scholarly journals Effect of 6-Hydroxydopamine on Host Resistance against Listeria monocytogenes Infection

2001 ◽  
Vol 69 (12) ◽  
pp. 7234-7241 ◽  
Author(s):  
Tomisato Miura ◽  
Tsuyoshi Kudo ◽  
Akitomo Matsuki ◽  
Kenji Sekikawa ◽  
Yoh-Ichi Tagawa ◽  
...  
Keyword(s):  
Nervous System ◽  
Listeria Monocytogenes ◽  
Sympathetic Nervous System ◽  
Cell Cultures ◽  
Host Resistance ◽  
Chemical Sympathectomy ◽  
Tnf Α ◽  
Ifn Γ ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine

ABSTRACT Recent studies have shown that immunocompetent cells bear receptors of neuropeptides and neurotransmitters and that these ligands play roles in the immune response. In this study, the role of the sympathetic nervous system in host resistance against Listeria monocytogenes infection was investigated in mice pretreated with 6-hydroxydopamine (6-OHDA), which destroys sympathetic nerve termini. The norepinephrine contents of the plasma and spleens were significantly lower in 6-OHDA-treated mice than in vehicle-treated mice. The 50% lethal dose of L. monocytogenes was about 20 times higher for 6-OHDA-treated mice than for vehicle-treated mice. Chemical sympathectomy by 6-OHDA upregulated interleukin-12 (IL-12) and tumor necrosis factor-alpha (TNF-α) production in enriched dendritic cell cultures and gamma interferon (IFN-γ) and TNF-α production in spleen cell cultures, whereas chemical sympathectomy had no apparent effect on phagocytic activities, listericidal activities, and nitric oxide production in peritoneal exudate cells and splenic macrophages. Augmentation of host resistance against L. monocytogenesinfection by 6-OHDA was abrogated in IFN-γ−/− or TNF-α−/− mice, suggesting that upregulation of IFN-γ, IL-12, and TNF-α production may be involved in 6-OHDA-mediated augmentation of antilisterial resistance. Furthermore, adoptive transfer of spleen cells immune to L. monocytogenes from 6-OHDA-treated mice resulted in untreated naive recipients that had a high level of resistance against L. monocytogenesinfection. These results suggest that the sympathetic nervous system may modulate host resistance against L. monocytogenesinfection through regulation of production of IFN-γ, IL-12, and TNF-α, which are critical in antilisterial resistance.

Central and peripheral mechanisms of arterial pressure lability following baroreceptor denervation

1987 ◽  
Vol 65 (8) ◽  
pp. 1615-1618 ◽  
Author(s):  
R. H. Alper ◽  
H. J. Jacob ◽  
M. J. Brody
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Humoral Factors ◽  
Neural Transmission ◽  
Sympathetic Transmission ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine ◽  
Alpha Adrenergic Agonist ◽  
Arterial Pressure Lability

Deafferentation of sinoaortic baroreceptors produces a marked increase in the lability of arterial pressure that is sustained chronically. Studies reviewed in this paper were designed to determine the mechanisms responsible for generating arterial pressure lability. Pharmacological interruption of the humoral vasopressin and angiotensin systems failed to alter arterial pressure lability. In contrast, blockade of sympathetic nervous system transmission at both ganglionic and alpha-adrenergic receptor levels significantly attenuated lability. A similar effect was observed with the peripheral neurotoxin, 6-hydroxydopamine. After blockade of sympathetic transmission, a further reduction in lability was produced by blocking the renin–angiotensin or vasopressin systems. The dissociation of the level of arterial pressure from lability was achieved with parachloroamphetamine which raised arterial pressure but reduced lability. A substantial peripheral contribution to lability was obtained in experiments in which the alpha-adrenergic agonist, phenylephrine, produced a marked increase in lability in both normal and baroreceptor-denervated animals in which humoral and neural transmission were blocked. These data demonstrate that following baroreceptor deafferentation, arterial pressure lability is produced primarily by the sympathetic nervous system and secondarily by circulating humoral factors that appear to act on vascular smooth muscle to induce fluctuations in the level of arterial pressure.

Delayed stress-induced colonic hypersensitivity in male Wistar rats: role of neurokinin-1 and corticotropin-releasing factor-1 receptors

2004 ◽  
Vol 286 (4) ◽  
pp. G683-G691 ◽  
Author(s):  
Ines Schwetz ◽  
Sylvie Bradesi ◽  
James A. McRoberts ◽  
Marciano Sablad ◽  
Jerry C. Miller ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Wistar Rats ◽  
Corticotropin Releasing Factor ◽  
Chemical Sympathectomy ◽  
Visceromotor Response ◽  
Male Wistar Rats ◽  
Sympathetic Nervous ◽  
Neurokinin 1

The mechanism(s) underlying stress-induced colonic hypersensitivity (SICH) are incompletely understood. Our aims were to assess the acute and delayed (24 h) effect of water avoidance (WA) stress on visceral nociception in awake male Wistar rats and to evaluate the role of two stress-related modulation systems: the substance P/neurokinin-1 receptor (SP/NK1R) and the corticotropin-releasing factor (CRF)/CRF1 receptor (CRF/CRF1R) systems, as well as the possible involvement of the sympathetic nervous system. Visceral pain responses were measured as the visceromotor response to colorectal distension (CRD) at baseline, immediately after WA and again 24 h later. The NK1R antagonists RP-67580 and SR-140333 and the CRF1R antagonist CP-154526 were injected 15 min before WA or 1 h before the CRD on day 2. Chemical sympathectomy was performed by repeated injection of 6-hydroxydopamine. WA stress resulted in a significant increase in the visceromotor response on day 2, but no change immediately after WA. Injection of CP-154526 abolished delayed SICH when applied either before WA stress or before the CRD on day 2. Both NK1R antagonists only decreased SICH when injected before the CRD on day 2. Chemical sympathectomy did not affect delayed SICH. Our results indicate that in male Wistar rats, both NK1R and CRF1R activation, but not sympathetic nervous system activation, play a role in the development of SICH.

Circulatory and humoral responses of sympathectomized fetal sheep to hypoxemia

1983 ◽  
Vol 245 (5) ◽  
pp. H767-H772 ◽  
Author(s):  
H. S. Iwamoto ◽  
A. M. Rudolph ◽  
B. L. Mirkin ◽  
L. C. Keil
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Fetal Sheep ◽  
Vascular Responses ◽  
Fetal Survival ◽  
Placental Blood ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine ◽  
Humoral Responses

In fetal sheep, hypoxemia causes arterial hypertension, bradycardia, a redistribution of blood flow, and an increase in plasma vasopressin and catecholamine concentrations. To assess the role of the sympathetic nervous system in mediating these responses, we administered 6-hydroxydopamine to 11 chronically catheterized fetal sheep. Some of the responses to acute hypoxemia, achieved by administration of a low-O2 gas mixture to the ewe, were similar to those in intact fetal sheep. Fetal arterial O2 tension decreased from 22 +/- 3 to 12 +/- 3 (SD) Torr; fetal heart rate decreased transiently; combined ventricular output and umbilical-placental blood flow, as measured by the radionuclide-labeled microsphere technique, were maintained; cerebral, myocardial, and adrenal blood flow increased, and pulmonary blood flow decreased. However, there was no significant change in arterial pressure or blood flow to the peripheral, renal, and splanchnic circulations in the chemically sympathectomized fetuses in response to hypoxemia. The sympathetic nervous system is important in certain fetal vascular responses to hypoxemia but is not necessary for vascular responses in certain critical organs and thus is not crucial for fetal survival during hypoxia.

scholarly journals Sympathectomized tumor-bearing mice survive longer but develop bigger melanomas

2016 ◽  
Vol 50 (4) ◽  
pp. 207-214 ◽  
Author(s):  
L Horvathova ◽  
A Tillinger ◽  
A Padova ◽  
B Mravec
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Tumor Growth ◽  
Tumor Tissue ◽  
Melanoma Cells ◽  
Chemical Sympathectomy ◽  
Sympathetic Neurotransmission ◽  
Tumor Mass ◽  
Tumor Bearing ◽  
Sympathetic Nervous

AbstractObjectives. Previously we have shown that 20 days after the tumor cells injection smaller melanomas have been developed in chemically sympathectomized mice in comparison with animals having intact sympathetic nervous system. However, it is known that chemical sympathectomy reduces the sympathetic neurotransmission only temporarily. In the present study, we monitored the survival of the sympathectomized mice with melanoma with an attempt to find out how long the suppressing effect of sympathectomy on the melanoma growth may endure.Methods. The chemical sympathectomy was performed by intraperitoneal injection of neurotoxin 6-hydroxydopamine in male C57BL/6J mice. Seven days later, the animals were injected subcutaneously with B16-F10 melanoma cells. Then, melanoma development, survival of the tumor-bearing mice and weight of the developed tumor mass were analyzed.Results. Sympathectomy delayed the development of the palpable tumors (18th day vs.14th day) and significantly prolonged the survival of the tumor-bearing mice (median 34 days vs. 29 days). However, the weight of the developed melanoma was significantly increased in the sympathectomized mice in comparison with the animals having intact sympathetic nervous system.Conclusions. The data of the present study showed that effect of the chemical sympathectomy, performed before the tumor growth induction, persisted even at the time when sympathetic nerves started to regenerate that resulted in a prolonged survival of the mice with melanoma. However, comparing to our previous study, in which we have shown a reduced tumor mass in earlier stages of the tumor growth, specifically 20 days after melanoma cells injection, now we indicate that in later stages of the melanoma progression, the tumor mass was significantly increased in sympathectomized animals. These contra-intuitive findings may indicate that interventions affecting the sympathetic nervous system may exert complex effect on the tumor progression. Based on these data we may suggest that the potential therapeutic interventions affecting the sympathetic signaling in the tumor tissue and its microenvironment should attenuate the sympathetic neurotransmission not only temporarily but till the complete regression of the tumor tissue.

Sympathectomy and beta-adrenergic blockade during lung maturation stimulated by TRH and cortisol in fetal sheep

1993 ◽  
Vol 75 (1) ◽  
pp. 141-147 ◽  
Author(s):  
J. C. Schellenberg ◽  
G. C. Liggins ◽  
J. A. Kitterman ◽  
C. C. Lee
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Adrenergic Blockade ◽  
Lung Maturation ◽  
Fetal Sheep ◽  
Beta Adrenergic ◽  
Adrenergic Mechanisms ◽  
Adrenergic Blocker ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine

To test whether beta-adrenergic mechanisms and the sympathetic nervous system are involved in the synergistic action of thyrotropin-releasing hormone (TRH) and cortisol on lung maturation, fetal sheep (n = 32) were infused from 121 to 128 days of gestation with saline, TRH + cortisol, TRH + cortisol + beta-adrenergic blocker, or TRH + cortisol after chemical sympathectomy with 6-hydroxydopamine. TRH + cortisol increased lung distensibility and stability and alveolar concentrations of saturated phosphatidylcholine two- to threefold over control fetuses. beta-Adrenergic blockade prevented the increase in distensibility in response to TRH + cortisol. Sympathectomy did not impair the increase in distensibility and stability in response to TRH + cortisol but inhibited the increase in alveolar total phospholipids. Tissue concentrations of saturated phosphatidylcholine increased in TRH + cortisol-treated fetuses after either sympathectomy or beta-adrenergic blockade. We concluded that during lung maturation by TRH + cortisol 1) sympathetic mechanisms are requisite for surfactant release, 2) nonneurogenic beta-adrenergic mechanisms are requisite for the maturation of the mechanical properties of the lung and 3) stimulation of surfactant synthesis is independent of beta-adrenergic action and the sympathetic nervous system.

Low back pain in athletes can be controlled with acupuncture by a catecholaminergic pathway: clinical trial

2020 ◽  
Vol 38 (6) ◽  
pp. 388-395 ◽  
Author(s):  
Lourdes Arriaga-Pizano ◽  
Daniel Cuauhtémoc Gómez-Jiménez ◽  
Luis Angel Flores-Mejía ◽  
Yobana Pérez-Cervera ◽  
Carlos Josué Solórzano-Mata ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Nervous System ◽  
Low Back Pain ◽  
Back Pain ◽  
Sympathetic Nervous System ◽  
Pharmacological Treatment ◽  
Enzyme Linked Immunosorbent Assay ◽  
Low Back ◽  
Tnf Α ◽  
Sympathetic Nervous

Background: Activation of the sympathetic nervous system attenuates inflammation via catecholamines. Recent evidence has shown that electroacupuncture (EA) activates neuronal networks involved in the release of dopamine and norepinephrine that control systemic inflammation. In muscle, catecholamines are related to cyclic adenosine monophosphate (cAMP). This signaling molecule has been implicated in recovery from sustained contractile activity, which may induce muscular pain, such as that which occurs during low back pain (LBP). Objective: Our aim was to evaluate the effects of EA used for the control of LBP on the activation of the sympathetic nervous system in a randomized controlled clinical trial in athletes. Methods: Two groups of athletes with acute or chronic low back pain were studied. EA, sham EA and pharmacological treatment (diclofenac sodium) were evaluated. The outcome measures included a pain score represented by a visual analogue scale (VAS) and serum levels of catecholamines quantified by enzyme-linked immunosorbent assay. In addition, blood was collected into chilled heparin tubes, placed in 96-well cell culture plates and incubated with an equal volume of Roswell Park Memorial Institute (RPMI) medium, with lipopolysaccharide (LPS) alone or with catecholamines. Tumor necrosis factor (TNF)-α levels in the supernatants were analyzed. Results: The results indicated that the initial pain ratings did not differ between the groups analyzed. EA induced epinephrine secretion but not norepinephrine or dopamine secretion. Although EA and pharmacological treatment did not differ in terms of pain relief, in vitro epinephrine and norepinephrine reduced TNF-α production in response to LPS stimuli. Conclusion: EA activates the sympathetic nervous system and induces the release of epinephrine, which could ameliorate inflammation and protect muscular tissue in addition to relieving pain.

Comparison of the Visceral Antinociceptive Effects of Spinally Administered MPV-2426 (Fadolmidine) and Clonidine in the Rat

2003 ◽  
Vol 98 (1) ◽  
pp. 189-194 ◽  
Author(s):  
Antti Pertovaara ◽  
Jaakko Kalmari
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Antinociceptive Effect ◽  
Descending Pathways ◽  
Colorectal Distension ◽  
Adrenoceptor Agonist ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine ◽  
Dose Dependent

Background The authors determined the visceral antinociceptive effect induced by MPV-2426 (fadolmidine), a selective alpha 2 -adrenoceptor agonist, in rats with and without inflammation of the colon. They also determined whether the sympathetic nervous system or intact descending pathways are critical for the alpha 2 -adrenoceptor-induced visceral antinociception. Methods Spinal neuronal responses evoked by colorectal distension were recorded in pentobarbitone-anesthetized rats. MPV-2426 was administered onto the spinal cord. Clonidine was used as a reference alpha 2 -adrenoceptor agonist. Inflammation of the colon was induced by turpentine. Sympathectomy was induced by 6-hydroxydopamine. A midthoracic transection of the spinal cord was performed to study the role of descending pathways. Results Spinal administration of MPV-2426 produced a dose-dependent attenuation of responses evoked by colorectal distension, and this effect was of the same percentual magnitude in inflamed as in noninflamed animals. Clonidine and MPV-2426 induced equipotent visceral antinociception. The effect by spinally administered MPV-2426 was enhanced by a chemical sympathectomy but not influenced by spinal transection. Conclusions Spinally administered MPV-2426 produces a dose-dependent visceral antinociception as well in animals with an inflammation of the colon as in controls. The visceral antinociceptive effect induced by spinal MPV-2426 is equipotent to that of spinal clonidine. An intact sympathetic nervous system or intact brainstem-spinal pathway is not critical for the MPV-2426-induced visceral antinociception.

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