Last-order interneurones controlling activity of elbow extensor motoneurones during forelimb fictive locomotion in the cat

1991 ◽  
Vol 121 (1-2) ◽  
pp. 37-39 ◽  
Author(s):  
Yoichiro Ichikawa ◽  
Yumiko Terakado ◽  
Takashi Yamaguchi
Keyword(s):  
Fictive Locomotion ◽  
Extensor Motoneurones ◽  
Elbow Extensor

scholarly journals Disynaptic group I excitation of synergist ankle extensor motoneurones during fictive locomotion in the cat.

1995 ◽  
Vol 487 (2) ◽  
pp. 527-539 ◽  
Author(s):  
D A McCrea ◽  
S J Shefchyk ◽  
M J Stephens ◽  
K G Pearson
Keyword(s):  
Fictive Locomotion ◽  
Group I ◽  
Extensor Motoneurones

Critical Points in the Forelimb Fictive Locomotor Cycle and Motor Coordination: Evidence From the Effects of Tonic Proprioceptive Perturbations in the Cat

2004 ◽  
Vol 92 (3) ◽  
pp. 1329-1341 ◽  
Author(s):  
Philippe Saltiel ◽  
Serge Rossignol
Keyword(s):  
Critical Points ◽  
Motor Coordination ◽  
Morphological Characteristics ◽  
Neural Mechanisms ◽  
Fictive Locomotion ◽  
Abrupt Increase ◽  
Cycle Structure ◽  
Flexion Extension ◽  
Muscle Nerve ◽  
Elbow Extensor

During locomotion, the limbs of one girdle must remain coordinated in different conditions. To understand the neural mechanisms underlying such coordination, tonic protraction/ retraction of one shoulder or tonic flexion/extension of one elbow was applied during fictive locomotion in high decerebrate and paralyzed cats. We studied bilateral changes in the timing and amplitude characteristics of electroneurographic (ENG) muscle nerve bursts of cleidobrachialis (ClB, elbow flexor and shoulder protractor) and the two heads of triceps (long, TriLo, elbow extensor and shoulder retractor and lateral, TriLa, elbow extensor). Perturbations induced bilateral changes in amplitude and timing of ENG bursts that were anchored on certain critical points in the cycle. These critical points could correspond to morphological characteristics within the bursts or to bilateral onsets or offsets of ENG bursts. For instance, in response to shoulder and elbow perturbations, burst changes occur in relation to a fixed point, labeled point C, occurring at about mid-extensor burst and corresponding to a simultaneous abrupt increase in TriLa amplitude and a decrease in amplitude of contralateral ClB. At a point labeled B, corresponding to about mid-flexor burst, ClB amplitude increases above control with elbow extension or starts decreasing with shoulder protraction. Although cycle reorganization is specific for each type of tonic perturbation, a common feature is that the changes in burst duration are achieved through discrete shifts between consecutive critical points. It is postulated that coordination may be based on a discrete temporal cycle structure along which critical points delimiting burst components are shifted.

Tonic and phasic synaptic input to spinal cord motoneurons during fictive locomotion in frog embryos

1982 ◽  
Vol 48 (6) ◽  
pp. 1279-1288 ◽  
Author(s):  
S. R. Soffe ◽  
A. Roberts
Keyword(s):  
Spinal Cord ◽  
Synaptic Input ◽  
Inhibitory Interneurons ◽  
Fictive Locomotion ◽  
Inhibitory Pathway ◽  
Intact Side ◽  
Rhythmic Motor ◽  
Postsynaptic Potential ◽  
Late Developmental Stage ◽  
Motor Root

1. In curarized, late developmental stage Xenopus embryos, episodes of rhythmic motor root discharge, termed fictive swimming (17), may be evoked by touch or by dimming the lights, as in unparalyzed animals. Motoneurons are tonically depolarized throughout each episode, are phasically excited to fire 1 spike per cycle, and receive a midcycle inhibitory postsynaptic potential (IPSP) in phase with motor root activity on the opposite side. 2. Rostral hemisection of the spinal cord abolishes motor root discharge on the operated side caudal to the cut but leaves activity on the intact side unaffected. In motoneurons, the tonic depolarization is abolished on the hemisected side but is still present on the intact side. This is evidence that the tonic depolarization is a descending drive. 3. Midcycle IPSPs normally seen in motoneurons during fictive swimming are abolished by rostral hemisection of the opposite side of the cord but are still recorded on the cut side. The simplest conclusion is that the inhibitory interneurons responsible lie on the opposite side of the spinal cord to the motoneurons they inhibit, and so represent a reciprocal inhibitory pathway. 4. The phasic excitatory postsynaptic potentials (EPSPs), which drive motoneuron spikes during swimming, are still present on the intact side of a rostrally hemisected cord but are abolished on the operated side. We conclude that the excitatory interneurons responsible lie on the same side of the cord as the motoneurons they excite.

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)

Inhibitory synaptic input to edge cells during fictive locomotion

1987 ◽  
Vol 409 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Simon Alford ◽  
Thelma L. Williams
Keyword(s):  
Synaptic Input ◽  
Fictive Locomotion ◽  
Inhibitory Synaptic Input

5-HT Prolongs Ventral Root Bursting Via Presynaptic Inhibition of Synaptic Activity During Fictive Locomotion in Lamprey

2005 ◽  
Vol 93 (2) ◽  
pp. 980-988 ◽  
Author(s):  
Eric J. Schwartz ◽  
Tatyana Gerachshenko ◽  
Simon Alford
Keyword(s):  
Synaptic Transmission ◽  
Presynaptic Inhibition ◽  
Cellular Level ◽  
Ventral Horn ◽  
Pattern Generation ◽  
Ventral Root ◽  
Synaptic Activity ◽  
Fictive Locomotion ◽  
Cellular Mechanisms ◽  
Bath Application

Locomotor pattern generation is maintained by integration of the intrinsic properties of spinal central pattern generator (CPG) neurons in conjunction with synaptic activity of the neural network. In the lamprey, the spinal locomotor CPG is modulated by 5-HT. On a cellular level, 5-HT presynaptically inhibits synaptic transmission and postsynaptically inhibits a Ca2+-activated K+ current responsible for the slow afterhyperpolarization (sAHP) that follows action potentials in ventral horn neurons. To understand the contribution of these cellular mechanisms to the modulation of the spinal CPG, we have tested the effect of selective 5-HT analogues against fictive locomotion initiated by bath application of N-methyl-d-aspartate (NMDA). We found that the 5-HT1D agonist, L694-247, dramatically prolongs the frequency of ventral root bursting. Furthermore, we show that L694-247 presynaptically inhibits synaptic transmission without altering postsynaptic Ca2+ -activated K+ currents. We also confirm that 5-HT inhibits synaptic transmission at concentrations that modulate locomotion. To examine the mechanism by which selective presynaptic inhibition modulates the frequency of fictive locomotion, we performed voltage- and current-clamp recordings of CPG neurons during locomotion. Our results show that 5-HT decreases glutamatergic synaptic drive within the locomotor CPG during fictive locomotion. Thus we conclude that presynaptic inhibition of neurotransmitter release contributes to 5-HT–mediated modulation of locomotor activity.

Variability of Positioning Accuracy following a Maximum Isometric Contraction

1987 ◽  
Vol 64 (3) ◽  
pp. 759-764 ◽  
Author(s):  
Bruce R. Etnyre ◽  
Eva J. Lee ◽  
Hally B. W. Poindexter
Keyword(s):  
Isometric Contraction ◽  
Constant Error ◽  
Elbow Extension ◽  
Positioning Accuracy ◽  
Extensor Muscles ◽  
Delay Times ◽  
Contraction Times ◽  
The Subject ◽  
Experimental Trials ◽  
Elbow Extensor

The purpose of this study was to examine the effects of different contraction times and delay times prior to a positioning task. While blindfolded, each of 25 subjects learned to produce elbow-extension movements to a short and a long target using a kinesthesiometer. The subject then produced 30 trials without feedback to each target. These control trials were preceded by a foreperiod of 0-, 3-, or 6-sec. delay. The 60 experimental trials were identical to control trials except the subject isometrically contracted elbow extensor muscles for 3 or 6 sec. prior to each trial. Following each isometric contraction the subject delayed movement for 0, 3, or 6 sec. The 3-sec. and 6-sec. prepositioning contractions produced greater undershooting and variability than no prepositioning contractions, and the 0-sec. delay produced less constant error than either the 3- or 6-sec. delay. It was concluded that following isometric contraction, undershooting a target occurred and this effect did not dissipate within a 6-sec. period.

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