Spinoreticular neurons that receive group III input are inhibited by MLR stimulation

2002 ◽  
Vol 93 (1) ◽  
pp. 92-98 ◽  
Author(s):  
Alexandr M. Degtyarenko ◽  
Marc P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Tibial Nerve ◽  
Afferent Input ◽  
Ventrolateral Medulla ◽  
Central Command ◽  
Mesencephalic Locomotor Region ◽  
Group Iii ◽  
Tibial Nerve Stimulation ◽  
Muscle Afferent ◽  
Stimulation Of

In decerebrate paralyzed cats, we examined the responses of 18 spinoreticular neurons to electrical stimulation of the mesencephalic locomotor region. The activity of each of the spinoreticular neurons was recorded extracellularly from laminae IV through VI of the L7 and S1 spinal cord. In addition, each of the 18 spinoreticular neurons received group III afferent input from the tibial nerve. Spinoreticular projections were established for each of 18 neurons by antidromic invasion of the ventro lateral medulla at the P11 though P14 levels. The onset latencies and current thresholds for antidromic invasion from the ventro lateral medulla averaged 15.0 ± 3.8 ms and 117 ± 11 μA, respectively. Electrical stimulation of the mesencephalic locomotor region attenuated the spontaneous activity or the responses of each of the spinoreticular neurons to tibial nerve stimulation at currents that recruited group III afferents. Our data support the notion that thin-fiber muscle afferent input to the ventrolateral medulla is gated by a central command to exercise.

Central 5-HT1A modulation of cardiovascular responses to tibial nerve stimulation-evoked muscle contraction

1997 ◽  
Vol 272 (4) ◽  
pp. R1020-R1027 ◽  
Author(s):  
A. Ally ◽  
D. Caringi ◽  
D. M. Koester ◽  
T. Kobayashi ◽  
D. J. Mokler
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Muscle Tension ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Motor Threshold ◽  
Tibial Nerve Stimulation ◽  
Prior Administration ◽  
Stimulation Of

The effects of administering 8-hydroxy-2-(di-n-propylamine) tetralin [8-OH-DPAT, a serotonin 1A (5-HT1A) receptor agonist] into the rostral ventrolateral medulla (RVLM) on cardiovascular responses during tibial nerve stimulation-evoked muscle contraction were investigated using anesthetized rats. Stimulation of the tibial nerve (3 times motor threshold, 0.1 ms, 40 Hz) for 30 s increased mean arterial pressure (MAP), heart rate (HR), and muscle tension by 25 +/- 3 mmHg, 24 +/- 4 beats/min, and 299 +/- 35 g, respectively. Bilateral microdialysis of 8-OH-DPAT (10 mM) for 30 min attenuated the stimulation-evoked increases in MAP (8 +/- 2 mmHg) and HR (11 +/- 5 beats/min), without a change in muscle tension (292 +/- 30 g). However, administration of 1 mM 8-OH-DPAT had no effect on the cardiovascular responses. Thirty minutes of microdialysis of 8-OH-DPAT (10 mM) into the caudal ventrolateral medulla produced no effect on cardiovascular responses during muscle contraction. Prior administration of 10 mM 1-[2-methoxyphenyl]-4-[4-(2-phthalimido)-butyl]piperazine (NAN-190), a 5-HT1A receptor antagonist, for 30 min into the RVLM blocked the attenuating effects of subsequent microdialysis of 8-OH-DPAT (10 mM). Results suggest that activation of 5-HT1A receptors within the RVLM inhibit cardiovascular responses elicited during static muscle contraction.

scholarly journals Fatigue-incduced modulation of human soleus Hoffmann reflex under conditions of homosynaptic postactivation depression due to pair tibial nerve stimulation

2017 ◽  
Vol 74 (2) ◽  
pp. 55-59
Author(s):  
O. Kolosova
Keyword(s):  
Soleus Muscle ◽  
Tibial Nerve ◽  
Voluntary Contraction ◽  
H Reflex ◽  
Afferent Nerves ◽  
Tibial Nerve Stimulation ◽  
Static Contraction ◽  
Conditioned Responses ◽  
Postactivation Depression ◽  
Stimulation Of

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.

Central command, but not muscle reflex, stimulates cutaneous sympathetic efferents of cats

1998 ◽  
Vol 274 (5) ◽  
pp. H1552-H1559 ◽  
Author(s):  
Janeen M. Hill ◽  
Marc P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Blocking Agent ◽  
Muscle Afferents ◽  
Group Iii ◽  
Hairy Skin ◽  
Sympathetic Efferents ◽  
Muscle Reflex ◽  
Decerebrate Cats ◽  
Sympathetic Discharge ◽  
Stimulation Of

We determined the effects of stimulation of the mesencephalic locomotor region (MLR) and the muscle reflex, each evoked separately, on the discharge of cutaneous sympathetic fibers innervating the hairy skin of decerebrate cats. Electrical stimulation of the MLR was performed while the cats were paralyzed with vecuronium bromide. The muscle reflex was evoked while the cats were not paralyzed by electrical stimulation of the tibial nerve at current intensities that did not activate directly group III and IV muscle afferents. MLR stimulation increased, on average, the discharge of the 23 cutaneous sympathetic fibers tested ( P < 0.05). The muscle reflex, in contrast, had no overall effect on the discharge of 21 sympathetic fibers tested ( P > 0.05). Both maneuvers markedly increased mean arterial pressure and heart rate ( P < 0.05). Prevention of the baroreceptor reflex with the α-adrenergic blocking agent phentolamine did not reveal a stimulatory effect of the muscle reflex on cutaneous sympathetic discharge. We conclude that the MLR is a more important mechanism than is the muscle reflex in controlling sympathetic discharge to hairy skin during dynamic exercise.

Stimulation of the caudal ventrolateral medulla decreases total lung resistance in dogs

1987 ◽  
Vol 63 (3) ◽  
pp. 912-917 ◽  
Author(s):  
J. C. Connelly ◽  
L. W. McCallister ◽  
M. P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Adrenergic Blockade ◽  
Homocysteic Acid ◽  
Caudal Ventrolateral Medulla ◽  
Airway Caliber ◽  
Lung Resistance ◽  
Total Lung Resistance ◽  
Stimulation Of

Although the role played by the caudal ventrolateral medulla in the regulation of the cardiovascular system has been extensively investigated, little is known about the role played by this area in the regulation of airway caliber. Therefore, in alpha-chloralose-anesthetized dogs, we used both electrical and chemical means to stimulate the caudal ventrolateral medulla while we monitored changes in total lung resistance breath by breath. We found that electrical stimulation (25 microA) of 26 sites in this area significantly decreased total lung resistance from 7.1 +/- 0.4 to 5.7 +/- 0.3 cmH2O.1'1.s (P less than 0.001). The bronchodilation evoked by electrical stimulation was unaffected by beta-adrenergic blockade but was abolished by cholinergic blockade. In addition, chemical stimulation of seven sites in the caudal ventrolateral medulla with microinjections of DL-homocysteic acid (0.2 M; 66 nl), which stimulates cell bodies but not fibers of passage, also decreased total lung resistance from 8.3 +/- 1.1 to 6.5 +/- 0.8 cmH2O.l'1.s (P less than 0.01). In contrast, microinjections of DL-homocysteic acid into the nucleus ambiguus (n = 6) increased total lung resistance from 7.5 +/- 0.5 to 9.2 +/- 0.4 cmH2O.l'1.s (P less than 0.05). We conclude that the caudal ventrolateral medulla contains a pool of cell bodies whose excitation causes bronchodilation by withdrawing cholinergic input to airway smooth muscle.

Short-Latency Crossed Inhibitory Responses in the Human Soleus Muscle

2009 ◽  
Vol 102 (6) ◽  
pp. 3596-3605 ◽  
Author(s):  
Peter W. Stubbs ◽  
Natalie Mrachacz-Kersting
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Muscle Activation ◽  
Tibial Nerve ◽  
Voluntary Contraction ◽  
Short Latency ◽  
Afferent Feedback ◽  
Medial Plantar Nerve ◽  
Muscle Activation Patterns ◽  
Tibial Nerve Stimulation

Even though interlimb coordination is critical in bipedal locomotion, the role of muscle afferent mediated feedback is unknown. The aim of this study was to establish if ipsilateral muscle generated afferent feedback can influence contralateral muscle activation patterns in the human lower limb and to elucidate the mechanisms involved. The effect of ipsilateral tibial nerve stimulation on contralateral soleus (cSOL) responses were quantified. Three interventions were investigated, 1) electrical stimulation applied to the tibial nerve at stimulation intensities from 0 to 100% of maximal M-wave (M-max) with the cSOL contracted from 5 to 15% of maximal voluntary contraction (MVC) and 15 to 30% MVC, 2) ispsilateral tibial nerve stimulation at 75% M-max prior to, during, and following the application of ischemia to the ipsilateral thigh. 3) Electrical stimulation applied to the ipsilateral sural (SuN) and medial plantar nerves at stimulation intensities from 1 to 3 times perceptual threshold. A short-latency depression in the cSOL electromyogram (EMG; onset: 37–41 ms) was observed following ipsilateral tibial nerve stimulation. The magnitude of this depression increased ( P = 0.0005 and P = 0.000001) with increasing stimulus intensities. Ischemia delayed the time of the minimum of the cSOL depression ( P = 0.04). SuN and medial plantar nerve stimulation evoked a longer latency depression [average; 91.2 ms (SuN); 142 ms (medial plantar nerve)] and therefore do not contribute to the response. This is the first study to demonstrate a short-latency depression in the cSOL following ipsilateral tibial nerve stimulation. Due to its short latency, the response is spinally mediated. The involvement of crossed spinal interneurons receiving input from low-threshold muscle afferents is discussed.

Rostral ventrolateral medullary opioid receptor activation modulates pressor response to muscle contraction

1998 ◽  
Vol 274 (1) ◽  
pp. H139-H146 ◽  
Author(s):  
Daryl Caringi ◽  
David J. Mokler ◽  
David M. Koester ◽  
Ahmmed Ally
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Ventrolateral Medulla ◽  
Tibial Nerve Stimulation ◽  
Isometric Muscle Contraction ◽  
Isometric Muscle

The effects of an opioid agonist, [d-Ala2]methionine enkephalinamide (DAME), administered into the rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses to isometric muscle contraction were determined in anesthetized rats. A 30-s contraction evoked by tibial nerve stimulation increased mean arterial pressure (MAP) and heart rate (HR) by 34 ± 6 mmHg and 40 ± 7 beats/min, respectively, with a developed tension of 322 ± 30 g, after bilateral insertion of microdialysis probes into the rVLM. Thirty-minute dialysis of DAME (10 and 100 μM) attenuated the contraction-evoked cardiovascular changes dose dependently (10 μM: MAP = 25 ± 4 mmHg, HR = 27 ± 3 beats/min, tension = 333 ± 25 g; 100 μM: MAP = 14 ± 4 mmHg, HR = 16 ± 5 beats/min, tension = 330 ± 34 g). Preadministration of an opioid antagonist, naloxone (100 μM), augmented contraction-evoked MAP and HR responses and blocked effects of 100 μM DAME. Microdialysis of DAME into the cVLM produced no changes in the pressor response to contraction. At end of each experiment, tibial nerve stimulation after neuromuscular blockade evoked no MAP or HR change. Results demonstrate that opioid receptor activation within the rVLM modulates cardiovascular responses to isometric muscle contraction.

Effects of ventrolateral medullary AMPA-receptor antagonism on pressor response during muscle contraction

1997 ◽  
Vol 272 (6) ◽  
pp. H2774-H2781 ◽  
Author(s):  
T. Kobayashi ◽  
D. Caringi ◽  
D. J. Mokler ◽  
A. Ally
Keyword(s):  
Heart Rate ◽  
Muscle Contraction ◽  
Ampa Receptors ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Contrast Administration ◽  
Tibial Nerve Stimulation ◽  
Before And After

Effects of administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration that preferentially blocks alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors into rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses elicited during static muscle contraction were investigated using anesthetized rats. Two microdialysis probes were inserted bilaterally into either the rVLM or the cVLM using stereotaxic guides. A tibial nerve stimulation-evoked static muscle contraction for 30 s increased mean arterial pressure (MAP) and heart rate (HR) by 27 +/- 3 mmHg and 28 +/- 4 beats/min, respectively. Microdialysis of CNQX into the rVLM for 30 min attenuated the contraction-evoked increases in MAP and HR (10 +/- 2 mmHg and 12 +/- 2 beats/min). Developed tensions were similar during the contractions before and after microdialyzing CNQX. In contrast, administration of CNQX into the cVLM potentiated the muscle contraction-evoked cardiovascular responses (MAP, 25 +/- 4 vs. 39 +/- 6 mmHg; HR, 27 +/- 3 vs. 42 +/- 3 beats/min), with no change in developed tensions. Results demonstrate that AMPA receptors within the rVLM and the cVLM appear to play opposite modulatory roles in the central integration of cardiovascular responses elicited during static muscle contraction.

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