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.

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.

Interaction of the Sympathetic Nervous System with Vasopressin and Renin in the Maintenance of Blood Pressure in Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 313s-317s ◽  
Author(s):  
Peter Hatzinikolaou ◽  
Irene Gavras ◽  
William G. North ◽  
Hans R. Brunner ◽  
Haralambos Gavras
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Close Correlation ◽  
Chemical Sympathectomy ◽  
Resting Blood Pressure ◽  
Sympathetic Nervous ◽  
Angiotensin Blockade ◽  
Stimulation Of ◽  
Intact Rats

1. Anephric and intact rats were submitted sequentially to catecholamine depletion (‘chemical sympathectomy’) vasopressin inhibition and angiotensin blockade whilst blood pressure and plasma levels of each hormone were monitored. 2. Depletion of catecholamines to 15–25% of baseline levels was associated with significant fall of blood pressure. A close correlation existed between these variables. 3. Chemical sympathectomy caused stimulation of plasma vasopressin, which reached excessively high levels in anephric animals. These were inversely correlated with the levels of depleted catecholamines. 4. Vasopressin inhibition after chemical sympathectomy caused profound and lasting hypotension in anephric rats but only a transient small fall in blood pressure in intact rats. Angiotensin blockade after chemical sympathectomy in intact rats caused a transient small fall in blood pressure; subsequent vasopressin inhibition in these rats caused profound lasting hypotension. 5. It is concluded that resting blood pressure is mainly sustained by the sympathetic nervous system, whereas renin and vasopressin are important back-up mechanisms to maintain compromised blood pressure.

Chemical sympathectomy alters regulation of body weight during prolonged ICV leptin infusion

2003 ◽  
Vol 284 (4) ◽  
pp. E778-E787 ◽  
Author(s):  
Robert L. Dobbins ◽  
Lidia S. Szczepaniak ◽  
Weiguo Zhang ◽  
J. Denis McGarry
Keyword(s):  
Physical Activity ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Sympathetic Nervous System ◽  
Metabolic Rate ◽  
Resting Metabolic Rate ◽  
Chemical Sympathectomy ◽  
Sympathetic Nervous

To assess the importance of the sympathetic nervous system in regulating body weight during prolonged leptin infusion, we evaluated food intake, body weight, and physical activity in conscious, unrestrained rats. Initial studies illustrated that prolonged intracerebroventricular (ICV) infusion of leptin enhanced substrate oxidation so that adipose tissue lipid stores were completely ablated, and muscle triglyceride and liver glycogen stores were depleted. After neonatal chemical sympathectomy, changes in weight and food intake were compared in groups of sympathectomized (SYM) and control (CON) adult animals during ICV infusion of leptin. CON animals lost 60 ± 9 g over 10 days vs. 25 ± 3 g in the SYM animals when food intake was matched between the two groups. Greater weight loss despite similar energy intake points to an important role of the sympathetic nervous system in stimulating energy expenditure during ICV leptin infusion by increasing the resting metabolic rate, since no differences in physical activity were observed between CON and SYM groups. In conclusion, activation of the SNS by leptin increases energy expenditure by augmenting the resting metabolic rate.

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.

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