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A-M Systems emg recording electrodes
Emg Recording Electrodes, supplied by A-M Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/emg+recording+electrodes/electrodes+emg+recording/bio_rxiv__64898__2026__04__01__715924-27-9-7
Average 86 stars, based on 1 article reviews
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Article Title: Cholinergic basal forebrain structures are involved in the mediation of the arousal effect of noradrenaline.
Article Snippet: .. The EMG recording electrodes (silver wires covered by Teflon , A-M Systems, Inc., Carlsborg, WA, USA) were implanted into the neck muscles. .. For the local administration of MTX and SAP, a unilateral microdialysis guide cannula (CMA/11 Guide; CMA/Microdialysis, Stockholm, Sweden) was implanted in such a way that the tip was located 2 mm above the target area in the BF (HDB/SI/MCPO; AP = 0.3; ML = 2.0; V = 6.5; Paxinos and Watson, 1998).

Article Title: Sensory-motor circuit is a therapeutic target for dystonia musculorum mice, a model of hereditary sensory and autonomic neuropathy 6
Article Snippet: .. Then, the EMG recording electrodes (bipolar wire electrodes; tip distance, 1 to 2 mm) made of 140-mm-diameter Teflon-coated seven-stranded stainless steel wire (A-M Systems) were implanted in the bellies of the triceps and biceps brachii muscles of the forelimb. ..

other:

Article Title: Hypoglossal motor output is altered by C4 epidural electrical stimulation via ascending spinal and peripheral feedback pathways
Article Snippet: Two 36 AWG perfluoroalkoxy-insulated seven-stranded stainless-steel wire (AM Systems) EMG recording electrodes were implanted at the base of the tongue (targeting the genioglossus muscle), and bilaterally on the diaphragm.

Article Title: Focal loss of the paranodal domain protein Neurofascin155 in the internal capsule impairs cortically induced muscle activity in vivo
Article Snippet: A pair of EMG recording electrodes made of 50-μm-diameter Teflon-coated stranded stainless-steel wires (A-M systems, Carlsberg, USA) were also surgically placed into the triceps brachii muscle of the forelimb contralateral to the side of the cortical stimulation electrodes.



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A) Diagram depicting the 1-nerve stimulation assay designed to reveal the contribution of dPVs to motor activity evoked by stimulation of ipsilateral cutaneous nerves. Nerve cuffs were implanted on the right sural nerve and left saphenous nerve. <t>EMG</t> <t>electrodes</t> were implanted into the right and left semitendinosus (St, knee flexor), right vastus lateralis (VL, knee extensor), left tibialis anterior (TA, ankle flexor) and right and left gastrocnemius (Gs, ankle extensor). EMG responses were recorded from hindlimb flexors and extensors following stimulation of cutaneous nerves (saphenous / sural nerve). B) Example St EMG responses to stimulation of the right saphenous nerve at 5 times threshold (see methods) in dPV norm (top) and dPV abl (bottom), during the experiment described in D. C) Latency to response to stimulation of the saphenous (left) or sural (right) nerves of ipsilateral hindlimb muscles during the experiment depicted in D. D) Top-diagram of the 2-nerve stimulation assay applied to reveal if dPVs mediate sensory-evoked ipsilateral inhibition. Bottom-experiment timeline. Nerve cuffs and EMG electrodes were placed as in D. Stimulation of the contralateral cutaneous nerve (saphenous/ sural) alone (black lightning) was used to calculate the expected response in the absence of sensory evoked ipsilateral inhibition. Following, both nerves were stimulated (yellow lightning), with variable delays and compared to the expected response to reveal ipsilateral inhibition. E) Top-expected Gs EMG response to stimulation of a single cutaneous nerve in dPV abl (left) and dPV norm (right), averaged over 20 responses. Bottom-expected responses (black) superimposed on single trial responses to stimulation of both cutaneous nerves (yellow). Left-response to stimulation of both nerves (15 ms delay), shows a “dip” that is absent in the expected response, indicating ipsilateral inhibition. Right-no “dip” is seen (0 ms delay), suggesting a loss of inhibition. For each mouse and each muscle, the delay in which responses were best aligned was chosen for further analysis. F) Percent inhibition (the percentage of trials where inhibition was detected) in hindlimb muscles, mediated by ipsilateral saphenous (left) and ipsilateral sural (right) nerves, following the experiment in G. Statistical analysis was done using Mann Withney test, with *p < 0.05 and **p < 0.005. Graphs show average +S.E.M. blue and red denote dPV norm and dPV abl , respectively.
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A) Diagram depicting the 1-nerve stimulation assay designed to reveal the contribution of dPVs to motor activity evoked by stimulation of ipsilateral cutaneous nerves. Nerve cuffs were implanted on the right sural nerve and left saphenous nerve. <t>EMG</t> <t>electrodes</t> were implanted into the right and left semitendinosus (St, knee flexor), right vastus lateralis (VL, knee extensor), left tibialis anterior (TA, ankle flexor) and right and left gastrocnemius (Gs, ankle extensor). EMG responses were recorded from hindlimb flexors and extensors following stimulation of cutaneous nerves (saphenous / sural nerve). B) Example St EMG responses to stimulation of the right saphenous nerve at 5 times threshold (see methods) in dPV norm (top) and dPV abl (bottom), during the experiment described in D. C) Latency to response to stimulation of the saphenous (left) or sural (right) nerves of ipsilateral hindlimb muscles during the experiment depicted in D. D) Top-diagram of the 2-nerve stimulation assay applied to reveal if dPVs mediate sensory-evoked ipsilateral inhibition. Bottom-experiment timeline. Nerve cuffs and EMG electrodes were placed as in D. Stimulation of the contralateral cutaneous nerve (saphenous/ sural) alone (black lightning) was used to calculate the expected response in the absence of sensory evoked ipsilateral inhibition. Following, both nerves were stimulated (yellow lightning), with variable delays and compared to the expected response to reveal ipsilateral inhibition. E) Top-expected Gs EMG response to stimulation of a single cutaneous nerve in dPV abl (left) and dPV norm (right), averaged over 20 responses. Bottom-expected responses (black) superimposed on single trial responses to stimulation of both cutaneous nerves (yellow). Left-response to stimulation of both nerves (15 ms delay), shows a “dip” that is absent in the expected response, indicating ipsilateral inhibition. Right-no “dip” is seen (0 ms delay), suggesting a loss of inhibition. For each mouse and each muscle, the delay in which responses were best aligned was chosen for further analysis. F) Percent inhibition (the percentage of trials where inhibition was detected) in hindlimb muscles, mediated by ipsilateral saphenous (left) and ipsilateral sural (right) nerves, following the experiment in G. Statistical analysis was done using Mann Withney test, with *p < 0.05 and **p < 0.005. Graphs show average +S.E.M. blue and red denote dPV norm and dPV abl , respectively.
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A) Diagram depicting the 1-nerve stimulation assay designed to reveal the contribution of dPVs to motor activity evoked by stimulation of ipsilateral cutaneous nerves. Nerve cuffs were implanted on the right sural nerve and left saphenous nerve. <t>EMG</t> <t>electrodes</t> were implanted into the right and left semitendinosus (St, knee flexor), right vastus lateralis (VL, knee extensor), left tibialis anterior (TA, ankle flexor) and right and left gastrocnemius (Gs, ankle extensor). EMG responses were recorded from hindlimb flexors and extensors following stimulation of cutaneous nerves (saphenous / sural nerve). B) Example St EMG responses to stimulation of the right saphenous nerve at 5 times threshold (see methods) in dPV norm (top) and dPV abl (bottom), during the experiment described in D. C) Latency to response to stimulation of the saphenous (left) or sural (right) nerves of ipsilateral hindlimb muscles during the experiment depicted in D. D) Top-diagram of the 2-nerve stimulation assay applied to reveal if dPVs mediate sensory-evoked ipsilateral inhibition. Bottom-experiment timeline. Nerve cuffs and EMG electrodes were placed as in D. Stimulation of the contralateral cutaneous nerve (saphenous/ sural) alone (black lightning) was used to calculate the expected response in the absence of sensory evoked ipsilateral inhibition. Following, both nerves were stimulated (yellow lightning), with variable delays and compared to the expected response to reveal ipsilateral inhibition. E) Top-expected Gs EMG response to stimulation of a single cutaneous nerve in dPV abl (left) and dPV norm (right), averaged over 20 responses. Bottom-expected responses (black) superimposed on single trial responses to stimulation of both cutaneous nerves (yellow). Left-response to stimulation of both nerves (15 ms delay), shows a “dip” that is absent in the expected response, indicating ipsilateral inhibition. Right-no “dip” is seen (0 ms delay), suggesting a loss of inhibition. For each mouse and each muscle, the delay in which responses were best aligned was chosen for further analysis. F) Percent inhibition (the percentage of trials where inhibition was detected) in hindlimb muscles, mediated by ipsilateral saphenous (left) and ipsilateral sural (right) nerves, following the experiment in G. Statistical analysis was done using Mann Withney test, with *p < 0.05 and **p < 0.005. Graphs show average +S.E.M. blue and red denote dPV norm and dPV abl , respectively.
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A) Diagram depicting the 1-nerve stimulation assay designed to reveal the contribution of dPVs to motor activity evoked by stimulation of ipsilateral cutaneous nerves. Nerve cuffs were implanted on the right sural nerve and left saphenous nerve. <t>EMG</t> <t>electrodes</t> were implanted into the right and left semitendinosus (St, knee flexor), right vastus lateralis (VL, knee extensor), left tibialis anterior (TA, ankle flexor) and right and left gastrocnemius (Gs, ankle extensor). EMG responses were recorded from hindlimb flexors and extensors following stimulation of cutaneous nerves (saphenous / sural nerve). B) Example St EMG responses to stimulation of the right saphenous nerve at 5 times threshold (see methods) in dPV norm (top) and dPV abl (bottom), during the experiment described in D. C) Latency to response to stimulation of the saphenous (left) or sural (right) nerves of ipsilateral hindlimb muscles during the experiment depicted in D. D) Top-diagram of the 2-nerve stimulation assay applied to reveal if dPVs mediate sensory-evoked ipsilateral inhibition. Bottom-experiment timeline. Nerve cuffs and EMG electrodes were placed as in D. Stimulation of the contralateral cutaneous nerve (saphenous/ sural) alone (black lightning) was used to calculate the expected response in the absence of sensory evoked ipsilateral inhibition. Following, both nerves were stimulated (yellow lightning), with variable delays and compared to the expected response to reveal ipsilateral inhibition. E) Top-expected Gs EMG response to stimulation of a single cutaneous nerve in dPV abl (left) and dPV norm (right), averaged over 20 responses. Bottom-expected responses (black) superimposed on single trial responses to stimulation of both cutaneous nerves (yellow). Left-response to stimulation of both nerves (15 ms delay), shows a “dip” that is absent in the expected response, indicating ipsilateral inhibition. Right-no “dip” is seen (0 ms delay), suggesting a loss of inhibition. For each mouse and each muscle, the delay in which responses were best aligned was chosen for further analysis. F) Percent inhibition (the percentage of trials where inhibition was detected) in hindlimb muscles, mediated by ipsilateral saphenous (left) and ipsilateral sural (right) nerves, following the experiment in G. Statistical analysis was done using Mann Withney test, with *p < 0.05 and **p < 0.005. Graphs show average +S.E.M. blue and red denote dPV norm and dPV abl , respectively.
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A) Diagram depicting the 1-nerve stimulation assay designed to reveal the contribution of dPVs to motor activity evoked by stimulation of ipsilateral cutaneous nerves. Nerve cuffs were implanted on the right sural nerve and left saphenous nerve. EMG electrodes were implanted into the right and left semitendinosus (St, knee flexor), right vastus lateralis (VL, knee extensor), left tibialis anterior (TA, ankle flexor) and right and left gastrocnemius (Gs, ankle extensor). EMG responses were recorded from hindlimb flexors and extensors following stimulation of cutaneous nerves (saphenous / sural nerve). B) Example St EMG responses to stimulation of the right saphenous nerve at 5 times threshold (see methods) in dPV norm (top) and dPV abl (bottom), during the experiment described in D. C) Latency to response to stimulation of the saphenous (left) or sural (right) nerves of ipsilateral hindlimb muscles during the experiment depicted in D. D) Top-diagram of the 2-nerve stimulation assay applied to reveal if dPVs mediate sensory-evoked ipsilateral inhibition. Bottom-experiment timeline. Nerve cuffs and EMG electrodes were placed as in D. Stimulation of the contralateral cutaneous nerve (saphenous/ sural) alone (black lightning) was used to calculate the expected response in the absence of sensory evoked ipsilateral inhibition. Following, both nerves were stimulated (yellow lightning), with variable delays and compared to the expected response to reveal ipsilateral inhibition. E) Top-expected Gs EMG response to stimulation of a single cutaneous nerve in dPV abl (left) and dPV norm (right), averaged over 20 responses. Bottom-expected responses (black) superimposed on single trial responses to stimulation of both cutaneous nerves (yellow). Left-response to stimulation of both nerves (15 ms delay), shows a “dip” that is absent in the expected response, indicating ipsilateral inhibition. Right-no “dip” is seen (0 ms delay), suggesting a loss of inhibition. For each mouse and each muscle, the delay in which responses were best aligned was chosen for further analysis. F) Percent inhibition (the percentage of trials where inhibition was detected) in hindlimb muscles, mediated by ipsilateral saphenous (left) and ipsilateral sural (right) nerves, following the experiment in G. Statistical analysis was done using Mann Withney test, with *p < 0.05 and **p < 0.005. Graphs show average +S.E.M. blue and red denote dPV norm and dPV abl , respectively.

Journal: bioRxiv

Article Title: Inhibitory interneurons within the deep dorsal horn integrate convergent sensory input to regulate motor performance

doi: 10.1101/2022.05.21.492933

Figure Lengend Snippet: A) Diagram depicting the 1-nerve stimulation assay designed to reveal the contribution of dPVs to motor activity evoked by stimulation of ipsilateral cutaneous nerves. Nerve cuffs were implanted on the right sural nerve and left saphenous nerve. EMG electrodes were implanted into the right and left semitendinosus (St, knee flexor), right vastus lateralis (VL, knee extensor), left tibialis anterior (TA, ankle flexor) and right and left gastrocnemius (Gs, ankle extensor). EMG responses were recorded from hindlimb flexors and extensors following stimulation of cutaneous nerves (saphenous / sural nerve). B) Example St EMG responses to stimulation of the right saphenous nerve at 5 times threshold (see methods) in dPV norm (top) and dPV abl (bottom), during the experiment described in D. C) Latency to response to stimulation of the saphenous (left) or sural (right) nerves of ipsilateral hindlimb muscles during the experiment depicted in D. D) Top-diagram of the 2-nerve stimulation assay applied to reveal if dPVs mediate sensory-evoked ipsilateral inhibition. Bottom-experiment timeline. Nerve cuffs and EMG electrodes were placed as in D. Stimulation of the contralateral cutaneous nerve (saphenous/ sural) alone (black lightning) was used to calculate the expected response in the absence of sensory evoked ipsilateral inhibition. Following, both nerves were stimulated (yellow lightning), with variable delays and compared to the expected response to reveal ipsilateral inhibition. E) Top-expected Gs EMG response to stimulation of a single cutaneous nerve in dPV abl (left) and dPV norm (right), averaged over 20 responses. Bottom-expected responses (black) superimposed on single trial responses to stimulation of both cutaneous nerves (yellow). Left-response to stimulation of both nerves (15 ms delay), shows a “dip” that is absent in the expected response, indicating ipsilateral inhibition. Right-no “dip” is seen (0 ms delay), suggesting a loss of inhibition. For each mouse and each muscle, the delay in which responses were best aligned was chosen for further analysis. F) Percent inhibition (the percentage of trials where inhibition was detected) in hindlimb muscles, mediated by ipsilateral saphenous (left) and ipsilateral sural (right) nerves, following the experiment in G. Statistical analysis was done using Mann Withney test, with *p < 0.05 and **p < 0.005. Graphs show average +S.E.M. blue and red denote dPV norm and dPV abl , respectively.

Article Snippet: Two nerve cuff electrodes and six EMG recording electrodes were attached to the headpiece pin connector (female, SAM1153-12; DigiKey Electronics Thief River Falls, MN) and covered with 3D printed cap.

Techniques: Activity Assay, Inhibition