Role of an Identified Looming-Sensitive Neuron in Triggering a Flying Locust's Escape

2006 ◽  
Vol 95 (6) ◽  
pp. 3391-3400 ◽  
Author(s):  
Roger D. Santer ◽  
F. Claire Rind ◽  
Richard Stafford ◽  
Peter J. Simmons
Keyword(s):  
Membrane Potential ◽  
Motor Neuron ◽  
High Frequency ◽  
Escape Behavior ◽  
Excitatory Input ◽  
Movement Detector ◽  
Stimulus Meaning ◽  
Contralateral Movement ◽  
Flight Motor

Flying locusts perform a characteristic gliding dive in response to predator-sized stimuli looming from one side. These visual looming stimuli trigger trains of spikes in the descending contralateral movement detector (DCMD) neuron that increase in frequency as the stimulus gets nearer. Here we provide evidence that high-frequency (>150 Hz) DCMD spikes are involved in triggering the glide: the DCMD is the only excitatory input to a key gliding motor neuron during a loom; DCMD-mediated EPSPs only summate significantly in this motor neuron when they occur at >150 Hz; when a looming stimulus ceases approach prematurely, high-frequency DCMD spikes are removed from its response and the occurrence of gliding is reduced; and an axon important for glide triggering descends in the nerve cord contralateral to the eye detecting a looming stimulus, as the DCMD does. DCMD recordings from tethered flying locusts showed that glides follow high-frequency spikes in a DCMD, but analyses could not identify a feature of the DCMD response alone that was reliably associated with glides in all trials. This was because, for a glide to be triggered, the high-frequency spikes must be timed appropriately within the wingbeat cycle to coincide with wing elevation. We interpret this as flight-gating of the DCMD response resulting from rhythmic modulation of the flight motor neuron's membrane potential during flight. This means that the locust's escape behavior can vary in response to the same looming stimulus, meaning that a predator cannot exploit predictability in the locust's collision avoidance behavior.

scholarly journals Gamma motor neurons survive and exacerbate alpha motor neuron degeneration in ALS

2016 ◽  
Vol 113 (51) ◽  
pp. E8316-E8325 ◽  
Author(s):  
Melanie Lalancette-Hebert ◽  
Aarti Sharma ◽  
Alexander K. Lyashchenko ◽  
Neil A. Shneider
Keyword(s):  
Motor Neuron ◽  
Mouse Models ◽  
Motor Neurons ◽  
Muscle Spindles ◽  
Excitatory Input ◽  
Synaptic Excitation ◽  
Fused In Sarcoma ◽  
Alpha Motor Neuron ◽  
Lateral Sclerosis

The molecular and cellular basis of selective motor neuron (MN) vulnerability in amyotrophic lateral sclerosis (ALS) is not known. In genetically distinct mouse models of familial ALS expressing mutant superoxide dismutase-1 (SOD1), TAR DNA-binding protein 43 (TDP-43), and fused in sarcoma (FUS), we demonstrate selective degeneration of alpha MNs (α-MNs) and complete sparing of gamma MNs (γ-MNs), which selectively innervate muscle spindles. Resistant γ-MNs are distinct from vulnerable α-MNs in that they lack synaptic contacts from primary afferent (IA) fibers. Elimination of these synapses protects α-MNs in the SOD1 mutant, implicating this excitatory input in MN degeneration. Moreover, reduced IAactivation by targeted reduction of γ-MNs in SOD1G93Amutants delays symptom onset and prolongs lifespan, demonstrating a pathogenic role of surviving γ-MNs in ALS. This study establishes the resistance of γ-MNs as a general feature of ALS mouse models and demonstrates that synaptic excitation of MNs within a complex circuit is an important determinant of relative vulnerability in ALS.

Arterial chemoreceptor input to respiratory hypoglossal motoneurons

1990 ◽  
Vol 69 (2) ◽  
pp. 700-709 ◽  
Author(s):  
S. W. Mifflin
Keyword(s):  
Membrane Potential ◽  
Upper Airway ◽  
Excitatory Input ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
End Tidal ◽  
Carotid Body Chemoreceptors ◽  
Excitatory Drive ◽  
Arterial Chemoreceptor

To better understand the role of the arterial chemoreceptors in the regulation of upper airway patency at the level of the oropharynx, intracellular recordings were obtained from inspiratory hypoglossal motoneurons (IHMs), and the responses to selective activation of the carotid body chemoreceptors were examined. In pentobarbital-anesthetized, vagotomized, paralyzed, and artificially ventilated cats, chemoreceptor activation enhanced the inspiratory depolarization of membrane potential in 32 of 36 IHMs. This was manifested as an increase in either the amplitude (n = 13) or duration (n = 3) or an increase in both amplitude and duration (n = 16) of the inspiratory membrane potential depolarization. The amplitude and duration of the inspiratory membrane potential depolarization increased 98 +/- 15% (n = 29) and 78 +/- 13% (n = 19), respectively. Similar patterns of enhanced activity (increased duration and/or amplitude of membrane depolarization) were observed in five expiratory hypoglossal motoneurons (EHMs) after chemoreceptor activation. In 16 of the 32 IHMs, chemoreceptor activation also evoked changes in IHM membrane potential during expiration: enhanced post-inspiratory discharge (n = 6), expiratory depolarization/discharge (n = 6), and tonic depolarization/discharge, which persisted for several respiratory cycles (n = 4). The arterial chemoreceptors provide a powerful excitatory input to IHMs during both inspiration and expiration. This excitatory drive to IHMs and EHMs will aid in the maintenance of upper airway patency throughout the respiratory cycle during increases in end-tidal CO2.

Segmental giant: evidence for a driver neuron interposed between command and motor neurons in the crayfish escape system

1982 ◽  
Vol 47 (5) ◽  
pp. 761-781 ◽  
Author(s):  
A. Roberts ◽  
F. B. Krasne ◽  
G. Hagiwara ◽  
J. J. Wine ◽  
A. P. Kramer
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
High Frequency ◽  
Functional Significance ◽  
Escape Behavior ◽  
Dendritic Branch ◽  
Command Neurons ◽  
Firing Threshold ◽  
Conventional Tests ◽  
Bilateral Pair

1. The giant command neurons for tailflip escape behavior in crayfish have been thought to excite the nongiant fast flexor (tailflip producing) motor neurons (FFs) via monosynaptic connections. We show here that excitation of FFs instead occurs via a bilateral pair of segmental giant neurons (SGs) interposed between the command axons and FFs in each segment. 2. Anatomically, the SGs appear to make numerous contacts with ipsilateral command axons and FFs and fewer contacts contralaterally. In contrast, the command axons have only sparse direct connections to the FFs. An SG has an axon in the ipsilateral first ganglionic root and may be a modified swimmeret motor neuron. 3. Each SG is depolarized well beyond threshold by the firing of an ipsilateral command axon and is depolarized to near threshold by the firing of a contralateral command axon. The synapses between command axons and SGs are electrical and probably rectifying. 4. Each FF is excited to a level near firing threshold by the SG ipsilateral to its axon and is excited weakly by the contralateral SG. The synapses between SGs and FFs are electrical and nonrectifying. 5. Variations in excitatory postsynaptic potentials (EPSPs) recorded in FFs during prolonged, high-frequency firing of the command axons can be accounted for by refractoriness of SG spikes, as opposed to refractoriness of dendritic branch spikes as had previously been delivered. 6. These findings illustrate the limitations of conventional tests for monosynapticity. 7. The functional significance of having driver neurons interposed between command neurons and motor neurons is discussed.

Triggering of locust jump by multimodal inhibitory interneurons

1980 ◽  
Vol 43 (2) ◽  
pp. 257-278 ◽  
Author(s):  
K. G. Pearson ◽  
W. J. Heitler ◽  
J. D. Steeves
Keyword(s):  
Action Potentials ◽  
Sensory Modality ◽  
Excitatory Input ◽  
Movement Detector ◽  
Sensory Stimuli ◽  
Response Characteristics ◽  
Sensory Convergence ◽  
Contralateral Movement ◽  
Tail Flip ◽  
External Stimuli

1. The locust jump is triggered by a sudden inhibition of activity in hindleg flexor tibiae motoneurons following cocontraction of the hindleg flexor and extensor tibiae muscles. The main result of this investigation was the identification of two interneurons (one for each hindleg) that monosynaptically inhibit flexor tibiae motoneurons and whose properties are all consistent with them being the trigger interneurons for initiating a jump. 2. These interneurons receive strong excitatory input from many sensory modalities (visual, auditory, tactile, and proprioceptive). Because of their multimodal response characteristics, we designated them M-neurons. A particularly strong excitatory input to each M-neuron is from both descending contralateral movement detector (DCMD) interneurons. 3. The threshold for spike initiation in the M-neurons is high (approximately 14 mV). As a consequence, input from any one sensory modality alone rarely initiates action potentials. 4. Each M-neuron is depolarized by sensory input from leg proprioceptors. We propose that proprioceptive feedback during the cocontraction phase depolarizes the M-neurons to decrease their threshold, thus enabling extrinsic sensory stimuli to generate action potentials in both M-neurons and in so doing trigger a jump. The function of the proprioceptive gating of inhibitory transmission from the various sensory systems to the flexor motoneurons (via the M-neurons) is to ensure the development of a strong isometric contraction of the extensor tibiae muscle, and thus a powerful jump in response to external stimuli. 5. Insofar as the initiation of the locust jump depends on sensory convergence onto large identified interneurons, this behavior is similar to ballistic movements in some other animals such as the crayfish tail flip and the startle response in fish. The unique feature of the locust jump is that the trigger interneurons initiate the jump only after a preceding phase (cocontraction) has been accomplished.

Calculation-and-experimental estimation of the role of the frequency ratio in changing the endurance at two-frequency deformation modes

2019 ◽  
Vol 85 (1(I)) ◽  
pp. 64-71 ◽  
Author(s):  
M. M. Gadenin
Keyword(s):  
High Frequency ◽  
Experimental Studies ◽  
Low Frequency ◽  
Reduction Factor ◽  
Single Frequency ◽  
Cyclic Loads ◽  
Small Ratio ◽  
Harmonic Components ◽  
Deformation Modes

The cycle configuration at two-frequency loading regimes depends on the number of parameters including the absolute values of the frequencies and amplitudes of the low-frequency and high-frequency loads added during this mode, the ratio of their frequencies and amplitudes, as well as the phase shift between these harmonic components, the latter having a significant effect only with a small ratio of frequencies. Presence of such two-frequency regimes or service loading conditions for parts of machines and structures schematized by them can significantly reduce their endurance. Using the results of experimental studies of changes in the endurance of a two-frequency loading of specimens of cyclically stable, cyclically softened and cyclically hardened steels under rigid conditions we have shown that decrease in the endurance under the aforementioned conditions depends on the ratio of frequencies and amplitudes of operation low-frequency low-cycle and high-frequency vibration stresses, and, moreover, the higher the level of the ratios of amplitudes and frequencies of those stacked harmonic processes of loading the greater the effect. It is shown that estimation of such a decrease in the endurance compared to a single frequency loading equal in the total stress (strains) amplitudes can be carried out using an exponential expression coupling those endurances through a parameter (reduction factor) containing the ratio of frequencies and amplitudes of operation cyclic loads and characteristic of the material. The reduction is illustrated by a set of calculation-experimental curves on the corresponding diagrams for each of the considered types of materials and compared with the experimental data.

scholarly journals Intracellular Na+ Modulates Pacemaking Activity in Murine Sinoatrial Node Myocytes: An In Silico Analysis

2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Membrane Potential ◽  
In Silico ◽  
Sinoatrial Node ◽  
In Silico Analysis ◽  
Ankyrin B ◽  
Deficient Mice ◽  
Silico Analysis ◽  
Bursting Activity

Background: The mechanisms underlying dysfunction in the sinoatrial node (SAN), the heart’s primary pacemaker, are incompletely understood. Electrical and Ca2+-handling remodeling have been implicated in SAN dysfunction associated with heart failure, aging, and diabetes. Cardiomyocyte [Na+]i is also elevated in these diseases, where it contributes to arrhythmogenesis. Here, we sought to investigate the largely unexplored role of Na+ homeostasis in SAN pacemaking and test whether [Na+]i dysregulation may contribute to SAN dysfunction. Methods: We developed a dataset-specific computational model of the murine SAN myocyte and simulated alterations in the major processes of Na+ entry (Na+/Ca2+ exchanger, NCX) and removal (Na+/K+ ATPase, NKA). Results: We found that changes in intracellular Na+ homeostatic processes dynamically regulate SAN electrophysiology. Mild reductions in NKA and NCX function increase myocyte firing rate, whereas a stronger reduction causes bursting activity and loss of automaticity. These pathologic phenotypes mimic those observed experimentally in NCX- and ankyrin-B-deficient mice due to altered feedback between the Ca2+ and membrane potential clocks underlying SAN firing. Conclusions: Our study generates new testable predictions and insight linking Na+ homeostasis to Ca2+ handling and membrane potential dynamics in SAN myocytes that may advance our understanding of SAN (dys)function.

scholarly journals How Can We Manage Gallbladder Lesions by Transabdominal Ultrasound?

Diagnostics ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 784
Author(s):  
Shinji Okaniwa
Keyword(s):  
High Frequency ◽  
Layer Structure ◽  
Wall Layer ◽  
Pancreaticobiliary Maljunction ◽  
Doppler Imaging ◽  
Wall Thickening ◽  
Contrast Enhanced ◽  
Postural Changes ◽  
Venous Phase

The most important role of ultrasound (US) in the management of gallbladder (GB) lesions is to detect lesions earlier and differentiate them from GB carcinoma (GBC). To avoid overlooking lesions, postural changes and high-frequency transducers with magnified images should be employed. GB lesions are divided into polypoid lesions (GPLs) and wall thickening (GWT). For GPLs, classification into pedunculated and sessile types should be done first. This classification is useful not only for the differential diagnosis but also for the depth diagnosis, as pedunculated carcinomas are confined to the mucosa. Both rapid GB wall blood flow (GWBF) and the irregularity of color signal patterns on Doppler imaging, and heterogeneous enhancement in the venous phase on contrast-enhanced ultrasound (CEUS) suggest GBC. Since GWT occurs in various conditions, subdividing into diffuse and focal forms is important. Unlike diffuse GWT, focal GWT is specific for GB and has a higher incidence of GBC. The discontinuity and irregularity of the innermost hyperechoic layer and irregular or disrupted GB wall layer structure suggest GBC. Rapid GWBF is also useful for the diagnosis of wall-thickened type GBC and pancreaticobiliary maljunction. Detailed B-mode evaluation using high-frequency transducers, combined with Doppler imaging and CEUS, enables a more accurate diagnosis.

Effect of low chloride on relaxation in hamster diaphragm muscle

1986 ◽  
Vol 61 (1) ◽  
pp. 180-184 ◽  
Author(s):  
S. A. Esau ◽  
N. Sperelakis
Keyword(s):  
Membrane Potential ◽  
Muscle Fatigue ◽  
Time Constant ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Krebs Solution ◽  
Sarcolemmal Membrane ◽  
Cl Conductance

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.

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