidth, low-latency transmission path from peripheral nerve to VIM thalamus is consistent with the importance of rapid and accurate sensory information for the control of coordination and movement via the cerebello-thalamo-cortical pathway. Our results suggest the possibility of non-invasive modulation of thalamic activity in children with dystonia, and therefore the possibility that a subset of children could have beneficial clinical response without the need for invasive deep brain stimulation.

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High-frequency burst spiking in layer 5 thick-tufted pyramids of rat primary somatosensory cortex encodes exploratory touch

Communications Biology ◽

10.1038/s42003-021-02241-8 ◽

2021 ◽

Vol 4 (1) ◽

Author(s):

Christiaan P. J. de Kock ◽

Jean Pie ◽

Anton W. Pieneman ◽

Rebecca A. Mease ◽

Arco Bast ◽

...

Keyword(s):

Somatosensory Cortex ◽

Information Content ◽

High Frequency ◽

Temporal Structure ◽

Cell Types ◽

Primary Somatosensory Cortex ◽

Excitatory Cell ◽

Cortical Microcircuit ◽

Subcortical Regions ◽

Frequency Burst

AbstractDiversity of cell-types that collectively shape the cortical microcircuit ensures the necessary computational richness to orchestrate a wide variety of behaviors. The information content embedded in spiking activity of identified cell-types remain unclear to a large extent. Here, we recorded spike responses upon whisker touch of anatomically identified excitatory cell-types in primary somatosensory cortex in naive, untrained rats. We find major differences across layers and cell-types. The temporal structure of spontaneous spiking contains high-frequency bursts (≥100 Hz) in all morphological cell-types but a significant increase upon whisker touch is restricted to layer L5 thick-tufted pyramids (L5tts) and thus provides a distinct neurophysiological signature. We find that whisker touch can also be decoded from L5tt bursting, but not from other cell-types. We observed high-frequency bursts in L5tts projecting to different subcortical regions, including thalamus, midbrain and brainstem. We conclude that bursts in L5tts allow accurate coding and decoding of exploratory whisker touch.

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Encoding properties of the wing hinge stretch receptor in the hawkmothManduca sexta

Journal of Experimental Biology ◽

10.1242/jeb.204.21.3693 ◽

2001 ◽

Vol 204 (21) ◽

pp. 3693-3702 ◽

Cited By ~ 1

Author(s):

Mark A. Frye

Keyword(s):

Manduca Sexta ◽

Instantaneous Frequency ◽

High Frequency ◽

Dynamic Deformation ◽

Stretch Receptor ◽

Tonic Firing ◽

Frequency Burst ◽

Natural Dynamic ◽

Oscillation Rate

SUMMARYTo characterize the in vivo responses of the wing hinge stretch receptor of Manduca sexta, I recorded its activity and simultaneously tracked the up-and-down motion of the wing while the hawkmoth flew tethered in a wind tunnel. The stretch receptor fires a high-frequency burst of spikes near each dorsal stroke reversal. The onset of the burst is tightly tuned to a set-point in wing elevation, and the number of spikes contained within the burst encodes the maximal degree of wing elevation during the stroke. In an effort to characterize its mechanical encoding properties, I constructed an actuator that delivered deformations to the wing hinge and simultaneously recorded the resultant stretch and tension and the activity of the stretch receptor. Stimuli included stepwise changes in length as well as more natural dynamic deformation that was measured in vivo. Step changes in length reveal that the stretch receptor encodes the static amplitude of stretch with both phasic and tonic firing dynamics. In vivo sinusoidal deformation revealed (i) that the timing of stretch receptor activity is tightly phase-locked within the oscillation cycle, (ii) that the number of spikes per burst is inversely related to oscillation frequency and (iii) that the instantaneous frequency of the burst increases with oscillation rate. At all oscillation rates tested, the instantaneous frequency of the burst increases with amplitude.

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The locust jump. I. The motor programme

Journal of Experimental Biology ◽

10.1242/jeb.66.1.203 ◽

1977 ◽

Vol 66 (1) ◽

pp. 203-219

Author(s):

W. J. Heitler ◽

M. Burrows

Keyword(s):

High Frequency ◽

Tactile Stimulation ◽

The Body ◽

Flexor Muscle ◽

Tactile Stimuli ◽

Extensor Muscles ◽

Trigger Activity ◽

Three Stages ◽

Motor Programme ◽

Made In

A motor programme is described for defensive kicking in the locust which is also probably the programme for jumping. The method of analysis has been to make intracellular recordings from the somata of identified motornuerones which control the metathoracic tibiae while defensive kicks are made in response to tactile stimuli. Three stages are recognized in the programme. (1) Initial flexion of the tibiae results from the low spike threshold of tibial flexor motorneurones to tactile stimulation of the body. (2) Co-contraction of flexor and extensor muscles followa in which flexor and extensor excitor motoneurones spike at high frequency for 300-600 ms. the tibia flexed while the extensor muscle develops tension isometrically to the level required for a kick or jump. (3) Trigger activity terminates the co-contraction by inhibiting the flexor excitor motorneurones and simultaneously exciting the flexor inhibitors. This causes relaxation of the flexor muscle and allows the tibiae to extend. If the trigger activity does not occur, the jump or kick is aborted, and the tibiae remain flexed.

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High-frequency burst vagal nerve simulation therapy in a natural primate model of genetic generalized epilepsy

Epilepsy Research ◽

10.1016/j.eplepsyres.2017.10.010 ◽

2017 ◽

Vol 138 ◽

pp. 46-52 ◽

Cited By ~ 11

Author(s):

C.Á. Szabó ◽

F.S. Salinas ◽

A.M. Papanastassiou ◽

J. Begnaud ◽

M. Ravan ◽

...

Keyword(s):

High Frequency ◽

Vagal Nerve ◽

Primate Model ◽

Generalized Epilepsy ◽

Frequency Burst

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Blink-Perturbed Saccades in Monkey. II. Superior Colliculus Activity

Journal of Neurophysiology ◽

10.1152/jn.2000.83.6.3430 ◽

2000 ◽

Vol 83 (6) ◽

pp. 3430-3452 ◽

Cited By ~ 63

Author(s):

H.H.L.M. Goossens ◽

A. J. Van Opstal

Keyword(s):

Superior Colliculus ◽

Firing Rate ◽

High Frequency ◽

Displacement Vector ◽

Neural Mechanism ◽

Fixed Number ◽

Deep Layers ◽

The Mean ◽

Reflex Blinks ◽

Frequency Burst

Trigeminal reflex blinks evoked near the onset of a saccade cause profound spatial-temporal perturbations of the saccade that are typically compensated in mid-flight. This paper investigates the influence of reflex blinks on the discharge properties of saccade-related burst neurons (SRBNs) in intermediate and deep layers of the monkey superior colliculus (SC). Twenty-nine SRBNs, recorded in three monkeys, were tested in the blink-perturbation paradigm. We report that the air puff stimuli, used to elicit blinks, resulted in a short-latency (∼10 ms) transient suppression of saccade-related SRBN activity. Shortly after this suppression (within 10–30 ms), all neurons resumed their activity, and their burst discharge then continued until the perturbed saccade ended near the extinguished target. This was found regardless whether the compensatory movement was into the cell's movement field or not. In the limited number of trials where no compensation occurred, the neurons typically stopped firing well before the end of the eye movement. Several aspects of the saccade-related activity could be further quantified for 25 SRBNs. It appeared that 1) the increase in duration of the high-frequency burst was well correlated with the (two- to threefold) increase in duration of the perturbed movement. 2) The number of spikes in the burst for control and perturbed saccades was quite similar. On average, the number of spikes increased only 14%, whereas the mean firing rate in the burst decreased by 52%. 3) An identical number of spikes were obtained between control and perturbed responses when burst and postsaccadic activity were both included in the spike count. 4) The decrease of the mean firing rate in the burst was well correlated with the decrease in the velocity of perturbed saccades. 5) Monotonic relations between instantaneous firing rate and dynamic motor error were obtained for control responses but not for perturbed responses. And 6) the high-frequency burst of SRBNs with short-lead and long-lead presaccadic activity (also referred to as burst and buildup neurons, respectively) showed very similar features. Our findings show that blinking interacts with the saccade premotor system already at the level of the SC. The data also indicate that a neural mechanism, rather than passive elastic restoring forces within the oculomotor plant, underlies the compensation for blink-related perturbations. We propose that these interactions occur downstream from the motor SC and that the latter may encode the desired displacement vector of the eyes by sending an approximately fixed number of spikes to the brainstem saccadic burst generator.

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