scholarly journals Individual excitatory post-synaptic potentials due to muscle spindle Ia afferents in cat triceps surae motoneurones.

1981 ◽  
Vol 312 (1) ◽  
pp. 455-470 ◽  
Author(s):  
P J Harrison ◽  
A Taylor
1993 ◽  
Vol 70 (4) ◽  
pp. 1460-1468 ◽  
Author(s):  
R. K. Powers ◽  
F. R. Robinson ◽  
M. A. Konodi ◽  
M. D. Binder

1. We evoked steady-state synaptic potentials in triceps surae motoneurons of the cat by stimulating the hindlimb projection area of the contralateral magnocellular red nucleus at 200 Hz. We measured the effective synaptic currents (IN) underlying the synaptic potentials using a modified voltage-clamp technique. We also determined the effect of the rubrospinal input on the discharge rate of some of the motoneurons by inducing repetitive discharge with long injected current pulses during which the red nucleus stimulation was repeated. 2. At motoneuron resting potential, the distribution of IN from the red nucleus within the triceps surae pools was qualitatively similar to the distribution of synaptic potentials: 86% of the putative type F motoneurons received a net depolarizing IN from the red nucleus stimulation, whereas only 38% of the putative type S units did so. The mean values of IN were significantly different in the two groups [+4.1 +/- 5.0 nA (SD) for putative type F and -1.6 +/- 3.1 nA for putative type S]. 3. However, when the values of IN at threshold for repetitive firing were estimated, the distribution of IN from the red nucleus was quite different. At threshold, all of the putative type S units received hyperpolarizing IN but so did nearly half of the putative type F units. 4. As would be expected from the wide range of IN at threshold (-20 to +12 nA), the red nucleus input produced dramatically different effects on the discharge of different motoneurons.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 64 (5) ◽  
pp. 1380-1389 ◽  
Author(s):  
D. Zytnicki ◽  
J. Lafleur ◽  
G. Horcholle-Bossavit ◽  
F. Lamy ◽  
L. Jami

1. Triceps surae and plantaris (Pl) motoneurons were recorded intracellularly in chloralose or pentobarbital sodium (Nembutal)-anesthetized cats during unfused tetanic contractions of gastrocnemius medialis muscle (GM) produced by stimulating either a cut branch of the GM nerve or the muscle directly. 2. In alpha-motoneurons, during a series of GM twitches at 10/s, contraction-induced inhibitory potentials, probably the result of input from Golgi tendon organs (autogenetic inhibition), rapidly subsided before the end of the series. In contrast, excitatory potentials, probably the result of the activation of spindle primary endings during relaxation from contraction, persisted. 3. In gastrocnemius lateralis-soleus (GL-S) and Pl motoneurons lacking an excitatory connection with Ia afferents from GM, the sustained contraction of this muscle also elicited a declining inhibition. Rapid reduction of contraction-induced autogenetic inhibition was also observed in homonymous gamma-motoneurons. During unfused tetanic contractions lasting 0.5-4s, inhibitory potentials quickly subsided, but an abrupt increase in contractile force elicited a new series of decreasing inhibitory potentials. 4. The assumption that the inhibition induced by GM unfused tetanic contractions was due to activation of homonymous Ib afferents was supported by observations of the effects of electrical stimulation of the GM nerve. In Pl motoneurons lacking an excitatory connection with Ia afferents from GM, repetitive trains applied to the GM nerve, at a strength just above threshold for group I fibers, elicited rapidly declining inhibitory potentials similar to those produced by GM contraction. It was verified that during such stimulation, the amplitude of the group I afferent volleys did not decrease. 5. Reduction of contraction-induced Ib inhibition during sustained GM contraction was still present after a low spinalization of the preparation. As GM tendon organ discharges were verified to persist throughout prolonged contractions, the observed decline of autogenetic inhibition is likely to depend on a spinal mechanism, possibly involving presynaptic inhibition of Ib afferents and/or mutual inhibition of Ib-inhibitory interneurons.


2008 ◽  
Vol 43 (1) ◽  
pp. 29-36 ◽  
Author(s):  
J. Troy Blackburn ◽  
Darin A. Padua ◽  
Kevin M. Guskiewicz

Abstract Context: Greater musculotendinous stiffness may enhance spinal stretch reflex sensitivity by improving mechanical coupling of the muscle spindle and the stretch stimulus. This heightened sensitivity would correspond with a shorter latency and higher-amplitude reflex response, potentially enhancing joint stability. Objective: To compare spinal stretch reflex latency and amplitude across groups that differed in musculotendinous stiffness. Design: Static group comparisons. Setting: Research laboratory. Patients or Other Participants: Forty physically active individuals (20 men, 20 women). Intervention(s): We verified a sex difference in musculotendinous stiffness and compared spinal stretch reflex latency and amplitude in high-stiffness (men) and low-stiffness (women) groups. We also evaluated relationships between musculotendinous stiffness and spinal stretch reflex latency and amplitude, respectively. Main Outcome Measure(s): Triceps surae musculotendinous stiffness and soleus spinal stretch reflex latency and amplitude were assessed at 30% of a maximal voluntary isometric plantar-flexion contraction. Results: The high-stiffness group demonstrated significantly greater stiffness (137.41 ± 26.99 N/cm) than the low-stiffness group did (91.06 ± 20.10 N/cm). However, reflex latency (high stiffness = 50.11 ± 2.07 milliseconds, low stiffness = 48.26 ± 2.40 milliseconds) and amplitude (high stiffness = 0.28% ± 0.12% maximum motor response, low stiffness = 0.31% ± 0.16% maximum motor response) did not differ significantly across stiffness groups. Neither reflex latency (r = .053, P = .746) nor amplitude (r = .073, P = .653) was related significantly to musculotendinous stiffness. Conclusions: A moderate level of pretension (eg, 30%) likely eliminates series elastic slack; thus, a greater change in force per unit-of-length change (ie, heightened stiffness) would have minimal effects on coupling of the muscle spindle and the stretch stimulus and, therefore, on spinal stretch reflex sensitivity. It appears unlikely that differences in musculotendinous stiffness influenced spinal stretch reflex sensitivity when initiated from a moderate level of pretension. Consequently, differences in musculotendinous stiffness did not appear to influence dynamic joint stability with respect to reflexive neuromuscular control.


2018 ◽  
Vol 120 (5) ◽  
pp. 2484-2497 ◽  
Author(s):  
William P. Mayer ◽  
Andrew J. Murray ◽  
Susan Brenner-Morton ◽  
Thomas M. Jessell ◽  
Warren G. Tourtellotte ◽  
...  

Terrestrial animals increase their walking speed by increasing the activity of the extensor muscles. However, the mechanism underlying how this speed-dependent amplitude modulation is achieved remains obscure. Previous studies have shown that group Ib afferent feedback from Golgi tendon organs that signal force is one of the major regulators of the strength of muscle activity during walking in cats and humans. In contrast, the contribution of group Ia/II afferent feedback from muscle spindle stretch receptors that signal angular displacement of leg joints is unclear. Some studies indicate that group II afferent feedback may be important for amplitude regulation in humans, but the role of muscle spindle feedback in regulation of muscle activity strength in quadrupedal animals is very poorly understood. To examine the role of feedback from muscle spindles, we combined in vivo electrophysiology and motion analysis with mouse genetics and gene delivery with adeno-associated virus. We provide evidence that proprioceptive sensory feedback from muscle spindles is important for the regulation of the muscle activity strength and speed-dependent amplitude modulation. Furthermore, our data suggest that feedback from the muscle spindles of the ankle extensor muscles, the triceps surae, is the main source for this mechanism. In contrast, muscle spindle feedback from the knee extensor muscles, the quadriceps femoris, has no influence on speed-dependent amplitude modulation. We provide evidence that proprioceptive feedback from ankle extensor muscles is critical for regulating muscle activity strength as gait speed increases. NEW & NOTEWORTHY Animals upregulate the activity of extensor muscles to increase their walking speed, but the mechanism behind this is not known. We show that this speed-dependent amplitude modulation requires proprioceptive sensory feedback from muscle spindles of ankle extensor muscle. In the absence of muscle spindle feedback, animals cannot walk at higher speeds as they can when muscle spindle feedback is present.


1991 ◽  
Vol 65 (4) ◽  
pp. 914-926 ◽  
Author(s):  
J. P. Gossard ◽  
J. M. Cabelguen ◽  
S. Rossignol

1. Presynaptic activity of identified primary afferents from flexor, extensor, and bifunctional hindlimb muscles was studied with intra-axonal recordings during fictive locomotion. Fictive locomotion appeared spontaneously in decorticate cats (n = 9), with stimulation of the mesencephalic locomotor region (n = 4), and in spinal cats injected with clonidine or nialamide and L-DOPA (n = 4). Representative flexor and extensor muscle nerves, recorded to monitor the locomotor pattern and dorsal rootlets of the sixth and seventh lumbar segments, were recorded simultaneously to monitor dorsal root potentials (DRPs). 2. From responses to muscle stretches and, in some instances, twitch contractions of the parent muscle, 75% of the single units examined were putatively identified as spindle afferents (40/53). On the basis of conduction velocity and stimulation threshold, 73% of these were further classified as group I fibers (29/40), the rest as group II fibers. 3. All units (n = 53 with resting potential more negative than -45 mV) showed fluctuations of their membrane potential (up to 1.5 mV) at the rhythm of the fictive locomotion. Subsequent averaging of these fluctuations over several cycles revealed that 89% of all units displayed a predominant wave of depolarization during the flexor phase, followed by a trough of repolarization. In 79% of the units, there was also a second, usually smaller, depolarization during the extensor phase. The relative size of each wave of depolarization could vary with different episodes of fictive locomotion in the same unit and among various afferents from the same muscle in the same experiment. 4. The firing frequency of some afferents from the ankle flexor tibialis anterior (5/16) and the bifunctional muscle posterior biceps-semitendinosus (4/15) was phasically modulated along the fictive step cycle. The maximum frequency always occurred during the flexor phase, i.e., during the largest depolarization of the unit. Because of the absence of phasic sensory input in the curarized animal, we assume that the phasic discharges were generated within the spinal cord and antidromically propagated. Phasic firing was never encountered in afferents from extensor muscles such as triceps surae (0/15) and vastus lateralis (0/4). 5. The results demonstrate that the pattern of rhythmic depolarization accompanying fictive locomotion is similar for the majority of flexor, extensor, and bifunctional group I (and possibly group II) muscle spindle primary afferents. They further indicate that there is a specific phasic modulation of antidromic firing for some flexor and bifunctional muscle spindle afferents.(ABSTRACT TRUNCATED AT 400 WORDS)


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