Homosynaptic Depression Research Articles

Transspinal Focused Ultrasound Suppresses Spinal Reflexes in Healthy Rats

ObjectivesLow-intensity, focused ultrasound (FUS) is an emerging noninvasive neuromodulation approach, with improved spatial and temporal resolution and penetration depth compared to other noninvasive electrical stimulation strategies. FUS has been used to modulate circuits in the brain and the peripheral nervous system, however, its potential to modulate spinal circuits is unclear. In this study, we assessed the effect of trans-spinal FUS (tsFUS) on spinal reflexes in healthy rats. Materials and MethodstsFUS targeting different spinal segments was delivered for 1 minute, under anesthesia. Monosynaptic H-reflex of the sciatic nerve, polysynaptic flexor reflex of the sural nerve, and withdrawal reflex tested with a hot plate were measured before, during, and after tsFUS. ResultstsFUS reversibly suppresses the H-reflex in a spinal segment-, acoustic pressure- and pulse-repetition frequency (PRF)-dependent manner. tsFUS with high PRF augments the degree of homosynaptic depression of the H-reflex observed with paired stimuli. It suppresses the windup of components of the flexor reflex associated with slower, C-afferent, but not faster, A- afferent fibers. Finally, it increases the latency of the withdrawal reflex. tsFUS does not elicit neuronal loss in the spinal cord. ConclusionsOur study provides evidence that tsFUS reversibly suppresses spinal reflexes and suggests that tsFUS could be a safe and effective strategy for spinal cord neuromodulation in disorders associated with hyperreflexia, including spasticity after spinal cord injury and painful syndromes.

ID: 216418 Activation of Inhibitory Circuit in Reflex Motor Pathways by 10kHz Versus Single Pulse/Low Frequency SCS

High frequency (10kHz) spinal cord stimulation (SCS) is a well-established and expanding neuromodulatory technique for treating chronic pain. Despite clinical success, the cellular mechanisms of 10kHz SCS for activating neurons is still not fully understood. In previous preclinical work, we reported that 10kHz SCS activated the thigh muscle selectively, with very little activation by single pulse (low frequency) SCS. The toe muscle showed a similar but opposite selectivity, where single pulse/low frequency SCS resulted in more selective activation of the toe than 10kHzSCS. In the literature, both animal and human studies reported that use of a paired pulse protocol generates recurrent, presynaptic inhibition and homosynaptic depression depending on the delay between first and second pulses. Here we studied the activation of inhibitory circuits in reflex motor pathways using a paired pulse protocol of 10 kHz SCS vs. low frequency/single pulse SCS.

Lumbar trans-spinal direct current stimulation: A modeling-experimental approach to dorsal root ganglia stimulation.

The excitability of spinal motor neurons (MN) can be altered through subthreshold currents, such as transcutaneous spinal direct-current stimulation (tsDCS). Current evidence shows that tsDCS can interfere with ascending somatosensory pathways and lower motor neurons' (LMN) excitability, which points to its therapeutic potential for repairing altered spinal responses. We aim to define the best tsDCS montage for maximizing the electric field (E-field) in the lumbar spinal cord (L-SC) by computer modeling; and to apply this montage to measure the effect on LMN excitability and somatosensory evoked potentials (SSEP). A human volume conductor model was obtained from an available database. The E-field distribution was calculated considering three different electrode settings aiming at maximizing the field at L-SC and right dorsal root ganglia (DRG). The best electrode setting was then selected and applied in a blind crossover pseudo-randomized study including 14 subjects. tsDCS was delivered for 15 min (cathodal vs. sham) over L2 vertebra level (4 mA, 144 mC/cm2), and its effect on F-waves, H-reflex (including homosynaptic depression, HD) and SSEPs was investigated in the lower limbs. All simulated montages showed higher current density and E-field magnitudes between the electrodes (>0.15 V/m), with a major longitudinal component and with rostral-caudal direction. The induced E-field involved the sensory ganglia and was maximum in the right T8-left L2 montage, which was the one selected for the experimental protocol. We disclosed a statistically significant increase of the H-reflex amplitude at 0.1 Hz, after cathodal tsDCS (c-tsDCS) on both sides. No other significant change was observed. Our results can suggest the c-tsDCS applied to the L-SC and DRG can modulate synaptic efficiency increasing lower motor neurons response to Ia fibers excitation. The possible implications of our findings for treating clinical conditions will be addressed in future studies.

Exercise following immobility increases lower motor neuron excitability: F-wave and H-reflex studies

ObjectivesThe excitability of lower motor neurons can be explored non-invasively by several neurophysiological techniques, e.g., F-wave and H-reflex studies after a period of immobility and then after subsequent exercise. The aim of this study is to investigate the impact of exercise and high frequency repetitive nerve stimulation (RNS) following changes induced by 75 min of immobility. MethodsWe studied 10 healthy subjects following 75 min lower limb immobility, then randomized to RNS or cycling on different days. The neurophysiological studies of M-response, F-wave latency, F/M amplitude ratio and persistence; H-reflex threshold and latency, H/M amplitude ratio, and homosynaptic depression were performed at baseline, after immobility and immediately following the intervention, using stimulation of posterior tibial and peroneal nerves. ResultsAfter immobility F-wave latencies were delayed and homosynaptic depression at 2 Hz was increased (p < 0.025). RNS had no effect, but cycling exercise reduced H-reflex latencies (p = 0.025) and decreased homosynaptic depression at 2 Hz. DiscussionOur findings suggest that both proprioceptive stimulation and supraspinal pathways modulate intraspinal physiological changes after immobility. These observations suggest that specific exercise protocols may be useful in managing patients recovering from periods of immobility.

Repetitive transcranial magnetic stimulation on the modulation of cortical and spinal cord excitability in individuals with spinal cord injury.

Repetitive transcranial magnetic stimulation (rTMS) has been applied for modulating cortical excitability and treating spasticity in neurological lesions. However, it is unclear which rTMS frequency is most effective in modulating cortical and spinal excitability in incomplete spinal cord injury (SCI). To evaluate electrophysiological and clinical repercussions of rTMS compared to sham stimulation when applied to the primary motor cortex (M1) in individuals with incomplete SCI. A total of 11 subjects (35±12 years) underwent three experimental sessions of rTMS (10 Hz, 1 Hz and sham stimulation) in a randomized order at 90%intensity of the resting motor threshold and interspersed by a seven-day interval between sessions. The following outcome measures were evaluated: M1 and spinal cord excitability and spasticity in the moments before (baseline), immediately after (T0), 30 (T30) and 60 (T60) minutes after rTMS. M1 excitability was obtained through the motor evoked potential (MEP); spinal cord excitability by the Hoffman reflex (H-reflex) and homosynaptic depression (HD); and spasticity by the modified Ashworth scale (MAS). A significant increase in cortical excitability was observed in subjects submitted to 10 Hz rTMS at the T0 moment when compared to sham stimulation (p = 0.008); this increase was also significant at T0 (p = 0.009), T30 (p = 0.005) and T60 (p = 0.005) moments when compared to the baseline condition. No significant differences were observed after the 10 Hz rTMS on spinal excitability or on spasticity. No inter-group differences were detected, or in the time after application of 1 Hz rTMS, or after sham stimulation for any of the assessed outcomes. High-frequency rTMS applied to M1 was able to promote increased cortical excitability in individuals with incomplete SCI for at least 60 minutes; however, it did not modify spinal excitability or spasticity.

Excitatory postsynaptic calcium transients at Aplysia sensory-motor neuron synapses allow for quantal examination of synaptic strength over multiple days in culture.

A more thorough description of the changes in synaptic strength underlying synaptic plasticity may be achieved with quantal resolution measurements at individual synaptic sites. Here, we demonstrate that by using a membrane targeted genetic calcium sensor, we can measure quantal synaptic events at the individual synaptic sites of Aplysia sensory neuron to motor neuron synaptic connections. These results show that synaptic strength is not evenly distributed between all contacts in these cultures, but dominated by multiquantal sites of synaptic contact, likely clusters of individual synaptic sites. Surprisingly, most synaptic contacts were not found opposite presynaptic varicosities, but instead at areas of pre- and postsynaptic contact with no visible thickening of membranes. The release probability, quantal size, and quantal content can be measured over days at individual synaptic contacts using this technique. Homosynaptic depression was accompanied by a reduction in release site probability, with no evidence of individual synaptic site silencing over the course of depression. This technique shows promise in being able to address outstanding questions in this system, including determining the synaptic changes that maintain long-term alterations in synaptic strength that underlie memory.

Passive torque influences the Hoffmann reflex pathway during the loading and unloading phases of plantar flexor muscles stretching.

This study investigated the influence of passive tension on Hoffmann reflex during the loading (muscle stretched by passive joint movement) and unloading phase (joint returned to initial position) of muscle stretching. The maximal H‐reflex amplitude (H max) was recorded in soleus in 19 young adults during the loading and unloading phases of a passive 30° dorsiflexion, from 90° ankle angle (reference position). H max was evoked at similar angles (protocol‐1) or similar passive torque (PT; protocol‐2) during the loading and unloading phases, or during two loading phases separated by a 5‐min stretch hold at 30° ankle dorsiflexion relative to the reference position (protocol‐3). Homosynaptic depression (HD) was assessed with paired H reflexes (0.5‐s interstimulus interval) during the loading and unloading phases (protocol‐4; n=13). In protocol‐1, PT was lesser and H max greater during the unloading than the loading phase (p < 0.001). In protocol‐2, no difference in H max was observed between phases. In protocol‐3, PT was lesser and H max greater during the second than the first loading phase (p < 0.001). Changes in PT during in these three protocols were associated with those in H max (r 2 ≥ 0.97). In protocol‐4, HD increased and decreased during the loading and unloading phases, respectively (p < 0.001), without differing between phases. Additional experiments (n=12) showed a similar modulation of H max in gastrocnemius medialis during loading and unloading phases, while muscle fascicle length did not differ between phases. This study indicates that the H‐reflex modulation during muscle stretching relies in part on mechanisms associated with the PT developed by the muscle‐tendon unit.

A stimulus rate that is not influenced by homosynaptic post-activation depression in chronic stroke

Purpose To determine a stimulus rate that is not influenced by homosynaptic post-activation depression for H-reflex studies in patients with chronic spasticity. Materials and methods A cohort of 15 chronic stroke patients with soleus spasticity who received inpatient treatment at our rehabilitation centre participated in this study. The effect of stimulus frequency related depression on H-reflex size was tested using four different stimulus rates (0.1, 0.2, 0.3 and 1 Hz). The affected sides stibial nerve was stimulated by a bipolar electrode. The H-reflex was recorded from the affected sideed sidee sidehe affected smine stimulus frequency related depression of H-reflex size, amplitude of the first H-reflex response (H1) was used as control and amplitude of the second H-reflex response (H2) as test. Results H2 amplitude for frequency of 1 Hz, 0.3 Hz, 0.2 Hz and 0.1 Hz were 74.3, 84.1, 85.5 and 92.7% of H1, respectively. Depression of H2 amplitude was statistically significant for 1 Hz, 0.3 Hz and 0.2 Hz (p < 0.001, p = 0.002, p = 0.024, respectively). Conclusions Higher frequency stimulation of Ia afferents than 0.1 Hz induced a stimulus frequency-related depression of H-reflex size in patients with chronic spasticity. The optimal stimulus rate for H-reflex was found to be 0.1 Hz.

МОДУЛЯЦІЙНІ ВПЛИВИ СТОМЛЕННЯ НА Н-РЕФЛЕКС КАМБАЛОПОДІБНОГО М'ЯЗА В УМОВАХ ПАРНОЇ СТИМУЛЯЦІЇ ВЕЛИКОГОМІЛКОВОГО НЕРВА В НЕТРЕНОВАНИХ ТА ТРЕНОВАНИХ ЛЮДЕЙ

Monosynaptic reflex indices peculiarities, concerned with adaptative reactions to the long-term physical exercise, might add new data about mechanisms of human nervous system plasticity. The objective of the research was to investigate the influence of fatigue on human soleus H (Hoffmann) reflex in conditions of pair stimulation of tibial nerve with inter stimulus interval 500 m sin tenun trained people (age: M = 25,3, SE = 1,6 years) and ten trained athletes (age: M = 20,5, SE = 0,5 years). H-reflex study was performed using neurodiagnostic complex Nicolet Biomedical Viking Select (Viasys Health care, USA) at rest: before and after long-lasting isometric voluntary contraction of calf muscle, which caused the soleus muscle fatigue; the muscle force was equal to 75 % of maximal voluntary contraction. Test and conditioned responses (by means of stimulation with first and second impulses from pair) were registered. Homosynaptic postactivation depression (HPAD), associated with pair stimulation of tibial nerve, led to 56 % and 51 % inhibition of H-reflex in untrained and trained people at rest, respectively (p &lt; 0,05). After fatiguing voluntary contraction the amplitudes of test and conditioned soleus H-reflex were both reduced approximately in half. Then both H-reflex amplitudes subsequently recovered, more rapidly in trained people. Soleus H-reflex inhibition might be due to the activation of the groups III and IV afferent nerves under the influence of mechanical and metabolic changes in the muscle. It was also found that HPAD H-reflex inhibition intensity increased by 20 % in untrained people and by 15 % in trained ones at 90 s after fatiguing voluntary contraction (p &lt; 0,05). It is assumed that complex influence of fatigue and homosynaptic postactivation depression was more pronounced in untrained people in comparison with trained ones. It can be ascribed to athletes adaptation to the long-term physical exercise.

On the reflex mechanisms of cervical transcutaneous spinal cord stimulation in human subjects.

Transcutaneous and epidural electrical spinal cord stimulation techniques are becoming more valuable as electrophysiological and clinical tools. Recently, remarkable recovery of the upper limb sensorimotor function during cervical spinal stimulation was demonstrated. In the present study, we sought to elucidate the neural mechanisms underlying the effects of transcutaneous spinal cord stimulation (tSCS) of the cervical spine. We hypothesized that cervical tSCS can be used to selectively activate the sensory route entering the spinal cord and transsynaptically converge on upper limb motor pools. To test this hypothesis, we applied cervical tSCS using paired stimuli (homosynaptic depression) and during passive muscle stretching of the wrist flexor (presynaptic inhibition via Ia afferents), voluntary hand muscle contraction (descending facilitation of motoneuron pool), and muscle-tendon vibration of the wrist (presynaptic inhibition via afferent occlusion). Our results demonstrate significant inhibition of the second evoked response during paired stimulus delivery, inhibition of responses during passive muscle stretching and muscle-tendon vibration, and facilitation during voluntary muscle contraction, which share similarities with responses evoked during lumbosacral tSCS. These results indicate that the route of the stimulation current transmission passes via afferents in the dorsal roots through the spinal cord to activate the motor pools and potentially interneuronal networks projecting to upper limb muscles. Using a novel stimulation paradigm, our study is the first to present evidence of the sensory neuronal pathway of the cervical tSCS propagation. Overall, our work demonstrates the utility and sensitivity of cervical tSCS to engage the sensory pathway projecting to the upper limbs. NEW & NOTEWORTHY Despite therapeutic effects that have been demonstrated previously using noninvasive cervical spinal stimulation, it has been unclear whether, and to what degree, the stimulation can activate the sensory afferent system. Our study presents evidence that cervical transcutaneous spinal cord stimulation can engage the sensory pathways and transsynaptically converge on motor pools projecting to upper limb muscles, demonstrating the utility and sensitivity of cervical spinal stimulation for electrophysiological assessments and neurorehabilitation.

F157. Presynaptic inhibition of the soleus H reflex and gating of event-related potentials by ankle taps

Introduction A single tendon tap may cause at the same time inhibition of reflex responses through post-activation depression and reduction of the afferent volley reaching the cortex through sensory gating. We aimed at characterizing the temporal profile of the two effects and establish the differences in the timing and degree of inhibition between them. Methods In 10 healthy subjects aged 22–65 years we recorded both the H reflex from the soleus muscle and the long-latency evoked potentials (LLEPs) from Cz to electrical stimuli to the posterior tibial nerve at the popliteal fossa. Stimulus intensity was appropriate to induce an H reflex with a small or absent M wave. In test trials, the responses were conditioned by an Achilles tendon tap at interstimulus intervals 60, 80, 100, 200, 400, 800, 1200, 1600 and 2000 ms. Results The H reflex was inhibited test trials at short intervals with progressive recovery at long inte, reaching 72% of control values at the longest interval tested (2000 ms). The LLEPs were inhibited at short intervals, reaching 90% of control values at 200 ms. The M wave remained unmodified in all control and test trials. Conclusion Homosynaptic depression of the H reflex is far more powerful than gating of the same sensory volley by mechanical taps. The long lasting inhibition of the H reflex may imply the activation of inhibitory circuits that do not participate in afferent gating.

Effects of repetitive transcranial magnetic stimulation and trans-spinal direct current stimulation associated with treadmill exercise in spinal cord and cortical excitability of healthy subjects: A triple-blind, randomized and sham-controlled study.

Repetitive transcranial magnetic stimulation (rTMS) over motor cortex and trans-spinal direct current stimulation (tsDCS) modulate corticospinal circuits in healthy and injured subjects. However, their associated effects with physical exercise is still not defined. This study aimed to investigate the effect of three different settings of rTMS and tsDCS combined with treadmill exercise on spinal cord and cortical excitability of healthy subjects. We performed a triple blind, randomized, sham-controlled crossover study with 12 healthy volunteers who underwent single sessions of rTMS (1Hz, 20Hz and Sham) and tsDCS (anodal, cathodal and Sham) associated with 20 minutes of treadmill walking. Cortical excitability was assessed by motor evoked potential (MEP) and spinal cord excitability by the Hoffmann reflex (Hr), nociceptive flexion reflex (NFR) and homosynaptic depression (HD). All measures were assessed before, immediately, 30 and 60 minutes after the experimental procedures. Our results demonstrated that anodal tsDCS/treadmill exercise reduced MEP’s amplitude and NFR’s area compared to sham condition, conversely, cathodal tsDCS/treadmill exercise increased NFR’s area. High-frequency rTMS increased MEP’s amplitude and NFR’s area compared to sham condition. Anodal tsDCS/treadmill exercise and 20Hz rTMS/treadmill exercise reduced Hr amplitude up to 30 minutes after stimulation offset and no changes were observed in HD measures. We demonstrated that tsDCS and rTMS combined with treadmill exercise modulated cortical and spinal cord excitability through different mechanisms. tsDCS modulated spinal reflexes in a polarity-dependent way acting at local spinal circuits while rTMS probably promoted changes in the presynaptic inhibition of spinal motoneurons. In addition, the association of two neuromodulatory techniques induced long-lasting changes.

The CaV2\u03b11 EF-hand F helix tyrosine, a highly conserved locus for GPCR inhibition of CaV2 channels

The sensory neuron of Aplysia californica participates in several forms of presynaptic plasticity including homosynaptic depression, heterosynaptic depression, facilitation and the reversal of depression. The calcium channel triggering neurotransmitter release at most synapses is CaV2, consisting of the pore forming α1 subunit (CaV2α1), and auxiliary CaVβ, and CaVα2δ subunits. To determine the role of the CaV2 channel in presynaptic plasticity in Aplysia, we cloned Aplysia CaV2α1, CaVβ, and CaVα2δ and over-expressed the proteins in Aplysia sensory neurons (SN). We show expression of exogenous CaV2α1 in the neurites of cultured Aplysia SN. One proposed mechanism for heterosynaptic depression in Aplysia is through inhibition of CaV2. Here, we demonstrate that heterosynaptic depression of the CaV2 calcium current is inhibited when a channel with a Y-F mutation at the conserved Src phosphorylation site is expressed, showing the strong conservation of this mechanism over evolution. We also show that the Y-F mutation reduces heterosynaptic inhibition of neurotransmitter release, highlighting the physiological importance of this mechanism for the regulation of synaptic efficacy. These results also demonstrate our ability to replace endogenous CaV2 channels with recombinant channels allowing future examination of the structure function relationship of CaV2 in the regulation of transmitter release in this system.

The effects of cervical transcutaneous spinal direct current stimulation on motor pathways supplying the upper limb in humans.

Non-invasive, weak direct current stimulation can induce changes in excitability of underlying neural tissue. Many studies have used transcranial direct current stimulation to induce changes in the brain, however more recently a number of studies have used transcutaneous spinal direct current stimulation to induce changes in the spinal cord. This study further characterises the effects following cervical transcutaneous spinal direct current stimulation on motor pathways supplying the upper limb. In Study 1, on two separate days, participants (n = 12, 5 F) received 20 minutes of either real or sham direct current stimulation at 3 mA through electrodes placed in an anterior-posterior configuration over the neck (anode anterior). Biceps brachii, flexor carpi radialis and first dorsal interosseous responses to transcranial magnetic stimulation (motor evoked potentials) and cervicomedullary stimulation (cervicomedullary motor evoked potentials) were measured before and after real or sham stimulation. In Study 2, on two separate days, participants (n = 12, 7 F) received either real or sham direct current stimulation in the same way as for Study 1. Before and after real or sham stimulation, median nerve stimulation elicited M waves and H reflexes in the flexor carpi radialis. H-reflex recruitment curves and homosynaptic depression of the H reflex were assessed. Results show that the effects of real and sham direct current stimulation did not differ for motor evoked potentials or cervicomedullary motor evoked potentials for any muscle, nor for H-reflex recruitment curve parameters or homosynaptic depression. Cervical transcutaneous spinal direct current stimulation with the parameters described here does not modify motor responses to corticospinal stimulation nor does it modify H reflexes of the upper limb. These results are important for the emerging field of transcutaneous spinal direct current stimulation.

МОДУЛЯЦІЯ Н-РЕФЛЕКСУ КАМБАЛОПОДІБНОГО М'ЯЗУ ЛЮДИНИ, ПОВ'ЯЗАНА ЗІ СТОМЛЕННЯМ, ЗА УМОВ ГОМОСИНАПТИЧНОЇ ПОСТАКТИВАЦІЙНОЇ ДЕПРЕСІЇ ПРИ ПАРНІЙ СТИМУЛЯЦІЇ ВЕЛИКОГОМІЛКОВОГО НЕРВУ

The purpose of our work was to investigate in detail the influence of pair stimulation of tibial nerve (n.tibialis) on human soleus H-reflex amplitude at rest and after long-lasting voluntary contraction of calf muscle (m.m. gastrocnemius-soleus), which caused the fatigue of soleus muscle. The method of H-reflex of soleus muscle was used. Test and conditioned responses (by pair stimulation of n. tibialis) were registered. Homosynaptic postactivation depression led to inhibition of H-reflex at rest. After fatiguing voluntary static contraction the amplitudes of test and conditioned soleus H-reflex were significantly reduced. Then both H-reflex amplitudes subsequently recovered. Soleus H-reflex inhibition might be due to the activation of the groups III and IV afferent nerves under the influence of mechanical and metabolic changes in the muscle.

Paired associative transspinal and transcortical stimulation produces plasticity in human cortical and spinal neuronal circuits.

Anatomical, physiological, and functional connectivity exists between the neurons of the primary motor cortex (M1) and spinal cord. Paired associative stimulation (PAS) produces enduring changes in M1, based on the Hebbian principle of associative plasticity. The present study aimed to establish neurophysiological changes in human cortical and spinal neuronal circuits by pairing noninvasive transspinal stimulation with transcortical stimulation via transcranial magnetic stimulation (TMS). We delivered paired transspinal and transcortical stimulation for 40 min at precise interstimulus intervals, with TMS being delivered after (transspinal-transcortical PAS) or before (transcortical-transspinal PAS) transspinal stimulation. Transspinal-transcortical PAS markedly decreased intracortical inhibition, increased intracortical facilitation and M1 excitability with concomitant decreases of motor threshold, and reduced the soleus Hoffmann's reflex (H-reflex) low frequency-mediated homosynaptic depression. Transcortical-transspinal PAS did not affect intracortical circuits, decreased M1 excitability, and reduced the soleus H-reflex-paired stimulation pulses' mediated postactivation depression. Both protocols affected the excitation threshold of group Ia afferents and motor axons. These findings clearly indicate that the pairing of transspinal with transcortical stimulation produces cortical and spinal excitability changes based on the timing interval and functional network interactions between the two associated inputs. This new PAS paradigm may constitute a significant neuromodulation method with physiological impact, because it can be used to alter concomitantly excitability of intracortical circuits, corticospinal neurons, and spinal inhibition in humans.

Spinal Reflex Excitability and Homosynaptic Depression Following Bouts of Whole-Body Vibration of Varying Frequencies.

Spinal Reflex Excitability and Homosynaptic Depression Following Bouts of Whole-Body Vibration of Varying Frequencies.

The Effects of Plyometric Training on Spinal and Supraspinal Motor Control

Purpose: The purpose of this study was to determine the effects of plyometric training on spinal and supraspinal motor control in healthy active females. Methods: A 2 (Group) x 2 (Session) x 2 (Stance) mixed model design was used for homosynaptic depression (HD) and recurrent inhibition (RI) data. A 2 (Group) x 2 (Session) mixed model design was used for H:M ratios and V-waves (V:M ratios) data. Thirty-one participants were recruited to participate in the study. Participants participated in either the training or control group for 6-weeks. All participants were measured pre- and post-intervention on H:M ratios, HD, RI, and V-waves. Results: There were no statistically significant interactions for any of the dependent variables (p &gt; 0.05). There was a session main effect for RI (p = 0.01) as well as a group main effect (p = 0.01) and a stance main effect (p &lt; 0.01) for HD. Conclusions: Performing plyometric training does not modulate the spinal or supraspinal motor control based on the findings of this study. Plyometric training is not the only component that should be used in Anterior Cruciate Ligament Injury Prevention Programs to alter motor control. A more challenging and higher impact plyometric exercises are suggested to allow more demand on the neural drive of the physically active participants.

Persistent Associative Plasticity at an Identified Synapse Underlying Classical Conditioning Becomes Labile with Short-Term Homosynaptic Activation.

Activity-dependent changes in neural circuits mediate long-term memories. Some forms of long-term memories become labile and can be reversed with specific types of reactivations, but the mechanism is complex. At the cellular level, reactivations that induce a reversal of memory must evoke changes in neural circuits underlying the memory. What types of reactivations induce a labile state at neural connections that lead to reversal of different types of memory? We find that a critical neural connection in Aplysia, which is modified with different stimuli that mediate different types of memory, becomes labile with different types of reactivations. These results provide insights for developing strategies in alleviating maladaptive memories accompanying anxiety disorders.

Decline in the Recovery from Synaptic Depression in Heavier Aplysia Results from Decreased Serotonin-Induced Novel PKC Activation

The defensive withdrawal reflexes of Aplysia are important behaviors for protecting the animal from predation. Habituation and dishabituation allow for experience-dependent tuning of these reflexes and the mechanisms underlying these forms of behavioral plasticity involve changes in transmitter release from the sensory to motor neuron synapses through homosynaptic depression and the serotonin-mediated recovery from depression, respectively. Interestingly, dishabituation is reduced in older animals with no corresponding change in habituation. Here we show that the cultured sensory neurons of heavier animals (greater than 120g) that form synaptic connections with motor neurons have both reduced recovery from depression and reduced novel PKC Apl II activation with 5HT. The decrease in the recovery from depression correlated better with the size of the animal than the age of the animal. Much of this change in PKC activation and synaptic facilitation following depression can be rescued by direct activation of PKC Apl II with phorbol dibutyrate, suggesting a change in the signal transduction pathway upstream of PKC Apl II activation in the sensory neurons of larger animals.