scholarly journals Central efferent pathways mediating skin cooling-evoked sympathetic thermogenesis in brown adipose tissue

2007 ◽  
Vol 292 (1) ◽  
pp. R127-R136 ◽  
Author(s):  
Kazuhiro Nakamura ◽  
Shaun F. Morrison
Keyword(s):  
Heart Rate ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Receptor Agonist ◽  
Excitatory Amino Acid ◽  
Defense Responses ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Skin Cooling ◽  
Efferent Pathways

Control of thermoregulatory effectors by the autonomic nervous system is a critical component of rapid cold-defense responses, which are triggered by thermal information from the skin. However, the central autonomic mechanism driving thermoregulatory effector responses to skin thermal signals remains to be determined. Here, we examined the involvement of several autonomic brain regions in sympathetic thermogenic responses in brown adipose tissue (BAT) to skin cooling in urethane-chloralose-anesthetized rats by monitoring thermogenic [BAT sympathetic nerve activity (SNA) and BAT temperature], metabolic (expired CO2), and cardiovascular (arterial pressure and heart rate) parameters. Acute skin cooling, which did not reduce either rectal (core) or brain temperature, evoked increases in BAT SNA, BAT temperature, expired CO2, and heart rate. Skin cooling-evoked thermogenic, metabolic, and heart rate responses were inhibited by bilateral microinjections of bicuculline (GABAA receptor antagonist) into the preoptic area (POA), by bilateral microinjections of muscimol (GABAA receptor agonist) into the dorsomedial hypothalamic nucleus (DMH), or by microinjection of muscimol, glycine, 8-OH-DPAT (5-HT1A receptor agonist), or kynurenate (nonselective antagonist for ionotropic excitatory amino acid receptors) into the rostral raphe pallidus nucleus (rRPa) but not by bilateral muscimol injections into the lateral/dorsolateral part or ventrolateral part of the caudal periaqueductal gray. These results implicate the POA, DMH, and rRPa in the central efferent pathways for thermogenic, metabolic, and cardiac responses to skin cooling, and suggest that these pathways can be modulated by serotonergic inputs to the medullary raphe.

scholarly journals Activation of TRPV1 in nucleus tractus solitarius reduces brown adipose tissue thermogenesis, arterial pressure, and heart rate

2018 ◽  
Vol 315 (1) ◽  
pp. R134-R143 ◽  
Author(s):  
Mazher Mohammed ◽  
Christopher J. Madden ◽  
Michael C. Andresen ◽  
Shaun F. Morrison
Keyword(s):  
Heart Rate ◽  
Adipose Tissue ◽  
Arterial Pressure ◽  
Vagus Nerve ◽  
Brown Adipose Tissue ◽  
Nucleus Tractus Solitarius ◽  
Trpv1 Channels ◽  
Brown Adipose ◽  
Skin Cooling ◽  
Vagal Afferent

The sympathetic nerve activity (SNA) to brown adipose tissue (BAT) regulates BAT thermogenesis to defend body temperature in cold environments or to produce fever during immune responses. The vagus nerve contains afferents that inhibit the BAT SNA and BAT thermogenesis evoked by skin cooling. We sought to determine whether activation of transient receptor potential vanilloid 1 (TRPV1) channels in the nucleus tractus solitarius (NTS), which are prominently expressed in unmyelinated vagal afferents, would affect cold-evoked BAT thermogenesis, cardiovascular parameters, or their vagal afferent-evoked responses. In urethane-chloralose-anesthetized rats, during skin cooling, nanoinjection of the TRPV1-agonist resiniferatoxin in NTS decreased BAT SNA (from 695 ± 195% of baseline during cooling to 103 ± 8% of baseline after resiniferatoxin), BAT temperature (−0.8 ± 0.1°C), expired CO2 (−0.3 ± 0.04%), mean arterial pressure (MAP; −20 ± 5 mmHg), and heart rate (−44 ± 11 beats/min). Pretreatment of NTS with the TRPV1 antagonist capsazepine prevented these resiniferatoxin-mediated effects. Intravenous injection of the TRPV1 agonist dihydrocapsaicin also decreased all the measured variables (except MAP). Bilateral cervical or subdiaphragmatic vagotomy attenuated the decreases in BAT SNA and thermogenesis evoked by nanoinjection of resiniferatoxin in NTS but did not prevent the decreases in BAT SNA and BAT thermogenesis evoked by intravenous dihydrocapsaicin. We conclude that activation of TRPV1 channels in the NTS of vagus nerve intact rats inhibits BAT SNA and decreases BAT metabolism, blood pressure, and heart rate. In contrast, the inhibition of BAT thermogenesis following systemic administration of dihydrocapsaicin does not require vagal afferent activity, consistent with a nonvagal pathway through which systemic TRPV1 agonists can inhibit BAT thermogenesis.

CNS origins of the sympathetic nervous system outflow to brown adipose tissue

1999 ◽  
Vol 276 (6) ◽  
pp. R1569-R1578 ◽  
Author(s):  
Maryam Bamshad ◽  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Pseudorabies Virus ◽  
Critical Role ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Diet Induced Thermogenesis

Brown adipose tissue (BAT) plays a critical role in cold- and diet-induced thermogenesis. Although BAT is densely innervated by the sympathetic nervous system (SNS), little is known about the central nervous system (CNS) origins of this innervation. The purpose of the present experiment was to determine the neuroanatomic chain of functionally connected neurons from the CNS to BAT. A transneuronal viral tract tracer, Bartha’s K strain of the pseudorabies virus (PRV), was injected into the interscapular BAT of Siberian hamsters. The animals were killed 4 and 6 days postinjection, and the infected neurons were visualized by immunocytochemistry. PRV-infected neurons were found in the spinal cord, brain stem, midbrain, and forebrain. The intensity of labeled neurons in the forebrain varied from heavy infections in the medial preoptic area and paraventricular hypothalamic nucleus to few infections in the ventromedial hypothalamic nucleus, with moderate infections in the suprachiasmatic and lateral hypothalamic nuclei. These results define the SNS outflow from the brain to BAT for the first time in any species.

scholarly journals Inhibition of brown adipose tissue thermogenesis by neurons in the ventrolateral medulla and in the nucleus tractus solitarius

2010 ◽  
Vol 299 (1) ◽  
pp. R277-R290 ◽  
Author(s):  
Wei-Hua Cao ◽  
Christopher J. Madden ◽  
Shaun F. Morrison
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Receptor Agonist ◽  
Nucleus Tractus Solitarius ◽  
Ventrolateral Medulla ◽  
Prostaglandin E ◽  
Experimental Conditions ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Raphe Pallidus

Neurons in the ventrolateral medulla (VLM) and in the nucleus tractus solitarius (NTS) play important roles in the regulation of cardiovascular and other autonomic functions. In the present study, we demonstrate an inhibition of brown adipose tissue (BAT) thermogenesis evoked by activation of neurons in the VLM, as well as by neurons in the intermediate NTS, of chloralose/urethane-anesthetized, artificially ventilated rats. Activation of neurons in either rostral VLM or caudal VLM with N-methyl-d-aspartate (12 nmol) reversed the cold-evoked increase in BAT sympathetic nerve activity (SNA), BAT temperature, and end-expired CO2. Disinhibition of neurons in either VLM or NTS with the GABAA receptor antagonist, bicuculline (30 pmol), reversed the increases in BAT SNA, BAT temperature, and end-expired CO2 that were elicited 1) by cold defense; 2) during the febrile model of nanoinjection of prostaglandin E2 into the medial preoptic area; 3) by activation of neurons in the dorsomedial hypothalamus or in the rostral raphe pallidus (rRPa); or 4) by the μ-opioid receptor agonist fentanyl. Combined, but not separate, inhibitions of neurons in the VLM and in the NTS, with the GABAA receptor agonist, muscimol (120 pmol/site), produced increases in BAT SNA, BAT temperature, and expired CO2, which were reversed by nanoinjection of glycine (30 nmol) into the rRPa. These findings suggest that VLM and NTS contain neurons whose activation inhibits BAT thermogenesis, that these neurons receive GABAergic inputs that are active under these experimental conditions, and that neurons in both sites contribute to the tonic inhibition of sympathetic premotor neuronal activity in the rRPa that maintains a low level of BAT thermogenesis in normothermic conditions.

scholarly journals Centrally Administered Resistin Enhances Sympathetic Nerve Activity to the Hindlimb but Attenuates the Activity to Brown Adipose Tissue

Endocrinology ◽  
2011 ◽  
Vol 152 (7) ◽  
pp. 2626-2633 ◽  
Author(s):  
S. Kosari ◽  
J. A. Rathner ◽  
F. Chen ◽  
S. Kosari ◽  
E. Badoer
Keyword(s):  
Cardiovascular Disease ◽  
Heart Rate ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve ◽  
Energy Homeostasis ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Obesity And Diabetes ◽  
Brown Adipose

Resistin, an adipokine, is believed to act in the brain to influence energy homeostasis. Plasma resistin levels are elevated in obesity and are associated with metabolic and cardiovascular disease. Increased muscle sympathetic nerve activity (SNA) is a characteristic of obesity, a risk factor for diabetes and cardiovascular disease. We hypothesized that resistin affects SNA, which contributes to metabolic and cardiovascular dysfunction. Here we investigated the effects of centrally administered resistin on SNA to muscle (lumbar) and brown adipose tissue (BAT), outputs that influence cardiovascular and energy homeostasis. Overnight-fasted rats were anesthetized, and resistin (7 μg) was administered into the lateral cerebral ventricle (intracerebroventricular). The lumbar sympathetic nerve trunk or sympathetic nerves supplying BAT were dissected free, and nerve activity was recorded. Arterial blood pressure, heart rate, body core temperature, and BAT temperature were also recorded. Responses to resistin or vehicle were monitored for 4 h after intracerebroventricular administration. Acutely administered resistin increased lumbar SNA but decreased BAT SNA. Mean arterial pressure and heart rate, however, were not significantly affected by resistin. BAT temperature was significantly reduced by resistin, and there was a concomitant fall in body temperature. The findings indicate that resistin has differential effects on SNA to tissues involved in metabolic and cardiovascular regulation. The decreased BAT SNA and the increased lumbar SNA elicited by resistin suggest that it may contribute to the increased muscle SNA and reduced energy expenditure observed in obesity and diabetes.

scholarly journals Preoptic area cooling increases the sympathetic outflow to brown adipose tissue and brown adipose tissue thermogenesis

2018 ◽  
Vol 315 (4) ◽  
pp. R609-R618 ◽  
Author(s):  
Mazher Mohammed ◽  
Christopher J. Madden ◽  
Kim J. Burchiel ◽  
Shaun F. Morrison
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glutamate Receptor ◽  
Preoptic Area ◽  
Hypothalamic Nucleus ◽  
Ionotropic Glutamate Receptor ◽  
Receptor Antagonists ◽  
Efferent Pathway ◽  
Brown Adipose ◽  
Glutamate Receptor Antagonists

Modest cold exposures are likely to activate autonomic thermogenic mechanisms due to activation of cutaneous thermal afferents, whereas central thermosensitive neurons set the background tone on which this afferent input is effective. In addition, more prolonged or severe cold exposures that overwhelm cold defense mechanisms would directly activate thermosensitive neurons within the central nervous system. Here, we examined the involvement of the canonical brown adipose tissue (BAT) sympathoexcitatory efferent pathway in the response to direct local cooling of the preoptic area (POA) in urethane-chloralose-anesthetized rats. With skin temperature and core body temperature maintained between 36 and 39°C, cooling POA temperature by ~1–4°C evoked increases in BAT sympathetic nerve activity (SNA), BAT temperature, expired CO2, and heart rate. POA cooling-evoked responses were inhibited by nanoinjections of ionotropic glutamate receptor antagonists or the GABAA receptor agonist muscimol into the median POA or by nanoinjections of ionotropic glutamate receptor antagonists into the dorsomedial hypothalamic nucleus (bilaterally) or into the raphe pallidus nucleus. These results demonstrate that direct cooling of the POA can increase BAT SNA and thermogenesis via the canonical BAT sympathoexcitatory efferent pathway, even in the face of warm thermal input from the skin and body core.

Electrical stimulation of the posterior and ventromedial hypothalamic nuclei causes specific activation of shivering and nonshivering thermogenesis

1994 ◽  
Vol 72 (1) ◽  
pp. 89-96 ◽  
Author(s):  
J. A. Thornhill ◽  
I. Halvorson
Keyword(s):  
Adipose Tissue ◽  
Electrical Stimulation ◽  
Brown Adipose Tissue ◽  
Posterior Hypothalamus ◽  
Hypothalamic Nucleus ◽  
Ventromedial Hypothalamic Nucleus ◽  
Hypothalamic Nuclei ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Stimulation Of

Experiments were designed to determine in the same animal whether electrical stimulation of the posterior hypothalamus and ventromedial hypothalamic nucleus could specifically evoke shivering and nonshivering (brown adipose tissue) thermogenesis, respectively, in anesthetized, normothermic rats. Urethane-anesthetized, male Long–Evans rats, kept at 37 °C, had colonic (Tc), gastrocnemius muscle (Tm), intrascapular brown adipose tissue (TIBAT), and tail (Tt) temperatures measured via thermistor probes, and electromyogram activity (differential multiunit activity from bipolar recording electrodes within gastrocnemius muscle) recorded, before and after unilateral electrical stimulation (monophasic 0.5-ms pulses of 200 μA at 50 Hz for 30 s) of the posterior hypothalamus and ventromedial hypothalamic nucleus (via stereotaxically implanted concentric stimulating electrodes). Each rat showed shivering (increased electromyogram activity) following posterior hypothalamic stimulation, which caused an immediate rise in Tm values with no change in TIBAT or Tt values. Electrical stimulation of the ventromedial hypothalamic nucleus of the same animals elicited no shivering activity, but significant increases in TIBAT values occurred with no change in Tm or Tt values. Results confirm that stimulation of the posterior and ventromedial hypothalamic nuclei in rodents specifically activates shivering and nonshivering (brown adipose tissue) effector mechanisms, respectively, to raise core temperature.Key words: posterior hypothalamus, shivering thermogenesis, ventromedial hypothalamus, intrascapular brown adipose tissue thermogenesis.

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