scholarly journals A hypothalamic circuit that controls body temperature

2017 ◽  
Vol 114 (8) ◽  
pp. 2042-2047 ◽  
Author(s):  
Zheng-Dong Zhao ◽  
Wen Z. Yang ◽  
Cuicui Gao ◽  
Xin Fu ◽  
Wen Zhang ◽  
...  
Keyword(s):  
Body Temperature ◽  
Gabaergic Neurons ◽  
Designer Drugs ◽  
Electrophysiological Recording ◽  
Strong Increase ◽  
Temperature Sensitive ◽  
Neural Pathways ◽  
Dorsomedial Hypothalamus ◽  
Reduced Body ◽  
Stimulation Of

The homeostatic control of body temperature is essential for survival in mammals and is known to be regulated in part by temperature-sensitive neurons in the hypothalamus. However, the specific neural pathways and corresponding neural populations have not been fully elucidated. To identify these pathways, we used cFos staining to identify neurons that are activated by a thermal challenge and found induced expression in subsets of neurons within the ventral part of the lateral preoptic nucleus (vLPO) and the dorsal part of the dorsomedial hypothalamus (DMD). Activation of GABAergic neurons in the vLPO using optogenetics reduced body temperature, along with a decrease in physical activity. Optogenetic inhibition of these neurons resulted in fever-level hyperthermia. These GABAergic neurons project from the vLPO to the DMD and optogenetic stimulation of the nerve terminals in the DMD also reduced body temperature and activity. Electrophysiological recording revealed that the vLPO GABAergic neurons suppressed neural activity in DMD neurons, and fiber photometry of calcium transients revealed that DMD neurons were activated by cold. Accordingly, activation of DMD neurons using designer receptors exclusively activated by designer drugs (DREADDs) or optogenetics increased body temperature with a strong increase in energy expenditure and activity. Finally, optogenetic inhibition of DMD neurons triggered hypothermia, similar to stimulation of the GABAergic neurons in the vLPO. Thus, vLPO GABAergic neurons suppressed the thermogenic effect of DMD neurons. In aggregate, our data identify vLPO→DMD neural pathways that reduce core temperature in response to a thermal challenge, and we show that outputs from the DMD can induce activity-induced thermogenesis.

Mechanism of reduced water intake in rats at high altitude

1981 ◽  
Vol 240 (3) ◽  
pp. R187-R191 ◽  
Author(s):  
R. M. Jones ◽  
C. Terhaard ◽  
J. Zullo ◽  
S. M. Tenney
Keyword(s):  
Polyethylene Glycol ◽  
Angiotensin Ii ◽  
Body Temperature ◽  
Diabetes Insipidus ◽  
Water Intake ◽  
Hypobaric Hypoxia ◽  
Reduced Body ◽  
Osmotic Stimulation ◽  
Reduced Water ◽  
Stimulation Of

Water intake was reduced during the 1st day of hypobaric hypoxia (inspired O2 pressure of 75 Torr) to 35-40% of the normoxic level in both normal rats (N) and rats with diabetes insipidus (DI). Analysis of water intake under graded saline loads at several inspired O2 levels (inspired O2 fractional concentrations of 0.105, 0.120, and 0.2095) indicated that hypoxia increased the threshold for osmotic stimulation of drinking without changing the sensitivity of the response in both N and DI rats. Nephrectomized N rats reduced water intake during hypoxia to 33% of the nephrectomized normoxic level of intake, and nephrectomized DI rats reduced intake to 47% of the nephrectomized normoxic intake. From these results it is concluded that reduced angiotensin II formation was not the factor responsible for reduced water intake during hypoxia. Polyethylene glycol-induced hypovolemia resulted in increased water intake during normoxia, but during hypoxia it was reduced to 29% of the normoxic rate. Reduced body temperature and hyperventilation were not the source of hypoxic attenuation of thirst. The mechanism may reside beyond the central integration of osmotic and nonosmotic information, or at the osmotic sensing mechanism itself.

scholarly journals 2010 Carl Ludwig Distinguished Lectureship of the APS Neural Control and Autonomic Regulation Section: Central neural pathways for thermoregulatory cold defense

2011 ◽  
Vol 110 (5) ◽  
pp. 1137-1149 ◽  
Author(s):  
Shaun F. Morrison
Keyword(s):  
Body Temperature ◽  
Heat Loss ◽  
Preoptic Area ◽  
Functional Organization ◽  
Inhibitory Input ◽  
Neural Pathways ◽  
Dorsomedial Hypothalamus ◽  
Brown Adipose ◽  
Premotor Neurons ◽  
Raphe Pallidus

Central neural circuits orchestrate the homeostatic repertoire to maintain body temperature during environmental temperature challenges and to alter body temperature during the inflammatory response. This review summarizes the research leading to a model representing our current understanding of the neural pathways through which cutaneous thermal receptors alter thermoregulatory effectors: the cutaneous circulation for control of heat loss, and brown adipose tissue, skeletal muscle, and the heart for thermogenesis. The activation of these effectors is regulated by parallel but distinct, effector-specific core efferent pathways within the central nervous system (CNS) that share a common peripheral thermal sensory input. The thermal afferent circuit from cutaneous thermal receptors includes neurons in the spinal dorsal horn projecting to lateral parabrachial nucleus neurons that project to the medial aspect of the preoptic area. Within the preoptic area, warm-sensitive, inhibitory output neurons control heat production by reducing the discharge of thermogenesis-promoting neurons in the dorsomedial hypothalamus. The rostral ventromedial medulla, including the raphe pallidus, receives projections form the dorsomedial hypothalamus and contains spinally projecting premotor neurons that provide the excitatory drive to spinal circuits controlling the activity of thermogenic effectors. A distinct population of warm-sensitive preoptic neurons controls heat loss through an inhibitory input to raphe pallidus sympathetic premotor neurons controlling cutaneous vasoconstriction. The model proposed for central thermoregulatory control provides a platform for further understanding of the functional organization of central thermoregulation.

Effects of intrahypothalamic injections of GABA, muscimol, pentobarbital, and L-glutamic acid on feed intake of satiated sheep

1989 ◽  
Vol 67 (1) ◽  
pp. 5-9 ◽  
Author(s):  
S. A. Wandji ◽  
J. R. Seoane ◽  
A. G. Roberge ◽  
L. Bédard ◽  
L. Thibault
Keyword(s):  
Glutamic Acid ◽  
Feed Intake ◽  
Feeding Behaviour ◽  
Ventromedial Hypothalamus ◽  
Neural Pathways ◽  
Direct Stimulation ◽  
Dorsomedial Hypothalamus ◽  
Cranial Implants ◽  
Stimulation Of

Five wethers were surgically prepared with cranial implants to study the role of gabaminergic neural pathways on the hypothalamic control of feeding behaviour in ruminants. In the first experiment, the animals were injected (1 μL) with a physiological Tyrode (0.95%) solution, muscimol (0.5 and 1.0 nmol), GABA (0.5 and 1.0 nmol), and L-glutamic acid (0.5 and 1.0 nmol). Feed intake following injections of muscimol (1.0 nmol) and L-glutamic acid (0.5 and 1.0 nmol) was twice as large as that following the Tyrode solution, at 60-min postinjections. These results, however, were not statistically significant (p = 0.12–0.15). In the second experiment, the animals were injected (1 μL) with saline, muscimol (0.8 nmol), L-glutamic acid (0.8 nmol), and pentobarbital (0.26 μmol). Fifteen minutes after the injections, pentobarbital had induced a significant feeding response when compared with control values (p < 0.01), whereas the effect of L-glutamic acid was not significant. However, 30 min after the injections, feed intake of sheep having received L-glutamic acid was higher than that obtained with the control injections (p < 0.01). The response to pentobarbital was stronger than that to either muscimol or L-glutamic acid. Histological analyses of brain tissue indicated that injections were performed in the ventromedial hypothalamus of four sheep and in the dorsomedial hypothalamus of the other. The data indicate that L-glutamic acid stimulates feed intake by acting either as a precursor of GABA or by a direct stimulation of glutaminergic neural pathways involved in the control of feed intake.Key words: Feeding behaviour, glutamic acid, GABA, sheep.

scholarly journals A refined method to monitor arousal from hibernation in the European hamster

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Fredrik A. F. Markussen ◽  
Vebjørn J. Melum ◽  
Béatrice Bothorel ◽  
David G. Hazlerigg ◽  
Valérie Simonneaux ◽  
...  
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Behavioural Adaptation ◽  
Ventilation Frequency ◽  
Reduced Body ◽  
Brown Adipose ◽  
Invasive Method ◽  
Warming Rate ◽  
Core Body ◽  
Environmental Temperatures

Abstract Background Hibernation is a physiological and behavioural adaptation that permits survival during periods of reduced food availability and extreme environmental temperatures. This is achieved through cycles of metabolic depression and reduced body temperature (torpor) and rewarming (arousal). Rewarming from torpor is achieved through the activation of brown adipose tissue (BAT) associated with a rapid increase in ventilation frequency. Here, we studied the rate of rewarming in the European hamster (Cricetus cricetus) by measuring both BAT temperature, core body temperature and ventilation frequency. Results Temperature was monitored in parallel in the BAT (IPTT tags) and peritoneal cavity (iButtons) during hibernation torpor-arousal cycling. We found that increases in brown fat temperature preceded core body temperature rises by approximately 48 min, with a maximum re-warming rate of 20.9℃*h-1. Re-warming was accompanied by a significant increase in ventilation frequency. The rate of rewarming was slowed by the presence of a spontaneous thoracic mass in one of our animals. Core body temperature re-warming was reduced by 6.2℃*h-1 and BAT rewarming by 12℃*h-1. Ventilation frequency was increased by 77% during re-warming in the affected animal compared to a healthy animal. Inspection of the position and size of the mass indicated it was obstructing the lungs and heart. Conclusions We have used a minimally invasive method to monitor BAT temperature during arousal from hibernation illustrating BAT re-warming significantly precedes core body temperature re-warming, informing future study design on arousal from hibernation. We also showed compromised re-warming from hibernation in an animal with a mass obstructing the lungs and heart, likely leading to inefficient ventilation and circulation.

The Validity of Temperature-Sensitive Ingestible Capsules for Measuring Core Body Temperature in Laboratory Protocols

2011 ◽  
Vol 28 (8) ◽  
pp. 719-726 ◽  
Author(s):  
David Darwent ◽  
Xuan Zhou ◽  
Cameron van den Heuvel ◽  
Charli Sargent ◽  
Greg D. Roach
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Temperature Sensitive ◽  
Core Body

What's hot and what's not: defining torpor in free-ranging birds and mammals

2001 ◽  
Vol 79 (10) ◽  
pp. 1885-1890 ◽  
Author(s):  
Robert MR Barclay ◽  
Cori L Lausen ◽  
Lydia Hollis
Keyword(s):  
Body Temperature ◽  
The Body ◽  
Temperature Sensitive ◽  
The Past ◽  
Data Loggers ◽  
Temperature Thresholds ◽  
Radio Transmitters ◽  
Species Specific ◽  
Free Ranging ◽  
Lowered Body

With the development of small implantable data loggers and externally attached temperature-sensitive radio transmitters, increasing attention is being paid to determining the thermoregulatory strategies of free-ranging birds and mammals. One of the constraints of such studies is that without a direct measure of metabolic rate, it is difficult to determine the significance of lowered body temperatures. We surveyed the literature and found that many different definitions have been used to discriminate torpor from normothermy. Many studies use arbitrary temperature thresholds without regard for the normothermic body temperature of the individuals or species involved. This variation makes comparison among studies difficult and means that ecologically and energetically significant small reductions in body temperature may be overlooked. We suggest that normothermic body temperature for each individual animal should be determined and that torpor be defined as occurring when the body temperature drops below that level. When individuals' active temperatures are not available, a species-specific value should be used. Of greater value, however, are the depth and duration of torpor bouts. We suggest several advantages of this definition over those used in the past.

Respiratory responses to noxious and nonnoxious heating of skin in cats

1984 ◽  
Vol 57 (6) ◽  
pp. 1738-1741 ◽  
Author(s):  
T. G. Waldrop ◽  
D. E. Millhorn ◽  
F. L. Eldridge ◽  
L. E. Klingler
Keyword(s):  
Body Temperature ◽  
Skin Temperature ◽  
Core Body Temperature ◽  
Warm Receptors ◽  
End Tidal ◽  
Core Body ◽  
Decerebrate Cats ◽  
Skin Temperatures ◽  
Respiratory Responses ◽  
Stimulation Of

Respiratory responses to increased skin temperatures were recorded in anesthetized cerebrate and in unanesthetized decerebrate cats. All were vagotomized, glomectomized, and paralyzed. Core body temperature and end-tidal Pco2 were kept constant with servoncontrollers. Stimulation of cutaneous nociceptors by heating the skin to 46 degrees C caused respiration to increase in both cerebrate and decerebrate cats. An even larger facilitation of respiration occurred when the skin temperature was elevated to 51 degrees C. However, respiration did not increase in either group of cats when the skin was heated to 41 degrees C to activate cutaneous warm receptors. The phenomenon of sensitization of nociceptors was observed. Spinal transection prevented all the respiratory responses to cutaneous heating. We conclude that noxious, but not nonnoxious, increases in skin temperature cause increases in respiratory output.

Temperature regulation in lizards: effects of hypoxia

1985 ◽  
Vol 248 (5) ◽  
pp. R595-R600 ◽  
Author(s):  
J. W. Hicks ◽  
S. C. Wood
Keyword(s):  
Body Temperature ◽  
Temperature Regulation ◽  
Adaptation To Hypoxia ◽  
Metabolic Demand ◽  
Reduced Body ◽  
Life Saving ◽  
Preferred Body Temperature ◽  
Rate Of Cooling ◽  
Temperature Exposure ◽  
Hypoxic Gas Mixture

Temperature regulation during external (lowered lung PO2) and internal hypoxia (anemia) was examined in four species of lizards. Exposure to a hypoxic gas mixture in a thermogradient resulted in the animals lowering their selected (preferred) body temperature. A 50% reduction in the O2 carrying capacity of the blood also reduced the selected body temperature. Lizards "shuttle" when forced to select a temperature either above or below their normal selected temperature. Exposure to hypoxia decreases the upper and lower exit temperatures during shuttling. Furthermore, a decrease in the inspired O2 causes the rate of heating to no longer exceed the rate of cooling as is normal. The behavioral reduction of body temperature and the altered neural and physiological aspects of temperature regulation appear to be generalized responses to impaired O2 transport and not PO2 per se. The reduced body temperature, by lowering metabolic demand, provides an effective, even life-saving, adaptation to hypoxia.

Chemical stimulation of the dorsomedial hypothalamus evokes non-shivering thermogenesis in anesthetized rats

2002 ◽  
Vol 928 (1-2) ◽  
pp. 113-125 ◽  
Author(s):  
Maria V. Zaretskaia ◽  
Dmitry V. Zaretsky ◽  
Anantha Shekhar ◽  
Joseph A. DiMicco
Keyword(s):  
Chemical Stimulation ◽  
Dorsomedial Hypothalamus ◽  
Anesthetized Rats ◽  
Shivering Thermogenesis ◽  
Stimulation Of

scholarly journals Activation of Norepinephrine Neurons in the NTS (A2 population) is Sufficient to Suppress Pulsatile LH Secretion in Female Mice

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A531-A531
Author(s):  
Richard B McCosh ◽  
Michael J Kreisman ◽  
Katherine Tian ◽  
Steven A Thomas ◽  
Kellie M Breen
Keyword(s):  
Acute Stress ◽  
Cell Activity ◽  
Metabolic Stress ◽  
Pulse Frequency ◽  
Designer Drugs ◽  
Transduction Efficiency ◽  
Neural Pathways ◽  
Wild Type ◽  
Female Mice ◽  
Lh Secretion

Abstract The overarching goal of this work is to identify neural pathways underlying inhibition of pulsatile luteinizing hormone (LH) secretion during stress. Stress-induced suppression of LH secretion is mediated, at least in part, by suppression of arcuate kisspeptin (ARCKiss1) neurons. The mechanisms by which acute stress suppresses ARCKiss1 cell activity are largely unknown; however, several lines of evidence support the hypothesis that A2 neurons (norepinephrine [NE] neurons in the nucleus of the solitary tract [NTS] of the brainstem) are involved. First, A2 cells are activated during several reactive stress paradigms. Second, NE administered into the paraventricular nucleus, which is innervated by A2 neurons, suppressed pulsatile LH secretion. Finally, ablation of brainstem NE neurons restored estrous cyclicity following chronic glucoprivation (chronic metabolic stress model). The present study employed chemogenetics to test the hypothesis that A2 neurons are sufficient to suppress pulsatile LH secretion in ovariectomized female dopamine beta-hydroxylase (DBH) Cre positive and negative (wild type) mice. Mice received bilateral injections of either a Cre-dependent stimulatory Designer Receptor Exclusively Activated by Designer Drugs (DREADD) virus (AAV1-DIO-hM3Dq-mCherry) or a control virus (AAV1-DIO-mCherry) into the NTS. Mice were randomly assigned to receive either clozapine N-oxide (CNO, specific DREADD agonist; 1mg/kg, i.p.) or saline and blood samples were collected at 6-min intervals for 60 min before and 90 min after injection. Two weeks later, mice received the alternate treatment in a cross-over design (n= 5-10/grp). During the pre-injection period, all mice had clear LH pulses (mean: 6.0 ± 0.2 ng/mL, pulses/60 min: 3.4 ± 1.5). In DBH Cre- (wild type) mice with hM3D virus and DBH Cre+ with mCherry virus (both control groups), neither CNO nor saline altered mean LH or LH pulse frequency. However, DBH Cre+ mice with hM3D virus had a 54% reduction in mean LH (p &lt; 0.05) and 59% reduction in pulse frequency (p &lt; 0.05) following CNO; neither LH metric was altered in response to saline. To assess transduction efficiency, fixed neural tissue was collected. In tissue analyzed thus far, DBH Cre+ mice have mCherry labeling in ~70% of DBH-immunoreactive neurons in the NTS and &gt;90% of mCherry neurons contained DBH immunoreactivity. Three DBH Cre+ mice with hM3D virus mice had no LH response to CNO and may represent missed viral injections, which will be determined when tissue is analyzed. These data demonstrate that activation of A2 neurons is sufficient to impair pulsatile LH secretion in female mice. Moreover, these data support the broad hypothesis that the A2 population of neurons is critical for modulating neuroendocrine function during stress and raises the possibility that A2 neurons directly or indirectly influence ARCKiss1 cell activity.

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