Post-activation depression of primary afferents reevaluated in humans

Özyurt, Mustafa Görkem; Topkara, Betilay; Şenocak, Beatrice Selen; Budan, Abdullah Salih; Yüce, Murat; Türker, Kemal S.

doi:10.1016/j.jelekin.2020.102460

Cited by 9 publications

(4 citation statements)

References 63 publications

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“…We studied this depression through paired-pulse H-reflex conditioning (see methods; Figures S16A-S16D), and we detected impairments in mSOD1 mice at different intervals in all ages test: in early juvenile (P18-23) animals, we detected a 15% reduction at 5 sec conditioning interval; in young adults (P56-67) we found a reduction at 500 ms; for 3-months-old adults (P87-108) 200 ms and 1 sec conditionings were reduced by ~20%. Although the intervals affected vary between agegroups, which could be attributed to the inter-individual variability of post-activation depression 57 , our EMG data indicate that the Ia depression is altered in mSOD1 mice.…”

Section: Early Reduction In Recurrent Inhibition Is Compensated In La...mentioning

confidence: 66%

Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration

Nascimento,

Özyurt,

Halablab

et al. 2024

Preprint

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SummaryIn neurological conditions affecting the brain, early-stage neural circuit adaption is key for long-term preservation of normal behaviour. We tested if motoneurons and respective microcircuits also adapt in the initial stages of disease progression in a mouse model of progressive motoneuron degeneration. Using a combination ofin vitroandin vivoelectrophysiology and super-resolution microscopy, we found that, preceding muscle denervation and motoneuron death, recurrent inhibition mediated by Renshaw cells is reduced in half due to impaired quantal size associated with decreased glycine receptor density. Additionally, higher probability of release from proprioceptive Ia terminals leads to increased monosynaptic excitation to motoneurons. Surprisingly, the initial impairment in recurrent inhibition is not a widespread feature of inhibitory spinal circuits, such as group I inhibitory afferents, and is compensated at later stages of disease progression. We reveal that in disease conditions, spinal microcircuits undergo specific multiphasic homeostatic compensations to preserve force output.

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Section: Early Reduction In Recurrent Inhibition Is Compensated In La...mentioning

confidence: 66%

Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration

Nascimento,

Özyurt,

Halablab

et al. 2024

Preprint

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“…The data from the current study suggests that, in persons with SCI, a larger number of pulses is required to elicit maximal reflex depression in comparison to individuals who are neurologically intact. In contrast, people who are neurologically intact demonstrate reflex depression that does not significantly change with repeated conditioning stimuli [ 17 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

“…The application of these findings is limited to LFD protocols utilizing 1 Hz of stimulation as there are multiple physiological mechanisms operating at different timepoints believed to be contributing to alterations in reflex excitability [ 24 ]. Changing the interpulse interval could result in the evaluation of mechanisms where these findings may not apply.…”

Section: Limitationsmentioning

confidence: 99%

Optimizing assessment of low frequency H-reflex depression in persons with spinal cord injury

Creech,

Hope,

Zarkou

et al. 2024

PLoS ONE

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Considering the growing interest in clinical applications of neuromodulation, assessing effects of various modulatory approaches is increasingly important. Monosynaptic spinal reflexes undergo depression following repeated activation, offering a means to quantify neuromodulatory influences. Following spinal cord injury (SCI), changes in reflex modulation are associated with spasticity and impaired motor control. To assess disrupted reflex modulation, low-frequency depression (LFD) of Hoffman (H)-reflex excitability is examined, wherein the amplitudes of conditioned reflexes are compared to an unconditioned control reflex. Alternatively, some studies utilize paired-pulse depression (PPD) in place of the extended LFD train. While both protocols induce similar amounts of H-reflex depression in neurologically intact individuals, this may not be the case for persons with neuropathology. We compared the H-reflex depression elicited by PPD and by trains of 3–10 pulses to an 11-pulse LFD protocol in persons with incomplete SCI. The amount of depression produced by PPD was less than an 11-pulse train (mean difference = 0.137). When compared to the 11-pulse train, the 5-pulse train had a Pearson’s correlation coefficient (R) of 0.905 and a coefficient of determination (R2) of 0.818. Therefore, a 5-pulse train for assessing LFD elicits modulation similar to the 11-pulse train and thus we recommend its use in lieu of longer trains.

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“…The P-AD occurs when a peripheral nerve is electrically stimulated at frequencies >1 Hz, consequently, the amplitude of the following H-reflexes recorded at a selected muscle decreases as compared to the first one ( Ishikawa et al, 1966 ; Crone and Nielsen, 1989 ; Hultborn et al, 1996 ). Although the mechanisms of P-AD are not fully understood, results in healthy subjects indicate that both presynaptic and postsynaptic mechanisms contribute to this phenomenon ( Özyurt et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Post-activation depression of the Hoffman reflex is not altered by galvanic vestibular stimulation in healthy subjects

Alvarado-Navarrete,

Pliego-Carrillo,

Ledesma-Ramírez

et al. 2023

Front. Integr. Neurosci.

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The comprehension of the neural elements interacting in the spinal cord affected by vestibular input will contribute to the understanding of movement execution in normal and pathological conditions. In this context, Hoffman’s reflex (H-reflex) has been used to evaluate transient excitability changes on the spinal cord descending pathways. The post-activation depression (P-AD) of the H-reflex consists of evoking consecutive responses (>1 Hz) provoking an amplitude depression, which has been shown to diminish in pathological conditions (i.e., spasticity, diabetic neuropathy). Galvanic Vestibular Stimulation (GVS) is a non-invasive method that activates the vestibular afferents and has been used to study the excitability of the H-reflex applied as a conditioning pulse. To our knowledge, there are no reports evaluating the P-AD during and after GVS. Our primary aim was to determine if GVS alters the P-AD evoked by stimulating the tibial nerve at 0.1, 1, 5, and 10 Hz, recording in the gastrocnemius and soleus muscles. Direct current stimulation of 2.0 ± 0.6 mA with the cathode ipsilateral (Ipsi) or contralateral (Contra) to the H-reflex electrode montage was applied bilaterally over the mastoid process in 19 healthy subjects. The P-AD’s immediate post-GVS response (P Ipsi, P Contra) was also analyzed. Secondarily, we analyzed the excitability of the H-reflex during GVS. Responses evoked at 0.1 Hz with GVS, post-GVS, and a Control (no GVS) condition were used for comparisons. Our results show that P-AD persisted in all subjects despite increased excitability induced by GVS: statistical significance was found when comparing P-AD at 1, 5, and 10 Hz with the corresponding condition (Control, Ipsi, P Ipsi, Contra, P Contra) at 0.1 Hz (p < 0.001). Additionally, the increase in excitability produced by GVS was quantified for the first H-reflex of each P-AD stimulation frequency. The percentage change for all GVS conditions surpassed the Control by at least 20%, being statistically significant for Contra compared to Control (p < 0.01). In summary, although GVS increases the excitability of the vestibulospinal pathway at a premotor level, the neural inhibitory mechanism present in P-AD remains unaltered in healthy subjects.

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Post-activation depression of primary afferents reevaluated in humans

Cited by 9 publications

References 63 publications

Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration

Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration

Optimizing assessment of low frequency H-reflex depression in persons with spinal cord injury

Post-activation depression of the Hoffman reflex is not altered by galvanic vestibular stimulation in healthy subjects

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