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.

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.

Extracellular serotonin changes in VLM during muscle contraction: effects of 5-HT1A-receptor activation

1997 ◽  
Vol 273 (6) ◽  
pp. H2899-H2909 ◽  
Author(s):  
Gudbjorn Asmundsson ◽  
Daryl Caringi ◽  
David J. Mokler ◽  
Toshio Kobayashi ◽  
Takeshi Ishide ◽  
...  
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Ventrolateral Medulla ◽  
Muscle Paralysis ◽  
Arterial Blood ◽  
Tibial Nerve Stimulation ◽  
Static Contraction

This study determined whether muscle contraction causes an increase in extracellular levels of serotonin (5-HT) in the rostral (rVLM) or caudal ventrolateral medulla (cVLM) in anesthetized rats. Muscle contraction, evoked by tibial nerve stimulation, increased mean arterial blood pressure (MAP) by 27 ± 4 mmHg ( n = 8). In addition, 5-HT levels in the rVLM were elevated by 65 ± 9% during the contraction ( n = 8). Results were similar over two repeated contractions. In contrast, muscle contraction increased MAP, but not 5-HT, levels in the cVLM ( n = 6). Tibial nerve stimulation after muscle paralysis had no effect on either MAP or 5-HT levels in both rVLM and cVLM. Microdialysis of a 5-HT1A agonist, 8-OH-DPAT (10 mM), into the rVLM for 30 min ( n = 6) blunted the MAP change and reduced 5-HT release during contraction. Administration of NAN-190, a 5-HT1A antagonist, into the rVLM had no effect on 5-HT release and cardiovascular responses during muscle contraction and blocked the changes in 5-HT, MAP, and heart rate to static contraction after subsequent microdialysis of 8-OH-DPAT. Results demonstrate that 5-HT levels in the rVLM increase during muscle contraction and that 5-HT1A-receptor activation in the rVLM blunts MAP response to muscle contraction via a decrease in the extracellular concentration of 5-HT.

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.

Role of ventrolateral medulla in reflex cardiovascular responses to activation of skin and muscle nerves

1995 ◽  
Vol 268 (6) ◽  
pp. R1464-R1471 ◽  
Author(s):  
P. Ruggeri ◽  
R. Ermirio ◽  
C. Molinari ◽  
F. R. Calaresu
Keyword(s):  
Nerve Stimulation ◽  
Sural Nerve ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Electrolytic Lesions ◽  
Cardiovascular Neurons ◽  
Muscle Nerve ◽  
Stimulation Of

Central neuronal circuits mediating reflex cardiovascular responses to skin and muscle nerve stimulation were studied in rats under urethan anesthesia. Responses of right rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) cardiovascular neurons to stimulation of contralateral skin and muscle afferent fibers were investigated. Stimulation of the tibial (muscle) nerve excited 19 (86%) of 22 CVLM neurons and inhibited 18 (82%) of 22 RVLM neurons. Stimulation of the sural (skin) nerve excited 20 (91%) of the 22 RVLM neurons but did not affect the firing rate of any of the 22 CVLM neurons. Electrolytic lesions of the CVLM abolished the depressor responses induced by stimulation of the tibial nerve without affecting the pressor response caused by sural nerve stimulation. Similarly, reversible blockade of the CVLM by microinjection of gamma-amino-butyric acid or CoCl2 abolished the depressor response to stimulation of the tibial nerve without affecting the pressor response induced by sural nerve stimulation. These results suggest that vasodepressor responses to muscle nerve activation are mediated by a neuronal inhibitory pathway to the RVLM relayed through the CVLM.

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.

scholarly journals Pudendal but not tibial nerve stimulation inhibits bladder contractions induced by stimulation of pontine micturition center in cats

2016 ◽  
Vol 310 (4) ◽  
pp. R366-R374 ◽  
Author(s):  
Timothy D. Lyon ◽  
Matthew C. Ferroni ◽  
Brian T. Kadow ◽  
Richard C. Slater ◽  
Zhaocun Zhang ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Area Under The Curve ◽  
Sympathetic Nerves ◽  
Detrusor Muscle ◽  
Tibial Nerve Stimulation ◽  
Parasympathetic Neurons ◽  
Bladder Disorders ◽  
Stimulation Of

This study examined the possibility that pudendal nerve stimulation (PNS) or tibial nerve stimulation (TNS) inhibits the excitatory pathway from the pontine micturition center (PMC) to the urinary bladder. In decerebrate cats under α-chloralose anesthesia, electrical stimulation of the PMC (40 Hz frequency, 0.2-ms pulse width, 10–25 s duration) using a microelectrode induced bladder contractions >20 cmH2O amplitude when the bladder was filled to 60–70% capacity. PNS or TNS (5 Hz, 0.2 ms) at two and four times the threshold (2T and 4T) to induce anal or toe twitch was applied to inhibit the PMC stimulation-induced bladder contractions. Propranolol, a nonselective β-adrenergic receptor antagonist, was administered intravenously (1 mg/kg iv) to determine the role of sympathetic pathways in PNS/TNS inhibition. PNS at both 2T and 4T significantly ( P < 0.05) reduced the amplitude and area under the curve of the bladder contractions induced by PMC stimulation, while TNS at 4T facilitated the bladder contractions. Propranolol completely eliminated PNS inhibition and TNS facilitation. This study indicates that PNS, but not TNS, inhibits PMC stimulation-induced bladder contractions via a β-adrenergic mechanism that may occur in the detrusor muscle as a result of reflex activity in lumbar sympathetic nerves. Neither PNS nor TNS activated a central inhibitory pathway with synaptic connections to the sacral parasympathetic neurons that innervate the bladder. Understanding the site of action involved in bladder neuromodulation is important for developing new therapies for bladder disorders.

Cobalt injections into the pedunculopontine nuclei attenuate the reflex diaphragmatic responses to muscle contraction in rats

2004 ◽  
Vol 96 (1) ◽  
pp. 301-307 ◽  
Author(s):  
Edward D. Plowey ◽  
Tony G. Waldrop
Keyword(s):  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Potential Role ◽  
Respiratory Activity ◽  
Tibial Nerve ◽  
Muscular Activity ◽  
Cardiovascular Responses ◽  
Pedunculopontine Nucleus ◽  
Hindlimb Muscle ◽  
Stimulation Of

Previous studies have suggested that neurons in the pedunculopontine nucleus (PPN) are activated during static muscle contraction. Furthermore, activation of the PPN, via electrical stimulation or chemical disinhibition, is associated with increases in respiratory activity observed via diaphragmatic electromyogram recordings. The present experiments address the potential for PPN involvement in the regulation of the reflex diaphragmatic responses to muscle contraction in chloralose-urethane anesthetized rats. Diaphragmatic responses to unilateral static hindlimb muscle contraction, evoked via electrical stimulation of the tibial nerve, were recorded before and subsequent to bilateral microinjections of a synaptic blockade agent (CoCl2) into the PPN. The peak reflex increases in respiratory frequency (9.0 ± 1.0 breaths/min) and minute integrated diaphragmatic electromyogram activity (14.6 ± 3.3 units/min) were attenuated after microinjection of CoCl2 into the PPN (2.6 ± 0.9 breaths/min and 4.6 ± 2.1 units/min, respectively). Consistent diaphragmatic responses were observed in the subset of animals that were barodenervated. Control experiments suggest no effects of PPN synaptic blockade on the cardiovascular responses to muscle contraction. The results are discussed in terms of a potential role for the PPN in modulation of the reflex respiratory adjustments that accompany muscular activity.

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