Endogenous Tachykinin Release Contributes to the Locomotor Activity in Lamprey

2007 ◽  
Vol 97 (5) ◽  
pp. 3331-3339 ◽  
Author(s):  
Carolina Thörn Pérez ◽  
Russell H. Hill ◽  
Sten Grillner
Keyword(s):  
Spinal Cord ◽  
Steady State ◽  
Locomotor Activity ◽  
Initial Period ◽  
Burst Frequency ◽  
Ongoing Activity ◽  
Initial Burst ◽  
Tachykinin Receptor ◽  
Spinal Network ◽  
Endogenous Release

Tachykinins are present in lamprey spinal cord. The goal of this study was to investigate whether an endogenous release of tachykinins contributes to the activity of the spinal network generating locomotor activity. The locomotor network of the isolated lamprey spinal cord was activated by bath-applied N-methyl-d-aspartate (NMDA) and the efferent activity recorded from the ventral roots. When spantide II, a tachykinin receptor antagonist, was bath-applied after reaching a steady-state burst frequency (>2 h), it significantly lowered the burst rate compared with control pieces from the same animal. In addition, the time to reach the steady-state burst frequency (>2 h) was lengthened in spantide II. These data indicate that an endogenous tachykinin release contributes to the ongoing activity of the locomotor network by modulating the glutamate–glycine neuronal network responsible for the locomotor pattern. We also explored the effects of a 10-min exogenous application of substance P (1 μM), a tachykinin, and showed that its effect on the burst rate depended on the initial NMDA induced burst frequency. At low initial burst rates (∼0.5 Hz), tachykinins caused a marked further slowing to 0.1 Hz, whereas at higher initial burst rates, it instead caused an enhanced burst rate as previously reported, and in addition, a slower modulation (0.1 Hz) of the amplitude of the motor activity. These effects occurred during an initial period of ∼1 h, whereas a modest long-lasting increase of the burst rate remained after >2 h.

scholarly journals Rostrocaudal Distribution of the C-Fos-Immunopositive Spinal Network Defined by Muscle Activity during Locomotion

2021 ◽  
Vol 11 (1) ◽  
pp. 69
Author(s):  
Natalia Merkulyeva ◽  
Vsevolod Lyakhovetskii ◽  
Aleksandr Veshchitskii ◽  
Oleg Gorskii ◽  
Pavel Musienko
Keyword(s):  
Spinal Cord ◽  
Locomotor Activity ◽  
Control Systems ◽  
Muscle Activity ◽  
Knee Extensors ◽  
Emg Activity ◽  
Lumbosacral Spinal Cord ◽  
Adductor Muscles ◽  
Spinal Network ◽  
Hip Flexor

The optimization of multisystem neurorehabilitation protocols including electrical spinal cord stimulation and multi-directional tasks training require understanding of underlying circuits mechanisms and distribution of the neuronal network over the spinal cord. In this study we compared the locomotor activity during forward and backward stepping in eighteen adult decerebrated cats. Interneuronal spinal networks responsible for forward and backward stepping were visualized using the C-Fos technique. A bi-modal rostrocaudal distribution of C-Fos-immunopositive neurons over the lumbosacral spinal cord (peaks in the L4/L5 and L6/S1 segments) was revealed. These patterns were compared with motoneuronal pools using Vanderhorst and Holstege scheme; the location of the first peak was correspondent to the motoneurons of the hip flexors and knee extensors, an inter-peak drop was presumably attributed to the motoneurons controlling the adductor muscles. Both were better expressed in cats stepping forward and in parallel, electromyographic (EMG) activity of the hip flexor and knee extensors was higher, while EMG activity of the adductor was lower, during this locomotor mode. On the basis of the present data, which showed greater activity of the adductor muscles and the attributed interneuronal spinal network during backward stepping and according with data about greater demands on postural control systems during backward locomotion, we suppose that the locomotor networks for movements in opposite directions are at least partially different.

The spinal GABA system modulates burst frequency and intersegmental coordination in the lamprey: differential effects of GABAA and GABAB receptors

1993 ◽  
Vol 69 (3) ◽  
pp. 647-657 ◽  
Author(s):  
J. Tegner ◽  
T. Matsushima ◽  
A. el Manira ◽  
S. Grillner
Keyword(s):  
Spinal Cord ◽  
Locomotor Activity ◽  
Gabaa Receptor ◽  
Gabab Receptor ◽  
Gaba Uptake ◽  
Phase Lag ◽  
Fictive Locomotion ◽  
Burst Frequency ◽  
Intersegmental Coordination ◽  
Burst Pattern

1. The effect of spinal GABAergic neurons on the segmental neuronal network generating locomotion has been analyzed in the lamprey spinal cord in vitro. It is shown that gamma-aminobutyric acid (GABA)A- and GABAB-mediated effects influence the burst frequency and the intersegmental coordination and that the GABA system is active during normal locomotor activity. 2. Fictive locomotor activity was induced by superfusing the spinal cord with a Ringer solution containing N-methyl-D-aspartate (NMDA, 150 microM). The efferent locomotor activity was recorded by suction electrodes from the ventral roots or intracellularly from interneurons or motoneurons. If a GABA uptake blocker was added to the perfusate, the burst rate decreased. This effect was counteracted by GABAB receptor blockade by phaclofen or 2-(OH)-saclofen. If instead a GABAB receptor agonist (baclofen) was added during fictive locomotion, a depression of the burst rate occurred. It was concluded that a GABAB receptor activation due to an endogenous release of GABA caused a depression of the burst activity with a maintained well-coordinated locomotor activity. 3. If a GABAA receptor antagonist (bicuculline) is applied during fictive locomotion elicited by NMDA, a certain increase of the burst rate occurred. Conversely, if a selective GABAA agonist (muscimol) was administered, the burst rate decreased. Similarly, if the GABAA receptor activity was potentiated by activation of a benzodiazepine site by diazepam, the burst rate was reduced. If, however the GABAergic effect was first enhanced by an uptake blocker (nipecotic acid), an administration of a GABAA antagonist (bicuculline) increased the burst rate, but in addition, the burst pattern became less regular with recurrent shorter periods without clear reciprocal burst activity. The GABAA receptor activity appears important for the rate control and for permitting a regular burst pattern. 4. The intersegmental coordination in the lamprey is characterized by a rostrocaudal constant phase lag of approximately 1% of the cycle duration between the activation of consecutive segments during forward swimming. This rostrocaudal phase lag can be reversed during backward swimming, which can be induced also experimentally in the isolated spinal cord by providing a higher excitability to the caudal segments. In a split-bath configuration, a GABA uptake blocker or a GABAB agonist was administered to the rostral part of the spinal cord, which caused a reversal of the phase lag as during backward swimming. If GABAA receptors were blocked under similar conditions, the intersegmental coordination became irregular. It is concluded that an increased GABA activity in a spinal cord region can modify the intersegmental coordination.(ABSTRACT TRUNCATED AT 400 WORDS)

The Spinal GABAergic System Is a Strong Modulator of Burst Frequency in the Lamprey Locomotor Network

2004 ◽  
Vol 92 (4) ◽  
pp. 2357-2367 ◽  
Author(s):  
David E. Schmitt ◽  
Russell H. Hill ◽  
Sten Grillner
Keyword(s):  
Spinal Cord ◽  
Detailed Analysis ◽  
Gabaergic Neurons ◽  
Ventral Root ◽  
Gabaergic System ◽  
Frequency Regulation ◽  
Fictive Locomotion ◽  
Burst Frequency ◽  
Pronounced Increase ◽  
Spinal Network

The spinal network coordinating locomotion is comprised of a core of glutamate and glycine interneurons. This network is modulated by several transmitter systems including spinal GABA interneurons. The purpose of this study is to explore the contribution of GABAergic neurons to the regulation of locomotor burst frequency in the lamprey model. Using gabazine, a competitive GABAA antagonist more specific than bicuculline, the goal was to provide a detailed analysis of the influence of an endogenous activation of GABAA receptors on fictive locomotion, as well as their possible interaction with GABAB and involvement of GABAC receptors. During N-methyl-d-aspartate (NMDA)-induced fictive locomotion (ventral root recordings in the isolated spinal cord), gabazine (0.1–100 μM) significantly increased the burst rate up to twofold, without changes in regularity or “burst quality.” Gabazine had a proportionately greater effect at higher initial burst rates. Picrotoxin (1–7.5 μM), a less selective GABAA antagonist, also produced a pronounced increase in frequency, but at higher concentrations, the rhythm deteriorated, likely due to the unspecific effects on glycine receptors. The selective GABAB antagonist CGP55845 also increased the frequency, and this effect was markedly enhanced when combined with the GABAA antagonist gabazine. The GABAC antagonist (1,2,5,6-tetrahydropyridine-4-yl)methylphosphinic acid (TPMPA) had no effect on locomotor bursting. Thus the spinal GABA system does play a prominent role in burst frequency regulation in that it reduces the burst frequency by ≤50%, presumably due to presynaptic and soma-dendritic effects documented previously. It is not required for burst generation, but acts as a powerful modulator.

scholarly journals Modulation of spinal motor networks by astrocyte-derived adenosine is dependent on D1-like dopamine receptor signaling

2018 ◽  
Vol 120 (3) ◽  
pp. 998-1009 ◽  
Author(s):  
David Acton ◽  
Matthew J. Broadhead ◽  
Gareth B. Miles
Keyword(s):  
Spinal Cord ◽  
Protein Kinase ◽  
Dopamine Receptor ◽  
Kinase Inhibitor ◽  
Ventral Horn ◽  
Skf 38393 ◽  
Network Activity ◽  
Related Activity ◽  
Burst Frequency ◽  
Spinal Motor

Astrocytes modulate many neuronal networks, including spinal networks responsible for the generation of locomotor behavior. Astrocytic modulation of spinal motor circuits involves release of ATP from astrocytes, hydrolysis of ATP to adenosine, and subsequent activation of neuronal A1 adenosine receptors (A1Rs). The net effect of this pathway is a reduction in the frequency of locomotor-related activity. Recently, it was proposed that A1Rs modulate burst frequency by blocking the D1-like dopamine receptor (D1LR) signaling pathway; however, adenosine also modulates ventral horn circuits by dopamine-independent pathways. Here, we demonstrate that adenosine produced upon astrocytic stimulation modulates locomotor-related activity by counteracting the excitatory effects of D1LR signaling and does not act by previously described dopamine-independent pathways. In spinal cord preparations from postnatal mice, a D1LR agonist, SKF 38393, increased the frequency of locomotor-related bursting induced by 5-hydroxytryptamine and N-methyl-d-aspartate. Bath-applied adenosine reduced burst frequency only in the presence of SKF 38393, as did adenosine produced after activation of protease-activated receptor-1 to stimulate astrocytes. Furthermore, the A1R antagonist 8-cyclopentyl-1,3-dipropylxanthine enhanced burst frequency only in the presence of SKF 38393, indicating that endogenous adenosine produced by astrocytes during network activity also acts by modulating D1LR signaling. Finally, modulation of bursting by adenosine released upon stimulation of astrocytes was blocked by protein kinase inhibitor-(14–22) amide, a protein kinase A (PKA) inhibitor, consistent with A1R-mediated antagonism of the D1LR/adenylyl cyclase/PKA pathway. Together, these findings support a novel, astrocytic mechanism of metamodulation within the mammalian spinal cord, highlighting the complexity of the molecular interactions that specify motor output. NEW & NOTEWORTHY Astrocytes within the spinal cord produce adenosine during ongoing locomotor-related activity or when experimentally stimulated. Here, we show that adenosine derived from astrocytes acts at A1 receptors to inhibit a pathway by which D1-like receptors enhance the frequency of locomotor-related bursting. These data support a novel form of metamodulation within the mammalian spinal cord, enhancing our understanding of neuron-astrocyte interactions and their importance in shaping network activity.

Evidence for at Least Two Tachykinin Receptor Subtypes in the Mammalian Spinal Cord

1987 ◽  
pp. 328-330 ◽  
Author(s):  
M. Wienrich ◽  
I. Lues ◽  
B. E. B. Sandberg ◽  
J. Harting
Keyword(s):  
Spinal Cord ◽  
Receptor Subtypes ◽  
Tachykinin Receptor

scholarly journals High-frequency epidural stimulation across the respiratory cycle evokes phrenic short-term potentiation after incomplete cervical spinal cord injury

2017 ◽  
Vol 118 (4) ◽  
pp. 2344-2357 ◽  
Author(s):  
Elisa J. Gonzalez-Rothi ◽  
Kristi A. Streeter ◽  
Marie H. Hanna ◽  
Anna C. Stamas ◽  
Paul J. Reier ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
High Frequency ◽  
Muscle Activation ◽  
Cervical Spinal Cord ◽  
Cervical Spinal Cord Injury ◽  
Burst Frequency ◽  
Epidural Stimulation ◽  
Term Potentiation ◽  
Cord Injury

C2 spinal hemilesion (C2Hx) paralyzes the ipsilateral diaphragm, but recovery is possible through activation of “crossed spinal” synaptic inputs to ipsilateral phrenic motoneurons. We tested the hypothesis that high-frequency epidural stimulation (HF-ES) would potentiate ipsilateral phrenic output after subacute and chronic C2Hx. HF-ES (300 Hz) was applied to the ventrolateral C4 or T2 spinal cord ipsilateral to C2Hx in anesthetized and mechanically ventilated adult rats. Stimulus duration was 60 s, and currents ranged from 100 to 1,000 µA. Bilateral phrenic nerve activity and ipsilateral hypoglossal (XII) nerve activity were recorded before and after HF-ES. Higher T2 stimulus currents potentiated ipsilateral phasic inspiratory activity at both 2 and 12 wk post-C2Hx, whereas higher stimulus currents delivered at C4 potentiated ipsilateral phasic phrenic activity only at 12 wk ( P = 0.028). Meanwhile, tonic output in the ipsilateral phrenic nerve reached 500% of baseline values at the high currents with no difference between 2 and 12 wk. HF-ES did not trigger inspiratory burst-frequency changes. Similar responses occurred following T2 HF-ES. Increases in contralateral phrenic and XII nerve output were induced by C4 and T2 HF-ES at higher currents, but the relative magnitude of these changes was small compared with the ipsilateral phrenic response. We conclude that following incomplete cervical spinal cord injury, HF-ES of the ventrolateral midcervical or thoracic spinal cord can potentiate efferent phrenic motor output with little impact on inspiratory burst frequency. However, the substantial increases in tonic output indicate that the uninterrupted 60-s stimulation paradigm used is unlikely to be useful for respiratory muscle activation after spinal injury. NEW & NOTEWORTHY Previous studies reported that high-frequency epidural stimulation (HF-ES) activates the diaphragm following acute spinal transection. This study examined HF-ES and phrenic motor output following subacute and chronic incomplete cervical spinal cord injury. Short-term potentiation of phrenic bursting following HF-ES illustrates the potential for spinal stimulation to induce respiratory neuroplasticity. Increased tonic phrenic output indicates that alternatives to the continuous stimulation paradigm used in this study will be required for respiratory muscle activation after spinal cord injury.

Dissolution behaviour of soil kaolinites in acidic solutions

Clay Minerals ◽  
2013 ◽  
Vol 48 (3) ◽  
pp. 447-461 ◽  
Author(s):  
K. Khawmee ◽  
A. Suddhiprakarn ◽  
I. Kheoruenromne ◽  
I. Bibi ◽  
B. Singh
Keyword(s):  
Steady State ◽  
Dissolution Rate ◽  
Initial Period ◽  
Reference Sample ◽  
Stoichiometric Ratio ◽  
Solution Ph ◽  
Weathered Soils ◽  
Dissolution Behaviour ◽  
Georgia Kaolinite ◽  
Highly Weathered Soils

AbstractHighly weathered soils of the tropics and subtropics commonly have kaolinitedominated clay fractions. Under acidic conditions prevailing in these soils kaolinite dissolution occurs, contributing to the high levels of soluble Al in these soils. This study evaluates the dissolution behaviour of kaolinites from subsurface horizons of highly weathered soils from Thailand, along with a soil kaolinite from Western Australia (WA kaolinite) and Georgia kaolinite (KGa-2). Kaolinite-dominated clay fractions were isolated from soils by sedimentation and chemically treated to remove iron oxides. The dissolution rate of kaolinites was measured in 0.01 M NaCl as a function of pH (1–4; HCl) at 25±1°C using non-stirred flow-through reactors. Kaolinite dissolution rates were calculated from the release of Al and Si at the steady state. In most of the experiments and at all pH values, the release of both Si and Al underwent a distinct transition from an initial period of rapid release to significantly slower release at the steady state. Aluminium and Si concentrations at the steady state were higher for soil kaolinites than the reference sample (KGa-2). At the steady state the dissolution of all kaolinites was stoichiometric except for the soil kaolinites from Thailand at pH 4, where the Al/Si ratio was well below the stoichiometric ratio. Log dissolution rate (RSi) of soil kaolinites ranged from –13.75 to –12.51, with the dissolution rate increasing significantly with decreasing solution pH. However, the dissolution rate was similar or pH independent between pH 2 and 3, which is the pH range of the point of zero net charge (PZNC) for both soil and reference kaolinites. The dissolution rate of soil kaolinite was significantly higher than the KGa-2 sample at pH < 3. The results obtained on kaolinite samples from highly weathered soils show that in highly acidic systems kaolinite is a source of soluble Al. Soil kaolinites with poorly ordered small crystals dissolve faster than better crystalline reference kaolinite (KGa-2) with larger crystals.

The Translesional Spinal Network and Its Reorganization after Spinal Cord Injury

2020 ◽  
pp. 107385842096627 ◽  
Author(s):  
Petr Krupa ◽  
Ahad M. Siddiqui ◽  
Peter J. Grahn ◽  
Riazul Islam ◽  
Bingkun K. Chen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Clinical Research ◽  
Functional Recovery ◽  
Motor Training ◽  
Motor Functions ◽  
Sensory Inputs ◽  
Cord Injury ◽  
Spinal Network ◽  
Motor Signals

Evidence from preclinical and clinical research suggest that neuromodulation technologies can facilitate the sublesional spinal networks, isolated from supraspinal commands after spinal cord injury (SCI), by reestablishing the levels of excitability and enabling descending motor signals via residual connections. Herein, we evaluate available evidence that sublesional and supralesional spinal circuits could form a translesional spinal network after SCI. We further discuss evidence of translesional network reorganization after SCI in the presence of sensory inputs during motor training. In this review, we evaluate potential mechanisms that underlie translesional circuitry reorganization during neuromodulation and rehabilitation in order to enable motor functions after SCI. We discuss the potential of neuromodulation technologies to engage various components that comprise the translesional network, their functional recovery after SCI, and the implications of the concept of translesional network in development of future neuromodulation, rehabilitation, and neuroprosthetics technologies.

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