Cold stress alters characteristics of sympathetic  nerve discharge bursts

Kenney, Michael J.; Claassen, Dale E.; Fels, Richard J.; Saindon, Cristina S.

doi:10.1152/jappl.1999.87.2.732

Cited by 32 publications

(53 citation statements)

References 40 publications

(81 reference statements)

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“…Our current results, however, show that low doses of leptin that fail to alter baseline SNA potentiate the response of thermogenic SNA to hypothermia. It was demonstrated previously that experimental hypothermia produces regionally nonuniform alterations in sympathetic nerve traffic (12). This report, however, is the first to describe the effects of leptin on changes in SNA during hypothermia.…”

Section: Discussionmentioning

confidence: 65%

Leptin Potentiates Thermogenic Sympathetic Responses to Hypothermia

Hausberg

Morgan²,

Mitchell³

et al. 2002

Diabetes

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Leptin contributes to the regulation of thermogenesis. In rodents, sympathetic nerve activity efferent to interscapular brown adipose tissue (IBAT-SNA) is involved. On the basis of the hypotheses that 1) leptin acutely potentiates hypothermia-induced increases in IBAT-SNA; 2) this action of leptin is specific to IBAT-SNA, i.e., it does not occur with renal sympathetic nerve activity (R-SNA); and 3) this effect of leptin depends on intact and functional leptin receptors, we measured IBAT-SNA and R-SNA in anesthetized lean and dietinduced obese Sprague-Dawley and in obese Zucker rats, randomly assigned to low-dose leptin or vehicle. Before the start of leptin or vehicle and 5 min, 90 min, and 180 min after, hypothermia (30°C) was induced. Compared with vehicle, leptin did not significantly alter baseline R-SNA or IBAT-SNA. In lean Sprague-Dawley rats, hypothermia-induced increases in IBAT-SNA were significantly augmented by leptin but not by vehicle. In obese Sprague-Dawley rats, leptin did not potentiate hypothermia-induced increases in IBAT-SNA. In Zucker rats, IBAT-SNA did not increase with hypothermia and leptin was not able to induce sympathoactivation with cooling. Changes in R-SNA during hypothermia were not significantly modified by leptin in either group. Thus, low-dose leptin, although not altering baseline SNA, acutely enhances hypothermia-induced sympathetic outflow to IBAT in lean rats. This effect is specific for thermogenic SNA because leptin does not significantly alter the response of R-SNA to hypothermia. The effect depends on intact and functional leptin receptors because it occurs neither in rats with a leptin receptor defect nor in rats with acquired leptin resistance.

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Section: Discussionmentioning

confidence: 65%

Leptin Potentiates Thermogenic Sympathetic Responses to Hypothermia

Hausberg

Morgan²,

Mitchell³

et al. 2002

Diabetes

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“…Sympathetic nerve potentials were full-wave rectified and integrated (time constant 10 ms), which produced a smooth tracing of the synchronized discharges (15)(16)(17). The level of activity in sympathetic nerves was quantified after integration as volts times seconds and corrected for background noise after ganglionic blockade (15 mg/kg trimethaphan camsylate) (15)(16)(17).…”

Section: Methodsmentioning

confidence: 99%

“…Importantly, the pattern of electrical stimulation of sympathetic nerves can influence renal function (6), neurotransmitter release (30), and vascular responses (28). The SND bursting pattern can be altered during various experimental interventions, including hyperthermia (15) and hypothermia (16). Alterations in the SND bursting pattern during elevations in internal body temperature contribute to hyperthermia-induced increases in the level of sympathetic nerve activity (15), suggesting that pattern transformation is a strategy used for mediating sympathoexcitation to acute heat stress.…”

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confidence: 99%

Role of paraventricular nucleus in regulation of sympathetic nerve frequency components

Kenney

Weiss

Mendes

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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.-Autospectral and coherence analyses were used to determine the role of and interactions between paraventricular nucleus (PVN) nitric oxide, ␥-aminobutyric acid (GABA), and the N-methyl-D-aspartic acid (NMDA)-glutamate receptor in regulation of sympathetic nerve discharge (SND) frequency components in anesthetized rats. Four observations were made. First, PVN microinjection of bicuculline (BIC) (GABA A receptor antagonist), but not single PVN injections of NMDA (excitatory amino acid) or N G -monomethyl-L-arginine (L-NMMA; a nitric oxide synthase inhibitor), altered SND frequency components. Second, combined PVN microinjections of L-NMMA and NMDA changed the SND bursting pattern; however, the observed pattern change was different from that produced by PVN BIC and not observed after sinoaortic denervation. Third, PVN microinjection of kynurenic acid prevented and reversed BIC-induced changes in the SND bursting pattern. Finally, vascular resistance (renal and splenic) was significantly increased after PVN BIC microinjection despite the lack of change in the level of renal and splenic SND. These data demonstrate that the PVN contains the neural substrate for altering SND frequency components and suggest complex interactions between specific PVN neurotransmitters and between PVN neurotransmitters and the arterial baroreceptor reflex in SND regulation. coherence function; autospectral analysis; Sprague-Dawley rats; sympathetic nerve discharge THE PARAVENTRICULAR NUCLEUS (PVN) of the hypothalamus is an important central nervous system site for autonomic and neuroendocrine regulation (4,22,32,33). The PVN contains a complex profile of excitatory and inhibitory neurotransmitters and neuromodulators (33). With respect to sympathetic nerve discharge (SND) regulation, PVN glutamate, nitric oxide (NO), and ␥-aminobutyric acid (GABA) have received considerable attention.Ionotropic glutamate receptor subunit mRNAs are expressed in the PVN (10) and glutamate administration into the PVN of conscious rats increases heart rate (HR) (24), arterial pressure (AP) (12, 24), renal SND (12), and plasma norepinephrine concentrations (24).In addition, PVN microinjection of the excitatory amino acid, N-methyl-D-aspartic acid (NMDA), increases renal SND and AP in anesthetized rats (21), suggesting that activation of PVN NMDA receptors is excitatory to SND.The results of several studies (11, 37) suggest that PVN NO is inhibitory to SND. PVN microinjection of nitroprusside, an NO donor, decreases AP (11, 37, 38), HR (37, 38), and renal SND (37, 38), whereas PVN administration of the nitric oxide synthase inhibitor, N G -monomethyl-L-arginine (L-NMMA), increases AP, HR, and renal SND (37). Activation of the NMDA receptor in the PVN releases NO, which inhibits NMDA-mediated increases in SND (21), suggesting interactions between excitatory and inhibitory PVN neurotransmitters in SND regulation.Concerning GABA, several lines of evidence suggest that a PVN GABAergic system tonically inhibits SND (25,26). PVN microinjection of muscimol, a GABA r...

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“…For monitoring during the experiment and for subsequent data analysis, the filtered neurograms were routed to an oscilloscope and a nerve traffic analyzer. Sympathetic nerve potentials were full-wave rectified, integrated (time constant 10 ms) and quantified as volts ϫ seconds (V ⅐ s) (19,20,28,29). SND was corrected for background noise after administration of the ganglionic blocker, trimethaphan camsylate (10 -15 mg/kg iv).…”

Section: Methodsmentioning

confidence: 99%

“…Acute cold stress increases plasma concentrations of norepinephrine and epinephrine (18,26,46,52), changes the pattern of synchronized SND bursts (28), influences the frequency-domain relationships between discharge bursts in regionally selective sympathetic nerves (28), and produces nonuniform changes in the level of sympathetic nerve activity to selected target organs (28). With regard to the latter, hypothermia increases lumbar and decreases renal SND without significantly changing the level of activity in the splanchnic and adrenal nerves in anesthetized rats (28) and activates preganglionic cervical SND in anesthetized rabbits (27). Considering immune system regulation, hypothermia alters the activity of splenic natural killer cells (11,25,36), augments the production of inflammatory cytokines in a cell line of peripheral blood monocytes (15), and increases cytokine gene expression in cultures of peripheral blood mononuclear cells (49).…”

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confidence: 99%

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system

Ganta

Helwig²,

Blecha³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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. Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system. Am J Physiol Regul Integr Comp Physiol 291: R558 -R565, 2006. First published February 9, 2006 doi:10.1152/ajpregu.00846.2005.-Splenic nerve denervation abrogates enhanced splenic cytokine gene expression responses to acute heating, demonstrating that hyperthermia-induced activation of splenic sympathetic nerve discharge (SND) increases splenic cytokine gene expression. Hypothermia alters SND responses; however, the role of the sympathetic nervous system in mediating splenic cytokine gene expression responses to hypothermia is not known. The purpose of the present study was to determine the effect of hypothermia on the relationship between the sympathetic nervous system and splenic cytokine gene expression in anesthetized F344 rats. Gene expression analysis was performed using a microarray containing 112 genes, representing inflammatory cytokines, chemokines, cytokine/chemokine receptors and housekeeping genes. A subset of differentially expressed genes was verified by real-time RT-PCR analysis. Splenic SND was decreased significantly during cooling (core temperature decreased from 38 to 30°C) in splenicintact rats but remained unchanged in sham-cooled splenic-intact rats (core temperature maintained at 38°C). Hypothermia upregulated the transcripts of several genes, including, chemokine ligands CCL2, CXCL2, CXCL10, and CCL20, and interleukins IL-1␣, IL-1␤, and IL-6. Gene expression responses to hypothermia were similar for the majority of cytokine genes in splenic-intact and splenic-denervated rats. These results suggest that hypothermia-enhanced splenic cytokine gene expression is independent of splenic SND.hypothermia; splenic cytokine gene expression; splenic sympathetic nerve discharge EVIDENCE FROM THE DISCIPLINES of neuroscience and immunology demonstrate bidirectional communication pathways between the sympathetic nervous system and the immune system (2, 3, 13, 38). Sympathetic innervation to the spleen provides a connection between central sympathetic neural circuits and immunocompetent cells in the spleen (1,6,9,16,17). For example, chemical sympathectomy alters splenic T and B cell proliferation and natural killer cell activity (36 -40, 45) and diminishes splenic production of immunoglobulin M (31). Results of our recent studies demonstrate that in rats with intact splenic nerves, whole body hyperthermia (19) and central ANG II infusion (20) increase splenic sympathetic nerve discharge (SND) and the expression of selective splenic cytokine genes. Splenic cytokine gene expression responses to whole body hyperthermia and central ANG II infusion are significantly reduced in splenic nerve-denervated compared with splenic nerve-intact rats (19,20), suggesting that activation of splenic SND can enhance splenic cytokine gene expression.Hypothermia, a common side effect of extreme cold environments, anesthesia, and serious traumatic injuries, alters the sympathetic nervous system and immune system regula...

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Cold stress alters characteristics of sympathetic nerve discharge bursts

Cited by 32 publications

References 40 publications

Leptin Potentiates Thermogenic Sympathetic Responses to Hypothermia

Leptin Potentiates Thermogenic Sympathetic Responses to Hypothermia

Role of paraventricular nucleus in regulation of sympathetic nerve frequency components

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system

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