Effect of percutaneous electrical stimulation of the spinal cord on the manifestation of reciprocal and presynaptic inhibition α-motor neurons of the lower leg muscles against the background of a weak isometric contraction in magnitude

The article presents the results of a study of the reflex mechanisms of reciprocal and presynaptic inhibition at rest and when performing an isometric reduction of 5% of MPS against the background of twenty-minute non-invasive electrical stimulation of the spinal cord. It was found that at rest against the background of electrical stimulation, reciprocal and presynaptic inhibition was inverted to their relief, and when performing plantar flexion of the foot, on the contrary, reciprocal and presynaptic inhibition increased, but the severity of presynaptic inhibition was greater. Key words: percutaneous electrical stimulation of the spinal cord, reciprocal inhibition, presynaptic inhibition, isometric contraction.

Mechanisms modulating spinal excitability after nerve stimulation inducing extra torque

The study included 3 experiments aiming to examine the mechanisms responsible for spinal excitability modulation, as assessed by the H-reflex, following stimulation trains delivered at two different frequencies (20 and 100Hz) inducing extra torque (ET). A first experiment (n=15) was conducted to evaluate changes in presynaptic inhibition acting on Ia afferents induced by these electrical stimulation trains, assessed by conditioning the soleus H-reflex (tibial nerve stimulation) with stimulation of the common peroneal nerve (D1 inhibition) and of the femoral nerve (heteronymous Ia facilitation, HF). A second experiment (n=12) permitted to investigate homosynaptic post-activation depression (HPAD) changes after the stimulation trains. A third experiment (n=14) analysed changes in motoneuron intrinsic properties after the stimulation trains, by electrically stimulating the descending corticospinal tract at the thoracic level, evoking thoracic motor evoked potentials (TMEP). Main results showed that in all experiments spinal excitability decreased after the 20-Hz train (P<0.05), while this parameter significantly increased after the 100-Hz stimulation (P<0.05). D1 and HF were not significantly modified after either stimulation. HPAD was significantly decreased only after the 20-Hz train, while TMEP was significantly increased only after the 100-Hz train (P<0.05). It is concluded that the decreased spinal excitability observed after the 20-Hz train cannot be attributed to D1 presynaptic inhibition but rather to increased HPAD of the Ia afferents terminals, while the increase of this parameter obtained after the 100-Hz train can be assigned to changes in intrinsic motoneuron properties allowing to maintain Ia - alpha motoneurons transmission efficacy.

Indirect Vibration of the Upper Limbs Alters Transmission Along Spinal but Not Corticospinal Pathways

The use of upper limb vibration (ULV) during exercise and rehabilitation continues to gain popularity as a modality to improve function and performance. Currently, a lack of knowledge of the pathways being altered during ULV limits its effective implementation. Therefore, the aim of this study was to investigate whether indirect ULV modulates transmission along spinal and corticospinal pathways that control the human forearm. All measures were assessed under CONTROL (no vibration) and ULV (30 Hz; 0.4 mm displacement) conditions while participants maintained a small contraction of the right flexor carpi radialis (FCR) muscle. To assess spinal pathways, Hoffmann reflexes (H-reflexes) elicited by stimulation of the median nerve were recorded from FCR with motor response (M-wave) amplitudes matched between conditions. An H-reflex conditioning paradigm was also used to assess changes in presynaptic inhibition by stimulating the superficial radial (SR) nerve (5 pulses at 300Hz) 37 ms prior to median nerve stimulation. Cutaneous reflexes in FCR elicited by stimulation of the SR nerve at the wrist were also recorded. To assess corticospinal pathways, motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation of the contralateral motor cortex were recorded from the right FCR and biceps brachii (BB). ULV significantly reduced H-reflex amplitude by 15.7% for both conditioned and unconditioned reflexes (24.0 ± 15.7 vs. 18.4 ± 11.2% Mmax; p &lt; 0.05). Middle latency cutaneous reflexes were also significantly reduced by 20.0% from CONTROL (−1.50 ± 2.1% Mmax) to ULV (−1.73 ± 2.2% Mmax; p &lt; 0.05). There was no significant effect of ULV on MEP amplitude (p &gt; 0.05). Therefore, ULV inhibits cutaneous and H-reflex transmission without influencing corticospinal excitability of the forearm flexors suggesting increased presynaptic inhibition of afferent transmission as a likely mechanism. A general increase in inhibition of spinal pathways with ULV may have important implications for improving rehabilitation for individuals with spasticity (SCI, stroke, MS, etc.).

GABAA presynaptic inhibition regulates the gain and kinetics of retinal output neurons

Output signals of neural circuits, including the retina, are shaped by a combination of excitatory and inhibitory signals. Inhibitory signals can act presynaptically on axon terminals to control neurotransmitter release and regulate circuit function. However, it has been difficult to study the role of presynaptic inhibition in most neural circuits due to lack of cell-type specific and receptor-type specific perturbations. In this study, we used a transgenic approach to selectively eliminate GABAA inhibitory receptors from select types of second order neurons - bipolar cells - in mouse retina and examined how this affects the light response properties of the well-characterized ON alpha ganglion cell retinal circuit. Selective loss of GABAA receptor-mediated presynaptic inhibition causes an enhanced sensitivity and slower kinetics of light-evoked responses from ON alpha ganglion cells thus highlighting the role of presynaptic inhibition in gain control and temporal filtering of sensory signals in a key neural circuit in the mammalian retina.

Age-Related Changes in Presynaptic Inhibition During Gait Initiation

Age-related changes in presynaptic inhibition (PSI) have not been observed during gait initiation, which requires anticipatory postural adjustment (APA). As APA is centrally modulated and is impaired in older compared to young adults, here we aimed to study the presynaptic control and co-contraction levels in the ankle muscles during gait initiation in older compared to young adults. Fifteen older (age range 65–80 years) and 15 young adults (age range 19–30 years) performed a gait initiation task on a force platform under 3 conditions: (i) without electrical stimulation; (ii) test Hoffman reflex (H-reflex); and (iii) conditioned H-reflex. H-reflexes were evoked on the soleus muscle when the APA amplitude exceeded 10%–20% of the average baseline mediolateral force. Participants also performed quiet stance as a control task. Results showed that both age groups presented similar PSI levels during quiet stance (p = .941), while in the gait initiation older adults presented higher PSI levels, longer duration, and lower amplitude of APA than young adults (p &lt; .05). Older adults presented higher co-contraction ratio in both tasks than young adults (p &lt; .05). Correlations between the PSI levels and the APA amplitude (r = −0.61, p = .008), and between the PSI levels and the co-contraction ratio during gait initiation (r = −0.64, p = .005) were found for older adults only. APA amplitude explained 49% of the variance of the PSI levels (p = .003). Our findings suggest that older compared to young adults have increased presynaptic control to compensate for the decreased supraspinal modulation on impaired APAs during gait initiation.