1,721,004 research outputs found
Role of Renshaw cells in amyotrophic lateral sclerosis
No full textAbstract
In this article the role of Renshaw cell involvement in experimental amyotrophic lateral sclerosis (ALS) is discussed, with an emphasis on the anatomy, physiology, and possible role in motor control of Renshaw cells. These cells are located in lamina VII of the spinal cord, are excited by motor axon collaterals, and inhibit homonymous and synergistic motoneurons in a negative-feedback fashion (recurrent inhibition). Early dysfunction and/or loss of Renshaw cells has been suggested to occur in experimental ALS, and the hypothesis has been put forward that this may be the event that makes motoneurons more susceptible to glutamatergic toxicity in ALS. However, Renshaw cell properties and connectivity-in particular, the lack of recurrent inhibition in the more distal muscles of the limbs where, on the contrary, initial wasting is prominent in human ALS-make it unlikely that impairment of Renshaw cells is a general feature of the human form of the disease.
PMID: 20082418 [PubMed - indexed for MEDLINE
More than at the Neuromuscular Synapse: Actions of Botulinum Neurotoxin A in the Central Nervous System
No full textA clinical maneuver to increase tremor differentiation between Parkinson disease and essential tremor
No full textEffect of chemically activated fine muscle afferents on spinal recurrent inhibition in humans
No full textOBJECTIVE:
To test the hypothesis that 'metabolites released during fatiguing muscle contractions excite group III-IV muscle nociceptive afferents, inhibiting homonymous motoneurones via Renshaw cells,' by recording changes in recurrent inhibition of soleus motoneurones when high-threshold, small-diameter afferents (group III-IV fibres) from the same muscle were tonically activated.
METHODS:
Experiments were performed in 7 healthy subjects at rest and during weak isometric voluntary contraction of the soleus muscle. Muscle nociceptive afferents were activated by local standardized injection of levo-ascorbic acid. Renshaw cells were orthodromically activated by a conditioning H reflex and the resulting recurrent inhibition of the soleus motoneurones was assessed by a subsequent test H reflex. An additional H reflex of the same size as the test reflex was used to assess motoneurone excitability.
RESULTS:
At rest, muscle nociceptive stimulation produced transient facilitation of both test H and reference H reflexes. Under weak voluntary contraction, muscle nociceptive stimulation produced long-lasting extra-inhibition and extra-facilitation of the test reflex and reference reflex respectively, the time course of which closely resembled that of the subjective muscle pain curve.
CONCLUSIONS:
Discharge of putative group III-IV muscle afferents facilitated homonymous recurrent inhibition. The filtering property of recurrent inhibition may contribute to limit motoneurone activity during muscle pain and/or adapt motoneurone firing rate to the modified contractile properties of motor units as muscle fatigue developed
Changes in Ia reciprocal inhibition from the peroneal nerve to the soleus alpha-motoneurons with different static body positions in man.
No full textExperiments were conducted in man to evaluate the changes in Ia inhibitory interneurons activated from the anterior tibial muscle and projecting to the soleus alpha-motoneurons in relation to different static body positions. Subjects were fixed to a tilting chair and the effects of body rotation were evaluated at 80 degrees (normal sitting position) and 40 degrees of backward inclination (head supine, nose-up). A test H-reflex was used to assess changes in excitability of the soleus alpha-motoneurons after a conditioning stimulus applied to the deep peroneal nerve. In 5 out of 6 subjects, we observed a significant increase in the reciprocal inhibition after backward inclination of the body (40 degrees) with respect to the control position (80 degrees). Such increase was attributed to facilitation of the Ia inhibitory interneurons projecting to the soleus motoneurons. We consider the possibility that the observed increment in reciprocal inhibition after backward inclination be sustained by variations of tonic vestibular activity
Evidence for Renshaw cell-motoneuron decoupling during tonic vestibular stimulation in man.
No full textThe influence of static head-body tilts in the sagittal plane on the activity of Renshaw cells coupled to the soleus extensor alpha-motoneurons was studied in eight human subjects. Head-body rotation was carried out using a tilting seat and its effect was evaluated at 80 degrees (normal sitting position) and at 40 degrees of backward inclination (nose-up). Renshaw cell activity was assessed through a specially designed method of paired H-reflexes first described by Bussel and Pierrot-Deseilligny. alpha-Motoneuron excitability was also independently studied by mapping a reference H-reflex amplitude as a function of static head-body displacements. In almost all subjects Renshaw cell activity was increased at 40 degrees backward inclination with respect to control values at 80 degrees. These changes were attributed to the tonic labyrinthine reflexes capable of decoupling Renshaw cell activity from their motoneurons when the body was tilted backward from the upright position. We discuss the hypothetical functional modalities of the recurrent inhibitory circuit during postural adjustments elicited by labyrinthine input
Depression of Renshaw recurrent inhibition by activation of corticospinal fibres in human upper and lower limb.
Full text link1. This study tested whether the recurrent inhibition of soleus and wrist flexor motoneurones could be modified by transcranial magnetic stimulation in human subjects. 2. Magnetic stimulation was given through a circular coil centred at the vertex. The intensity of the magnetic stimulus was subthreshold for evoking a motor response in the active soleus and wrist flexor muscles. The recurrent inhibition brought about by a conditioning H1 reflex discharge was estimated by a test H' reflex. The modifications of the recurrent inhibition after cortical stimulation were distinguished from the motoneuronal changes by comparing H' to a reference H reflex. 3. In the soleus motoneurones, the reference H reflex was inhibited at a minimum conditioning‐test interval of ‐2 ms (H reflex stimulus before magnetic stimulation). In contrast, the H' reflex was facilitated at minimum conditioning‐test intervals of +1 ms. In the wrist flexor motoneurones, both H' and reference H reflexes were facilitated. However, at lower cortical stimulus intensities, only the H' reflex was facilitated at minimum conditioning‐test intervals of +1 ms. 4. In both motoneurone pools, H' facilitation started 3‐4 ms later than the earliest changes in the reference H reflex. Also, the threshold of H' facilitation was lower than that of reference H reflex. 5. It is concluded that facilitation of the H' reflex is produced by corticospinal inhibition of Renshaw cells via a short interneuronal chain in both the upper and lower limb
Distribution of Ia effects onto human hand muscle motoneurones as revealed using an H reflex technique.
Full text link1. The possibility of eliciting H reflexes in relaxed hand muscles using a collision between the orthodromic impulses generated by magnetic cortical stimulation and the antidromic motor volley due to a supramaximal (SM) peripheral nerve stimulus was investigated in seven subjects. 2. Magnetic stimuli, applied through a circular coil (outer diameter, 13 cm) centred at the vertex, evoking EMG responses of 3-5 mV amplitude in the relaxed abductor digit minimi (ADM) muscle, and SM test stimuli to the ulnar nerve at the wrist producing a direct maximal motor response (Mmax) in the ADM muscle, were given either alone or combined. 3. In all subjects, combined cortical and SM ulnar stimulation produced a response after the Mmax with the latency of an H reflex evoked by the ulnar stimulus. This response occurred only within interstimulus intervals (1-20 ms) compatible with collision in the motor axons. The response behaved like an H reflex being time-locked to the SM ulnar stimulus, facilitated by voluntary activation of ADM muscle, depressed by vibration (4 s, 100 Hz) of ADM tendon and by a submotor-threshold ulnar nerve stimulus applied 50 and 80 ms before the combined stimulation, respectively. 4. In some subjects, it was also possible to distinguish an earlier response preceding the H reflex by 3 ms. Evidence is given that this response is probably of cortical origin. 5. Varying the intensity of magnetic stimulation resulted in a non-linear relationship between the H reflex size and the size of the cortical response. When the latter was between 5-25% of Mmax, H reflexes were small (2.5-7.5% of Mmax); with cortical responses between 25-50% of Mmax, there was a steep increase in H reflex amplitude (10-30% of Mmax). We suggest that this behaviour is due to an uneven distribution of Ia effects within the motoneurone pool
The H reflex recovery curve reinvestigated: low-intensity conditioning stimulation and nerve compression disclose differential effects of presumed group Ia fibres in man.
No full textThe recovery curve of the soleus H reflex, evoked by stimulation of the tibial nerve in the popliteal fossa, was studied by applying an electrical conditioning stimulus to the inferior soleus nerve. Under these conditions a long-latency facilitatory phase could be superimposed on a long-lasting inhibition, the excitability cycle being therefore similar to that obtained by means of a paired shock to the tibial nerve. In order to identify the afferent fibres responsible for the effects observed, various conditioning stimulus strengths and nerve compression were used. A low-intensity stimulus induced only a facilitatory phase, while the inhibition promptly ensued on increasing stimulus strength, which remained however subliminal for activation of group II fibres. During calf compression exerted by a sphygmomanometer cuff placed between the conditioning and test stimuli, the facilitatory effects disappeared within 10 to 15 min, and the inhibitory ones disappeared within 25 to 30 min from the onset of compression. Tonic voluntary contraction enhanced both the inhibition and the facilitation. In a subject with complete spinal section, both inhibitory and facilitatory phases could be demonstrated on low-intensity stimulation. The present data, and previous results of ours, allow the following conclusions. (1) Facilitation and inhibition are produced by fibres likely belonging to group Ia spindle afferents. (2) Both effects are of spinal origin. (3) The spinal circuits mediating the effects may be modulated by descending commands. (4) The facilitation is sustained by tonic supraspinal influences while the inhibition is independent of it. Arguments are proposed against the hypotheses that the inhibition be due to transmitter depletion or to presynaptic mechanisms
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