Activation of bulbospinal serotonergic neurons during cold exposure

1999 ◽  
Vol 77 (4) ◽  
pp. 250-258 ◽  
Author(s):  
Alicia M Passerin ◽  
Linda L Bellush ◽  
William N Henley
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cold Exposure ◽  
Metabolic Response ◽  
Dark Cycle ◽  
Temporal Aspects ◽  
Hydroxyindoleacetic Acid ◽  
Sympathetic Nervous ◽  
Induced Changes

In a four-part study, we expand on our previous report that bulbospinal serotonin (5HT) neuronal activation occurs with 24 h of cold exposure. To characterize temporal aspects, rats were exposed to 3°C or were maintained at 22°C for 2, 8, 48, or 96 h (experiment 1) or for 15, 30, or 60 min (experiment 2). To ensure that cold-induced changes in 5HT activity were not due to disturbances in diurnal pattern, rats in experiment 3 were exposed to cold (8 h) during the dark cycle. To explore the hypothesis that cold-induced 5HT activation is part of a broad metabolic response that includes activation of the sympathetic nervous system, metabolically impaired (hypothyroid) rats were exposed to 8°C in experiment 4. Significant increments in 5-hydroxyindoleacetic acid (5HIAA) concentration were evident by 60 min of cold exposure and existed at all later time points measured. These findings were most robust in spinal cord and rostral brainstem. Activation in spinal cord was also found when rats were exposed to 8 h of cold during the dark cycle, the active period for rats. In experiment 4, hypothyroid rats exhibited significantly greater norepinephrine excretion compared with control rats exposed to the same cold stimulus; this finding was accompanied by significantly greater increments in 5HIAA concentration in rostral brainstem and spinal cord of hypothyroid rats. In addition, significant elevations in tryptophan concentration were noted throughout the brainstem and spinal cord of cold-exposed, hypothyroid rats relative to room temperature, hypothyroid rats. This finding suggested that elevations in 5HIAA concentration in these rats were due to increases in precursor availability. The implications of these findings relative to autonomic and metabolic control are discussed.Key words: serotonin, spinal cord, raphe, cold, sympathetic nervous system.

Activation of spinal cord serotonergic neurons accompanies cold-induced sympathoexcitation

1994 ◽  
Vol 72 (8) ◽  
pp. 884-892 ◽  
Author(s):  
Alicia M. Passerin ◽  
William N. Henley
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Synthesis Inhibitor ◽  
Serotonergic Neurons ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Hydroxyindoleacetic Acid ◽  
Dopa Accumulation ◽  
Sympathetic Nervous

These studies examined the hypothesis that serotonergic neurons located in central sites known to be involved with autonomic regulation are activated by cold exposure, a potent stimulator of the sympathetic nervous system. In all experiments, rats were exposed to either 3 °C or 22 °C for 24 h. Significant increases (p < 0.05) in urinary norepinephrine excretion, depletions of myocardial norepinephrine, and enhanced myocardial L-DOPA accumulation following decarboxylase inhibition provided evidence of sympathoexcitation at 3 °C. Accumulations of the serotonin metabolite 5-hydroxyindoleacetic acid, in saline-injected rats, and 5-hydroxytryptophan in decarboxylase-inhibited rats were increased in spinal cord and brainstem regions of cold-exposed rats. Two hours after injection of the serotonin synthesis inhibitor p-chlorophenylalanine, significantly greater depletions of serotonin in spinal cord and 5-hydroxyindoleacetic acid in spinal cord and brainstem of cold-exposed rats were noted; synthesis inhibition also caused a larger drop in body temperature in cold-exposed rats. Microdissections of raphe nuclei and thoracic spinal cord sites indicated that the principal sites of serotonergic activation were the dorsal and intermediate spinal regions, and the raphe magnus. Thus, cold-induced sympathoexcitation was accompanied by activation of serotonergic neurons in spinal cord and brainstem regions known to be involved in autonomic regulation.Key words: serotonin, cold, stress, sympathetic nervous system, spinal cord.

Role of the sympathetic nervous system in CCl4 hepatotoxicity

1960 ◽  
Vol 198 (3) ◽  
pp. 669-676 ◽  
Author(s):  
Deane N. Calvert ◽  
Theodore M. Brody
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Liver Mitochondria ◽  
Central Vein ◽  
Fat Depots ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking ◽  
Stimulation Of

An hypothesis is proposed which states that the characteristic hepatic changes seen after the administration of carbon tetrachloride are the result of stimulation of central sympathetic areas which produce a massive discharge of the peripheral sympathetic nervous system. Stimulation of the sympathetic supply to the blood vessels of the liver results in restriction of blood flow in the liver, leading to anoxia and the characteristic necrosis around the central vein of the hepatic lobule. Similarly the discharge causes the release of unesterified fatty acids from the peripheral fat depots and the consequent deposition of lipid in the liver. This hypothesis is based upon experimental evidence using the following physiologic and pharmacologic maneuvers: adrenergic blocking agents, pretreatment with reserpine, adrenalectomy and section of the spinal cord—all are effective to a greater or lesser extent in preventing the changes characteristically seen in oxidative phosphorylation of the liver mitochondria, activation of a Mg-dependent ATPase and deposition of lipid in the liver. Transection of the spinal cord is the most effective treatment and prevents entirely the characteristic changes seen in the above-mentioned functions.

Diminished sympathetic nervous system activity in genetically obese (ob/ob) mouse

1983 ◽  
Vol 245 (2) ◽  
pp. E148-E154 ◽  
Author(s):  
J. B. Young ◽  
L. Landsberg
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cold Exposure ◽  
Feedback Regulation ◽  
Turnover Rates ◽  
Interscapular Brown Adipose Tissue ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Long Acting

The genetically obese (ob/ob) mouse exhibits defective thermoregulatory responses to cold exposure. Pathophysiological explanations for this phenomenon have focused on abnormalities in intracellular metabolism or insensitivity of peripheral tissues to the thermogenic effects of catecholamines. Because the sympathetic nervous system (SNS) is subject to feedback regulation, a peripheral impairment in thermogenesis should be associated with a compensatory increase in SNS activity. To examine SNS activity in the ob/ob mouse, norepinephrine (NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of ob/ob and lean mice. The results from studies utilizing radiolabeled NE or inhibition of NE biosynthesis with alpha-methyl-p-tyrosine to measure NE turnover demonstrated reductions in SNS activity of 33-56% in heart and of 45-73% in IBAT in ob/ob mice at ambient temperature (22 degrees C) compared with measurements in lean controls. During cold exposure (4 degrees C) NE turnover increased in heart and IBAT to a similar extent in both ob/ob and lean mice, but NE turnover rates in heart, and probably in IBAT as well, remained lower in the obese mice than in the lean despite the gradual development of hypothermia in the ob/ob mice during this period. Administration of naltrexone, a long-acting opiate antagonist, failed to reverse the suppression of SNS activity observed in the ob/ob mice. These data indicate that diminished SNS activity in ob/ob mice may be an additional factor contributing to the defective thermogenesis characteristic of these animals.

scholarly journals Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system

2019 ◽  
Vol 133 (9) ◽  
pp. 1097-1113 ◽  
Author(s):  
Ken Chen ◽  
Dongdong Sun ◽  
Shuang Qu ◽  
Yue Chen ◽  
Jialiang Wang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cold Exposure ◽  
Sodium Excretion ◽  
Adrenergic Receptor ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Sympathetic Nervous

Abstract Environmental temperature plays a role in the variation of blood pressure. Maternal cold stress could affect the physiological phenotype of the offspring, including blood pressure elevation. In the present study, we found that adult offspring of dams exposed to cold have increased systolic and diastolic blood pressure, and decreased urine volume and sodium excretion, accompanied by increased heart rate and heart rate variability, secondary to increased activity of the sympathetic nervous system. Renal denervation or adrenergic receptor blockade decreased blood pressure and increased sodium excretion. The increase in peripheral sympathetic nerve activity can be ascribed to the central nervous system because administration of clonidine, a centrally acting α2 adrenergic receptor agonist, lowered blood pressure to a greater degree in the prenatal cold-exposed than control offspring. Moreover, these prenatal cold-exposed offspring had hypothalamic paraventricular nucleus (PVN) disorder because magnetic resonance spectroscopy showed decreased N-acetylaspartate and increased choline and creatine ratios in the PVN. Additional studies found that prenatal cold exposure impaired the balance between inhibitory and excitatory neurons. This led to PVN overactivation that was related to enhanced PVN-angiotensin II type 1 (AT1) receptor expression and function. Microinjection of the AT1 receptor antagonist losartan in the PVN lowered blood pressure to a greater extent in prenatal cold-exposed that control offspring. The present study provides evidence for overactive peripheral and central sympathetic nervous systems in the pathogenesis of prenatal cold-induced hypertension. Central AT1 receptor blockade in the PVN may be a key step for treatment of this type hypertension.

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