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Jon E Welch - One of the best experts on this subject based on the ideXlab platform.
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stress and endotoxin induced increases in brain tryptophan and serotonin metabolism depend on sympathetic nervous system activity
Journal of Neurochemistry, 1991Co-Authors: Adrian J. Dunn, Jon E WelchAbstract:: Stressful treatments and immune challenges have been shown previously to elevate brain concentrations of tryptophan. The role of the autonomic nervous system in this neurochemical change was investigated using pharmacological treatments that inhibit autonomic effects. Pretreatment with the Ganglionic Blocker chlorisondamine did not alter the normal increases in catecholamine metabolites, but prevented the increase in brain tryptophan normally observed after footshock or restraint, except when the duration of the footshock period was extended to 60 min. The footshock-and restraint-related increases in 5-hydroxyindoleacetic acid (5-HIAA) were also prevented by chlorisondamine. The increases in brain tryptophan caused by intraperitoneal injection of endotoxin or interleukin-1 (IL-1) were also prevented by chlorisondamine pretreatment. The footshock-induced increases in brain tryptophan and 5-HIAA were attenuated by the β-adrenergic antagonist propranolol but not by the α-adrenergic antagonist phenoxybenzamine or the muscarinic cholinergic antagonist atropine. Thus the autonomic nervous system appears to be involved in the stress-related changes in brain tryptophan, and this effect is due to the sympathetic rather than the parasympathetic limb of the system. Moreover, the main effect of the sympathetic nervous system is exerted on β-as opposed to α-adrenergic receptors. We conclude that activation of the sympathetic nervous system is responsible for the stress-related increases in brain tryptophan, probably by enabling increased brain tryptophan uptake. Endotoxin and IL-1 also elevate brain tryptophan, presumably by a similar mechanism. The increase in brain tryptophan appears to be necessary to sustain the increased serotonin catabolism to S-HIAA that occurs in stressed animals, and which may reflect increased serotonin release.
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Stress- and endotoxin-induced increases in brain tryptophan and serotonin metabolism depend on sympathetic nervous system activity.
Journal of Neurochemistry, 1991Co-Authors: Adrian J. Dunn, Jon E WelchAbstract:: Stressful treatments and immune challenges have been shown previously to elevate brain concentrations of tryptophan. The role of the autonomic nervous system in this neurochemical change was investigated using pharmacological treatments that inhibit autonomic effects. Pretreatment with the Ganglionic Blocker chlorisondamine did not alter the normal increases in catecholamine metabolites, but prevented the increase in brain tryptophan normally observed after footshock or restraint, except when the duration of the footshock period was extended to 60 min. The footshock- and restraint-related increases in 5-hydroxyindoleacetic acid (5-HIAA) were also prevented by chlorisondamine. The increases in brain tryptophan caused by intraperitoneal injection of endotoxin or interleukin-1 (IL-1) were also prevented by chlorisondamine pretreatment. The footshock-induced increases in brain tryptophan and 5-HIAA were attenuated by the beta-adrenergic antagonist propranolol but not by the alpha-adrenergic antagonist phenoxybenzamine or the muscarinic cholinergic antagonist atropine. Thus the autonomic nervous system appears to be involved in the stress-related changes in brain tryptophan, and this effect is due to the sympathetic rather than the parasympathetic limb of the system. Moreover, the main effect of the sympathetic nervous system is exerted on beta- as opposed to alpha-adrenergic receptors. We conclude that activation of the sympathetic nervous system is responsible for the stress-related increases in brain tryptophan, probably by enabling increased brain tryptophan uptake. Endotoxin and IL-1 also elevate brain tryptophan, presumably by a similar mechanism. The increase in brain tryptophan appears to be necessary to sustain the increased serotonin catabolism to 5-HIAA that occurs in stressed animals, and which may reflect increased serotonin release.
Adrian J. Dunn - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms and Significance of the Increased Brain Uptake of Tryptophan
Neurochemical Research, 2005Co-Authors: Natalie R. Lenard, Adrian J. DunnAbstract:Changes in brain tryptophan concentrations may affect the synthesis of brain serotonin (5-hydroxytryptamine, 5-HT). Concentrations of tryptophan are regulated more than those of any other amino acid. Such stimuli as acute stress, carbohydrate ingestion, and treatment with various drugs increase the brain content of tryptophan. Treatment of rats and mice with interleukin-1 (IL-1), interleukin-6 (IL-6), lipopolysaccharide (LPS), and β-adrenoceptor agonists, as well as a variety of stressors, such as footshock and restraint, all increase brain concentrations of tryptophan. The peak effect following both acute stress and β-adrenoceptor agonist administration occurs within 30–60 min, whereas the peak effect following LPS and the cytokines occurs much later at around 4–8 h. Experiments using the Ganglionic Blocker chlorisondamine, and β-adrenoceptor antagonists suggest that the sympathetic nervous system plays an important role in the modulation of brain tryptophan concentrations. The mechanisms involved in the increases observed in brain tryptophan are discussed, as well as their possible biological significance.
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stress and endotoxin induced increases in brain tryptophan and serotonin metabolism depend on sympathetic nervous system activity
Journal of Neurochemistry, 1991Co-Authors: Adrian J. Dunn, Jon E WelchAbstract:: Stressful treatments and immune challenges have been shown previously to elevate brain concentrations of tryptophan. The role of the autonomic nervous system in this neurochemical change was investigated using pharmacological treatments that inhibit autonomic effects. Pretreatment with the Ganglionic Blocker chlorisondamine did not alter the normal increases in catecholamine metabolites, but prevented the increase in brain tryptophan normally observed after footshock or restraint, except when the duration of the footshock period was extended to 60 min. The footshock-and restraint-related increases in 5-hydroxyindoleacetic acid (5-HIAA) were also prevented by chlorisondamine. The increases in brain tryptophan caused by intraperitoneal injection of endotoxin or interleukin-1 (IL-1) were also prevented by chlorisondamine pretreatment. The footshock-induced increases in brain tryptophan and 5-HIAA were attenuated by the β-adrenergic antagonist propranolol but not by the α-adrenergic antagonist phenoxybenzamine or the muscarinic cholinergic antagonist atropine. Thus the autonomic nervous system appears to be involved in the stress-related changes in brain tryptophan, and this effect is due to the sympathetic rather than the parasympathetic limb of the system. Moreover, the main effect of the sympathetic nervous system is exerted on β-as opposed to α-adrenergic receptors. We conclude that activation of the sympathetic nervous system is responsible for the stress-related increases in brain tryptophan, probably by enabling increased brain tryptophan uptake. Endotoxin and IL-1 also elevate brain tryptophan, presumably by a similar mechanism. The increase in brain tryptophan appears to be necessary to sustain the increased serotonin catabolism to S-HIAA that occurs in stressed animals, and which may reflect increased serotonin release.
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Stress- and endotoxin-induced increases in brain tryptophan and serotonin metabolism depend on sympathetic nervous system activity.
Journal of Neurochemistry, 1991Co-Authors: Adrian J. Dunn, Jon E WelchAbstract:: Stressful treatments and immune challenges have been shown previously to elevate brain concentrations of tryptophan. The role of the autonomic nervous system in this neurochemical change was investigated using pharmacological treatments that inhibit autonomic effects. Pretreatment with the Ganglionic Blocker chlorisondamine did not alter the normal increases in catecholamine metabolites, but prevented the increase in brain tryptophan normally observed after footshock or restraint, except when the duration of the footshock period was extended to 60 min. The footshock- and restraint-related increases in 5-hydroxyindoleacetic acid (5-HIAA) were also prevented by chlorisondamine. The increases in brain tryptophan caused by intraperitoneal injection of endotoxin or interleukin-1 (IL-1) were also prevented by chlorisondamine pretreatment. The footshock-induced increases in brain tryptophan and 5-HIAA were attenuated by the beta-adrenergic antagonist propranolol but not by the alpha-adrenergic antagonist phenoxybenzamine or the muscarinic cholinergic antagonist atropine. Thus the autonomic nervous system appears to be involved in the stress-related changes in brain tryptophan, and this effect is due to the sympathetic rather than the parasympathetic limb of the system. Moreover, the main effect of the sympathetic nervous system is exerted on beta- as opposed to alpha-adrenergic receptors. We conclude that activation of the sympathetic nervous system is responsible for the stress-related increases in brain tryptophan, probably by enabling increased brain tryptophan uptake. Endotoxin and IL-1 also elevate brain tryptophan, presumably by a similar mechanism. The increase in brain tryptophan appears to be necessary to sustain the increased serotonin catabolism to 5-HIAA that occurs in stressed animals, and which may reflect increased serotonin release.
Mark S. Blumberg - One of the best experts on this subject based on the ideXlab platform.
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Effects of antihypertensive drugs on ultrasound production and cardiovascular responses in 15-day-old rats.
Behavioural brain research, 2002Co-Authors: Mark S. Blumberg, Greta Sokoloff, Robert F. Kirby, Tricia G Knoot, Sean J LewisAbstract:When exposed to extreme cold or injected with the alpha(2)-adrenoceptor agonist, clonidine, infant rats emit ultrasonic vocalizations (USVs). Based upon the cardiovascular changes that accompany these two manipulations, especially decreased venous return, it was hypothesized that USVs are the acoustic by-product of the abdominal compression reaction (ACR), a maneuver that increases venous return. If this hypothesis is correct, then other anithypertensive drugs that decrease venous return should evoke USVs. In Experiment 1, sodium nitroprusside (SNP, 400 microg/kg), a direct-acting dilator of arteries and veins, was administered to 15-day-old rats under thermoneutral conditions while cardiac rate and ultrasound production were monitored. In Experiment 2, femoral artery pressure was monitored after SNP administration. Infants responded to SNP administration with decreased arterial pressure and tachycardia and, in addition, significantly increased ultrasound production. In Experiment 3, chlorisondamine (5 mg/kg), a Ganglionic Blocker that causes vasodilation and bradycardia, and hydralazine (20 mg/kg), a selective dilator of arteries, was administered to 15-day-olds. As predicted, chlorisondamine evoked ultrasound production and hydralazine did not. These results introduce SNP and chlorisondamine as only the second and third known agents capable of independently evoking USVs in thermoneutral conditions, and provide further support for the notion that ultrasound production is triggered by decreased venous return.
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Effects of antihypertensive drugs on ultrasound production and cardiovascular responses in 15-day-old rats
2001Co-Authors: Mark S. Blumberg, Greta Sokoloff, Robert F. Kirby, Tricia G Knoot, Sean J LewisAbstract:When exposed to extreme cold or injected with the 2-adrenoceptor agonist, clonidine, infant rats emit ultrasonic vocalizations (USVs). Based upon the cardiovascular changes that accompany these two manipulations, especially decreased venous return, it was hypothesized that USVs are the acoustic by-product of the abdominal compression reaction (ACR), a maneuver that increases venous return. If this hypothesis is correct, then other anithypertensive drugs that decrease venous return should evoke USVs. In Experiment 1, sodium nitroprusside (SNP, 400 g/kg), a direct-acting dilator of arteries and veins, was administered to 15-day-old rats under thermoneutral conditions while cardiac rate and ultrasound production were monitored. In Experiment 2, femoral artery pressure was monitored after SNP administration. Infants responded to SNP administration with decreased arterial pressure and tachycardia and, in addition, significantly increased ultrasound production. In Experiment 3, chlorisondamine (5 mg/kg), a Ganglionic Blocker that causes vasodilation and bradycardia, and hydralazine (20 mg/kg), a selective dilator of arteries, was administered to 15-day-olds. As predicted, chlorisondamine evoked ultrasound production and hydralazine did not. These results introduce SNP and chlorisondamine as only the second and third known agents capable of independently evoking USVs in thermoneutral conditions, and provide further support for the notion that ultrasound production is triggered by decrease
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Further evidence that BAT thermogenesis modulates cardiac rate in infant rats
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1998Co-Authors: Greta Sokoloff, Robert F. Kirby, Mark S. BlumbergAbstract:Previous research in infant rats suggested that brown adipose tissue (BAT), by providing warm blood to the heart during moderate cold exposure, protects cardiac rate. This protective role for BAT thermogenesis was examined further in the present study. In experiment 1, 1-wk-old rats in a warm environment were pretreated with saline or chlorisondamine (a Ganglionic Blocker), and then BAT thermogenesis was stimulated by injection with the β3-agonist CL-316243. Inexperiment 2, pups were pretreated with chlorisondamine and injected with CL-316243, and after BAT thermogenesis was stimulated the interscapular region of the pups was cooled externally with a thermode. In both experiments, cardiac rate, oxygen consumption, and physiological temperatures were monitored. Activation of BAT thermogenesis substantially increased cardiac rate in saline- and chlorisondamine-treated pups, and focal cooling of the interscapular region was sufficient to lower cardiac rate. The results of these studies support the hypothesis...
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Active sleep in cold-exposed infant Norway rats and Syrian golden hamsters: the role of brown adipose tissue thermogenesis. Behav Neurosci 112:695–706
1998Co-Authors: Greta Sokoloff, Mark S. BlumbergAbstract:It was previously hypothesized that brown adipose tissue (BAT) thermogenesis helps to maintain high rates of myoclonic twitching during cold exposure in infant rats (M. S. Blumberg & M. A. Stolba, 1996). To test his hypothesis, the sensitivity of twitching to various levels of cold exposure was assessed in week-old rats that were untreated or whose BAT thermogenesis was inhibited using a Ganglionic Blocker. Because week-old golden hamsters do not exhibit BAT thermogenesis, their sleep behaviors during cold exposure also were examined. Additional investigations in infant rats were conducted inwhich supplemental heat was provided to the interscapular region using a thermode and in which BAT was activated pharmacologically in Ganglionically blocked pups. The results support he hypothesis that myoclonic twitching is sensitive to the prevailing air temperature and the activation of BAT thermogenesis. Brown adipose tissue (BAT) thermogenesis is a primary means of endogenous heat production in mammalian i fants (Brtick, 1992; Nedergaard, Connolly, & Cannon, 1986). Week-old rats during moderate cold exposure (i.e., air temperatures between 25-34 °C; see Blumberg & Sokoloff, in press) increase BAT thermogenesis, maintain cardiac rate, and do not emit ultrasonic vocalizations. In contrast, ex-treme cold exposure (i.e., air temperatures below 25 °C) overwhelm the ability of BAT thermogenesis to compensate for heat loss, resulting in bradycardia and ultrasound produc
Greta Sokoloff - One of the best experts on this subject based on the ideXlab platform.
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Further evidence that BAT thermogenesis modulates cardiac rate in infant rats
2014Co-Authors: Greta Sokoloff, Robert F. Kirby, S. Blumberg, Mark S. BlumAbstract:berg. Further evidence that BAT thermogenesis modulates cardiac rate in infant rats. Am. J. Physiol. 274 (Regulatory Integrative Comp. Physiol. 43): R1712–R1717, 1998.— Previous research in infant rats suggested that brown adi-pose tissue (BAT), by providing warm blood to the heart during moderate cold exposure, protects cardiac rate. This protective role for BAT thermogenesis was examined further in the present study. In experiment 1, 1-wk-old rats in a warm environment were pretreated with saline or chlorisondamine (a Ganglionic Blocker), and then BAT thermogenesis was stimulated by injection with the b3-agonist CL-316243. In experiment 2, pups were pretreated with chlorisondamine and injected with CL-316243, and after BAT thermogenesis was stimulated the interscapular region of the pups was cooled externally with a thermode. In both experiments
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Effects of antihypertensive drugs on ultrasound production and cardiovascular responses in 15-day-old rats.
Behavioural brain research, 2002Co-Authors: Mark S. Blumberg, Greta Sokoloff, Robert F. Kirby, Tricia G Knoot, Sean J LewisAbstract:When exposed to extreme cold or injected with the alpha(2)-adrenoceptor agonist, clonidine, infant rats emit ultrasonic vocalizations (USVs). Based upon the cardiovascular changes that accompany these two manipulations, especially decreased venous return, it was hypothesized that USVs are the acoustic by-product of the abdominal compression reaction (ACR), a maneuver that increases venous return. If this hypothesis is correct, then other anithypertensive drugs that decrease venous return should evoke USVs. In Experiment 1, sodium nitroprusside (SNP, 400 microg/kg), a direct-acting dilator of arteries and veins, was administered to 15-day-old rats under thermoneutral conditions while cardiac rate and ultrasound production were monitored. In Experiment 2, femoral artery pressure was monitored after SNP administration. Infants responded to SNP administration with decreased arterial pressure and tachycardia and, in addition, significantly increased ultrasound production. In Experiment 3, chlorisondamine (5 mg/kg), a Ganglionic Blocker that causes vasodilation and bradycardia, and hydralazine (20 mg/kg), a selective dilator of arteries, was administered to 15-day-olds. As predicted, chlorisondamine evoked ultrasound production and hydralazine did not. These results introduce SNP and chlorisondamine as only the second and third known agents capable of independently evoking USVs in thermoneutral conditions, and provide further support for the notion that ultrasound production is triggered by decreased venous return.
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Effects of antihypertensive drugs on ultrasound production and cardiovascular responses in 15-day-old rats
2001Co-Authors: Mark S. Blumberg, Greta Sokoloff, Robert F. Kirby, Tricia G Knoot, Sean J LewisAbstract:When exposed to extreme cold or injected with the 2-adrenoceptor agonist, clonidine, infant rats emit ultrasonic vocalizations (USVs). Based upon the cardiovascular changes that accompany these two manipulations, especially decreased venous return, it was hypothesized that USVs are the acoustic by-product of the abdominal compression reaction (ACR), a maneuver that increases venous return. If this hypothesis is correct, then other anithypertensive drugs that decrease venous return should evoke USVs. In Experiment 1, sodium nitroprusside (SNP, 400 g/kg), a direct-acting dilator of arteries and veins, was administered to 15-day-old rats under thermoneutral conditions while cardiac rate and ultrasound production were monitored. In Experiment 2, femoral artery pressure was monitored after SNP administration. Infants responded to SNP administration with decreased arterial pressure and tachycardia and, in addition, significantly increased ultrasound production. In Experiment 3, chlorisondamine (5 mg/kg), a Ganglionic Blocker that causes vasodilation and bradycardia, and hydralazine (20 mg/kg), a selective dilator of arteries, was administered to 15-day-olds. As predicted, chlorisondamine evoked ultrasound production and hydralazine did not. These results introduce SNP and chlorisondamine as only the second and third known agents capable of independently evoking USVs in thermoneutral conditions, and provide further support for the notion that ultrasound production is triggered by decrease
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Further evidence that BAT thermogenesis modulates cardiac rate in infant rats
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1998Co-Authors: Greta Sokoloff, Robert F. Kirby, Mark S. BlumbergAbstract:Previous research in infant rats suggested that brown adipose tissue (BAT), by providing warm blood to the heart during moderate cold exposure, protects cardiac rate. This protective role for BAT thermogenesis was examined further in the present study. In experiment 1, 1-wk-old rats in a warm environment were pretreated with saline or chlorisondamine (a Ganglionic Blocker), and then BAT thermogenesis was stimulated by injection with the β3-agonist CL-316243. Inexperiment 2, pups were pretreated with chlorisondamine and injected with CL-316243, and after BAT thermogenesis was stimulated the interscapular region of the pups was cooled externally with a thermode. In both experiments, cardiac rate, oxygen consumption, and physiological temperatures were monitored. Activation of BAT thermogenesis substantially increased cardiac rate in saline- and chlorisondamine-treated pups, and focal cooling of the interscapular region was sufficient to lower cardiac rate. The results of these studies support the hypothesis...
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Active sleep in cold-exposed infant Norway rats and Syrian golden hamsters: the role of brown adipose tissue thermogenesis. Behav Neurosci 112:695–706
1998Co-Authors: Greta Sokoloff, Mark S. BlumbergAbstract:It was previously hypothesized that brown adipose tissue (BAT) thermogenesis helps to maintain high rates of myoclonic twitching during cold exposure in infant rats (M. S. Blumberg & M. A. Stolba, 1996). To test his hypothesis, the sensitivity of twitching to various levels of cold exposure was assessed in week-old rats that were untreated or whose BAT thermogenesis was inhibited using a Ganglionic Blocker. Because week-old golden hamsters do not exhibit BAT thermogenesis, their sleep behaviors during cold exposure also were examined. Additional investigations in infant rats were conducted inwhich supplemental heat was provided to the interscapular region using a thermode and in which BAT was activated pharmacologically in Ganglionically blocked pups. The results support he hypothesis that myoclonic twitching is sensitive to the prevailing air temperature and the activation of BAT thermogenesis. Brown adipose tissue (BAT) thermogenesis is a primary means of endogenous heat production in mammalian i fants (Brtick, 1992; Nedergaard, Connolly, & Cannon, 1986). Week-old rats during moderate cold exposure (i.e., air temperatures between 25-34 °C; see Blumberg & Sokoloff, in press) increase BAT thermogenesis, maintain cardiac rate, and do not emit ultrasonic vocalizations. In contrast, ex-treme cold exposure (i.e., air temperatures below 25 °C) overwhelm the ability of BAT thermogenesis to compensate for heat loss, resulting in bradycardia and ultrasound produc
Patrice G. Guyenet - One of the best experts on this subject based on the ideXlab platform.
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C1 neurons mediate a stress-induced anti-inflammatory reflex in mice
Nature Neuroscience, 2017Co-Authors: Chikara Abe, Tsuyoshi Inoue, Mabel A Inglis, Kenneth E. Viar, Liping Huang, Diane L. Rosin, Ruth L. Stornetta, Mark D. Okusa, Patrice G. GuyenetAbstract:C1 neurons, located in the medulla oblongata, mediate adaptive autonomic responses to physical stressors (for example, hypotension, hemorrhage and presence of lipopolysaccharides). We describe here a powerful anti-inflammatory effect of restraint stress, mediated by C1 neurons: protection against renal ischemia-reperfusion injury. Restraint stress or optogenetic C1 neuron (C1) stimulation (10 min) protected mice from ischemia-reperfusion injury (IRI). The protection was reproduced by injecting splenic T cells that had been preincubated with noradrenaline or splenocytes harvested from stressed mice. Stress-induced IRI protection was absent in Chrna7 knockout ( a7nAChR ^−/−) mice and greatly reduced by destroying or transiently inhibiting C1. The protection conferred by C1 stimulation was eliminated by splenectomy, Ganglionic-Blocker administration or β_2-adrenergic receptor blockade. Although C1 stimulation elevated plasma corticosterone and increased both vagal and sympathetic nerve activity, C1-mediated IRI protection persisted after subdiaphragmatic vagotomy or corticosterone receptor blockade. Overall, acute stress attenuated IRI by activating a cholinergic, predominantly sympathetic, anti-inflammatory pathway. C1s were necessary and sufficient to mediate this effect. Acute stress elicits physiological and behavioral responses that enhance survival. This study in mice shows that stress reduces tissue injury in a model of renal ischemia-reperfusion injury by activating an anti-inflammatory response via the sympathetic system and the spleen. C1 neurons located in the brainstem mediate this protective effect of stress.
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C1 neurons mediate a stress-induced anti-inflammatory reflex in mice
Nature neuroscience, 2017Co-Authors: Chikara Abe, Tsuyoshi Inoue, Mabel A Inglis, Kenneth E. Viar, Liping Huang, Diane L. Rosin, Ruth L. Stornetta, Mark D. Okusa, Patrice G. GuyenetAbstract:C1 neurons, located in the medulla oblongata, mediate adaptive autonomic responses to physical stressors (for example, hypotension, hemorrhage and presence of lipopolysaccharides). We describe here a powerful anti-inflammatory effect of restraint stress, mediated by C1 neurons: protection against renal ischemia-reperfusion injury. Restraint stress or optogenetic C1 neuron (C1) stimulation (10 min) protected mice from ischemia-reperfusion injury (IRI). The protection was reproduced by injecting splenic T cells that had been preincubated with noradrenaline or splenocytes harvested from stressed mice. Stress-induced IRI protection was absent in Chrna7 knockout (a7nAChR-/-) mice and greatly reduced by destroying or transiently inhibiting C1. The protection conferred by C1 stimulation was eliminated by splenectomy, Ganglionic-Blocker administration or β2-adrenergic receptor blockade. Although C1 stimulation elevated plasma corticosterone and increased both vagal and sympathetic nerve activity, C1-mediated IRI protection persisted after subdiaphragmatic vagotomy or corticosterone receptor blockade. Overall, acute stress attenuated IRI by activating a cholinergic, predominantly sympathetic, anti-inflammatory pathway. C1s were necessary and sufficient to mediate this effect.
