Effect of fatigue-related group III/IV afferent firing on intracortical inhibition and facilitation in hand muscles

2020 ◽  
Vol 128 (1) ◽  
pp. 149-158 ◽  
Author(s):  
Christopher Latella ◽  
Onno van der Groen ◽  
Cassio V. Ruas ◽  
Janet L. Taylor

Fatiguing exercise causes a reduction in motor drive to the muscle. Group III/IV muscle afferent firing is thought to contribute to this process; however, the effect on corticospinal and intracortical networks is poorly understood. In two experiments, participants performed sustained maximal isometric finger abductions of the first dorsal interosseous (FDI) muscle, with postexercise blood flow occlusion (OCC) to maintain the firing of group III/IV afferents or without occlusion (control; CON). Before and after exercise, single- and paired-pulse transcranial magnetic stimulation (TMS) tested motor evoked potentials (MEPs), intracortical facilitation [ICF (12 ms)], and short-interval intracortical inhibition [SICI2 (2 ms), SICI3 (3 ms)]. Ulnar nerve stimulation elicited maximal M waves (MMAX). For experiment 1 ( n = 16 participants), TMS intensities were 70% and 120% of resting motor threshold (RMT) for the conditioning and MEP stimuli, respectively. For experiment 2 ( n = 16 participants), the MEP was maintained at 1 mV before and after exercise and the conditioning stimulus individualized. In experiment 1, MEP/MMAX was reduced after exercise (~48%, P = 0.007) but was not different between conditions. No changes occurred in ICF or SICI. In experiment 2, MEP/MMAX increased (~27%, P = 0.027) and less inhibition (SICI2: ~21%, P = 0.021) occurred after exercise for both conditions, whereas ICF decreased for CON only (~28%, P = 0.006). MEPs and SICI2 were modulated by fatiguing contractions but not by group III/IV afferent firing, whereas sustained afferent firing appeared to counteract postexercise reductions in ICF in FDI. The findings do not support the idea that actions of group III/IV afferents on motor cortical networks contribute to the reduction in voluntary activation observed in other studies. NEW & NOTEWORTHY This is the first study to investigate, in human hand muscles, the action of fatigue-related group III/IV muscle afferent firing on intracortical facilitation and inhibition. In fatigued and nonexercised hand muscles, intracortical inhibition is reduced after exercise but is not modulated differently by the firing of group III/IV afferents. However, facilitation is maintained for the fatigued muscle when group III/IV afferents fire, but these results are unlikely to explain the reduction in voluntary activation observed in other studies.

2018 ◽  
Vol 596 (19) ◽  
pp. 4789-4801 ◽  
Author(s):  
Simranjit K. Sidhu ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Dorothea Rosenberger ◽  
Jacob E. Jessop ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Eduardo Arruda Mello ◽  
Leonardo G. Cohen ◽  
Sarah Monteiro dos Anjos ◽  
Juliana Conti ◽  
Karina Nocelo F. Andrade ◽  
...  

Low-frequency repetitive transcranial magnetic stimulation of the unaffected hemisphere (UH-LF-rTMS) in patients with stroke can decrease interhemispheric inhibition from the unaffected to the affected hemisphere and improve hand dexterity and strength of the paretic hand. The objective of this proof-of-principle study was to explore, for the first time, effects of UH-LF-rTMS as add-on therapy to motor rehabilitation on short-term intracortical inhibition (SICI) and intracortical facilitation (ICF) of the motor cortex of the unaffected hemisphere (M1UH) in patients with ischemic stroke. Eighteen patients were randomized to receive, immediately before rehabilitation treatment, either active or sham UH-LF-rTMS, during two weeks. Resting motor threshold (rMT), SICI, and ICF were measured inM1UHbefore the first session and after the last session of treatment. There was a significant increase in ICF in the active group compared to the sham group after treatment, and there was no significant differences in changes in rMT or SICI. ICF is a measure of intracortical synaptic excitability, with a relative contribution of spinal mechanisms. ICF is typically upregulated by glutamatergic agonists and downregulated by gabaergic antagonists. The observed increase in ICF in the active group, in this hypothesis-generating study, may be related toM1UHreorganization induced by UH-LF-rTMS.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Florence Morin-Parent ◽  
Camille Champigny ◽  
Angelina Lacroix ◽  
François Corbin ◽  
Jean-François Lepage

AbstractFragile-X syndrome (FXS) is characterized by neurological and psychiatric problems symptomatic of cortical hyperexcitability. Recent animal studies identified deficient γ-aminobutyricacid (GABA) inhibition as a key mechanism for hyperexcitability in FXS, but the GABA system remains largely unexplored in humans with the disorder. The primary objective of this study was to assess GABA-mediated inhibition and its relationship with hyperexcitability in patients with FXS. Transcranial magnetic stimulation (TMS) was used to assess cortical and corticospinal inhibitory and excitatory mechanisms in 18 patients with a molecular diagnosis of FXS and 18 healthy controls. GABA-mediated inhibition was measured with short-interval intracortical inhibition (GABAA), long-interval intracortical inhibition (GABAB), and the corticospinal silent period (GABAA+B). Net intracortical facilitation involving glutamate was assessed with intracortical facilitation, and corticospinal excitability was measured with the resting motor threshold. Results showed that FXS patients had significantly reduced short-interval intracortical inhibition, increased long-interval intracortical inhibition, and increased intracortical facilitation compared to healthy controls. In the FXS group, reduced short-interval intracortical inhibition was associated with heightened intracortical facilitation. Taken together, these results suggest that reduced GABAA inhibition is a plausible mechanism underlying cortical hyperexcitability in patients with FXS. These findings closely match those observed in animal models, supporting the translational validity of these markers for clinical research.


Brain ◽  
2020 ◽  
Vol 143 (11) ◽  
pp. 3408-3421 ◽  
Author(s):  
Claudia Ammann ◽  
Michele Dileone ◽  
Cristina Pagge ◽  
Valentina Catanzaro ◽  
David Mata-Marín ◽  
...  

Abstract In Parkinson’s disease, striatal dopamine depletion produces profound alterations in the neural activity of the cortico-basal ganglia motor loop, leading to dysfunctional motor output and parkinsonism. A key regulator of motor output is the balance between excitation and inhibition in the primary motor cortex, which can be assessed in humans with transcranial magnetic stimulation techniques. Despite decades of research, the functional state of cortical inhibition in Parkinson’s disease remains uncertain. Towards resolving this issue, we applied paired-pulse transcranial magnetic stimulation protocols in 166 patients with Parkinson’s disease (57 levodopa-naïve, 50 non-dyskinetic, 59 dyskinetic) and 40 healthy controls (age-matched with the levodopa-naïve group). All patients were studied OFF medication. All analyses were performed with fully automatic procedures to avoid confirmation bias, and we systematically considered and excluded several potential confounding factors such as age, gender, resting motor threshold, EMG background activity and amplitude of the motor evoked potential elicited by the single-pulse test stimuli. Our results show that short-interval intracortical inhibition is decreased in Parkinson’s disease compared to controls. This reduction of intracortical inhibition was obtained with relatively low-intensity conditioning stimuli (80% of the resting motor threshold) and was not associated with any significant increase in short-interval intracortical facilitation or intracortical facilitation with the same low-intensity conditioning stimuli, supporting the involvement of cortical inhibitory circuits. Short-interval intracortical inhibition was similarly reduced in levodopa-naïve, non-dyskinetic and dyskinetic patients. Importantly, intracortical inhibition was reduced compared to control subjects also on the less affected side (n = 145), even in de novo drug-naïve patients in whom the less affected side was minimally symptomatic (lateralized Unified Parkinson’s Disease Rating Scale part III = 0 or 1, n = 23). These results suggest that cortical disinhibition is a very early, possibly prodromal feature of Parkinson’s disease.


2013 ◽  
Vol 124 (9) ◽  
pp. 1846-1852 ◽  
Author(s):  
Daisuke Sato ◽  
Koya Yamashiro ◽  
Takuya Yoshida ◽  
Hideaki Onishi ◽  
Yoshimitsu Shimoyama ◽  
...  

2006 ◽  
Vol 95 (6) ◽  
pp. 3371-3383 ◽  
Author(s):  
James P. Coxon ◽  
Cathy M. Stinear ◽  
Winston D. Byblow

Volitional inhibition is the voluntary prevention of a prepared movement. Here we ask whether primary motor cortex (M1) is a site of convergence of cortical activity associated with movement preparation and volitional inhibition. Volitional inhibition was studied by presenting a stop signal before execution of an anticipated response that requires a key lift to intercept a revolving dial. Motor evoked potentials (MEPs) were elicited in intrinsic hand muscles by transcranial magnetic stimulation (TMS) to assess corticomotor excitability and short interval intracortical inhibition (sICI) during task performance. The closer the stop cue was presented to the anticipated response, the harder it was for subjects to inhibit their response. Corticomotor pathway excitability was temporally modulated during volitional inhibition. Using subthreshold TMS, corticomotor excitability was reduced for Stop trials relative to Go trials from 140 ms after the cue. sICI was significantly greater for Stop trials compared with Go trials at a time that preceded the onset of muscle activity associated with the anticipated response. These results provide evidence that volitional inhibition is exerted at a cortical level and that inhibitory networks within M1 contribute to volitional inhibition of prepared action.


2011 ◽  
Vol 105 (4) ◽  
pp. 1594-1602 ◽  
Author(s):  
Demetris S. Soteropoulos ◽  
Monica A. Perez

Many bilateral motor tasks engage simultaneous activation of distal and proximal arm muscles, but little is known about their physiological interactions. Here, we used transcranial magnetic stimulation to examine motor-evoked potentials (MEPs), interhemispheric inhibition at a conditioning-test interval of 10 (IHI10) and 40 ms (IHI40), and short-interval intracortical inhibition (SICI) in the left first dorsal interosseous (FDI) muscle during isometric index finger abduction. The right side remained at rest or performed isometric voluntary contraction with the FDI, biceps or triceps brachii, or the tibialis anterior. Left FDI MEPs were suppressed to a similar extent during contraction of the right FDI and biceps and triceps brachii but remained unchanged during contraction of the right tibialis anterior. IHI10 and IHI40 were decreased during contraction of the right biceps and triceps brachii compared with contraction of the right FDI. SICI was increased during activation of the right biceps and triceps brachii and decreased during activation of the right FDI. The present results indicate that an isometric voluntary contraction with either a distal or a proximal arm muscle, but not a foot dorsiflexor, decreases corticospinal output in a contralateral active finger muscle. Transcallosal inhibitory effects were strong during bilateral activation of distal hand muscles and weak during simultaneous activation of a distal and a proximal arm muscle, whereas GABAergic intracortical activity was modulated in the opposite manner. These findings suggest that in intact humans crossed interactions at the level of the motor cortex involved different physiological mechanisms when bilateral distal hand muscles are active and when a distal and a proximal arm muscle are simultaneously active.


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