scholarly journals Neural control of fasting-induced torpor in mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Timna Hitrec ◽  
Marco Luppi ◽  
Stefano Bastianini ◽  
Fabio Squarcio ◽  
Chiara Berteotti ◽  
...  
Keyword(s):  
Body Temperature ◽  
Neural Control ◽  
Brain Regions ◽  
Early Gene ◽  
Brain Areas ◽  
Dorsomedial Hypothalamus ◽  
Brown Adipose ◽  
Cholera Toxin Subunit B ◽  
Raphe Pallidus ◽  
Subunit B

Abstract Torpor is a peculiar mammalian behaviour, characterized by the active reduction of metabolic rate, followed by a drop in body temperature. To enter torpor, the activation of all thermogenic organs that could potentially defend body temperature must be prevented. Most of these organs, such as the brown adipose tissue, are controlled by the key thermoregulatory region of the Raphe Pallidus (RPa). Currently, it is not known which brain areas mediate the entrance into torpor. To identify these areas, the expression of the early gene c-Fos at torpor onset was assessed in different brain regions in mice injected with a retrograde tracer (Cholera Toxin subunit b, CTb) into the RPa region. The results show a network of hypothalamic neurons that are specifically activated at torpor onset and a direct torpor-specific projection from the Dorsomedial Hypothalamus to the RPa that could putatively mediate the suppression of thermogenesis during torpor.

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.

Rhythms in Fos expression in brain areas related to the sleep-wake cycle in the diurnal Arvicanthis niloticus

2000 ◽  
Vol 278 (5) ◽  
pp. R1267-R1274 ◽  
Author(s):  
Colleen M. Novak ◽  
Laura Smale ◽  
Antonio A. Nunez
Keyword(s):  
Thalamic Nucleus ◽  
Brain Regions ◽  
Early Gene ◽  
Light Phase ◽  
Dark Cycle ◽  
Brain Areas ◽  
Tuberomammillary Nucleus ◽  
Fos Expression ◽  
The Difference ◽  
Arvicanthis Niloticus

Most mammals show daily rhythms in sleep and wakefulness controlled by the primary circadian pacemaker, the suprachiasmatic nucleus (SCN). Regardless of whether a species is diurnal or nocturnal, neural activity in the SCN and expression of the immediate-early gene product Fos increases during the light phase of the cycle. This study investigated daily patterns of Fos expression in brain areas outside the SCN in the diurnal rodent Arvicanthis niloticus. We specifically focused on regions related to sleep and arousal in animals kept on a 12:12-h light-dark cycle and killed at 1 and 5 h after both lights-on and lights-off. The ventrolateral preoptic area (VLPO), which contained cells immunopositive for galanin, showed a rhythm in Fos expression with a peak at zeitgeber time (ZT) 17 (with lights-on at ZT 0). Fos expression in the paraventricular thalamic nucleus (PVT) increased during the morning (ZT 1) but not the evening activity peak of these animals. No rhythm in Fos expression was found in the centromedial thalamic nucleus (CMT), but Fos expression in the CMT and PVT was positively correlated. A rhythm in Fos expression in the ventral tuberomammillary nucleus (VTM) was 180° out of phase with the rhythm in the VLPO. Furthermore, Fos production in histamine-immunoreactive neurons of the VTM cells increased at the light-dark transitions when A. niloticus show peaks of activity. The difference in the timing of the sleep-wake cycle in diurnal and nocturnal mammals may be due to changes in the daily pattern of activity in brain regions important in sleep and wakefulness such as the VLPO and the VTM.

scholarly journals Thermoregulatory inversion: a novel thermoregulatory paradigm

2017 ◽  
Vol 312 (5) ◽  
pp. R779-R786 ◽  
Author(s):  
Domenico Tupone ◽  
Georgina Cano ◽  
Shaun F. Morrison
Keyword(s):  
Body Temperature ◽  
Core Temperature ◽  
Neural Circuit ◽  
Core Body Temperature ◽  
Normal Body Temperature ◽  
Dorsomedial Hypothalamus ◽  
Pharmacological Mechanism ◽  
Brown Adipose ◽  
Skin Cooling ◽  
Core Body

To maintain core body temperature in mammals, the normal central nervous system (CNS) thermoregulatory reflex networks produce an increase in brown adipose tissue (BAT) thermogenesis in response to skin cooling and an inhibition of the sympathetic outflow to BAT during skin rewarming. In contrast, these normal thermoregulatory reflexes appear to be inverted in hibernation/torpor; thermogenesis is inhibited during exposure to a cold environment, allowing dramatic reductions in core temperature and metabolism, and thermogenesis is activated during skin rewarming, contributing to a return of normal body temperature. Here, we describe two unrelated experimental paradigms in which rats, a nonhibernating/torpid species, exhibit a “thermoregulatory inversion,” which is characterized by an inhibition of BAT thermogenesis in response to skin cooling, and a switch in the gain of the skin cooling reflex transfer function from negative to positive values. Either transection of the neuraxis immediately rostral to the dorsomedial hypothalamus in anesthetized rats or activation of A1 adenosine receptors within the CNS of free-behaving rats produces a state of thermoregulatory inversion in which skin cooling inhibits BAT thermogenesis, leading to hypothermia, and skin warming activates BAT, supporting an increase in core temperature. These results reflect the existence of a novel neural circuit that mediates inverted thermoregulatory reflexes and suggests a pharmacological mechanism through which a deeply hypothermic state can be achieved in nonhibernating/torpid mammals, possibly including humans.

SR59230A, a beta-3 adrenoceptor antagonist, inhibits ultradian brown adipose tissue thermogenesis and interrupts associated episodic brain and body heating

2011 ◽  
Vol 301 (4) ◽  
pp. R987-R994 ◽  
Author(s):  
Youichirou Ootsuka ◽  
Keerthi Kulasekara ◽  
Rodrigo Cunha de Menezes ◽  
William W. Blessing
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Neural Control ◽  
Substantial Contribution ◽  
Artery Blood Flow ◽  
Body Temperatures ◽  
Tail Artery ◽  
Brown Adipose

Brown adipose tissue (BAT) thermogenesis occurs episodically in an ultradian manner approximately every 80–100 min during the waking phase of the circadian cycle, together with highly correlated increases in brain and body temperatures, suggesting that BAT thermogenesis contributes to brain and body temperature increases. We investigated this in conscious Sprague-Dawley rats by determining whether inhibition of BAT thermogenesis via blockade of beta-3 adrenoceptors with SR59230A interrupts ultradian episodic increases in brain and body temperatures and whether SR59230A acts on BAT itself or via sympathetic neural control of BAT. Interscapular BAT (iBAT), brain, and body temperatures, tail artery blood flow, and heart rate were measured in unrestrained rats. SR59230A (1, 5, or 10 mg/kg ip), but not vehicle, decreased iBAT, body, and brain temperatures in a dose-dependent fashion (log-linear regression P < 0.01, R2 = 0.3, 0.4, and 0.4, respectively, n = 10). Ultradian increases in BAT, brain, and body temperature were interrupted by administration of SR59230A (10 mg/kg ip) compared with vehicle, resuming after 162 ± 24 min (means ± SE, n = 10). SR59230A (10 mg/kg ip) caused a transient bradycardia without any increase in tail artery blood flow. In anesthetized rats, SR59230A reduced cooling-induced increases in iBAT temperature without affecting cooling-induced increases in iBAT sympathetic nerve discharge. Inhibition of BAT thermogenesis by SR59230A, thus, reflects direct blockade of beta-3 adrenoceptors in BAT. Interruption of episodic ultradian increases in body and brain temperature by SR59230A suggests that BAT thermogenesis makes a substantial contribution to these increases.

The dorsomedial hypothalamus: a new player in thermoregulation

2007 ◽  
Vol 292 (1) ◽  
pp. R47-R63 ◽  
Author(s):  
Joseph A. DiMicco ◽  
Dmitry V. Zaretsky
Keyword(s):  
Sympathetic Nerve Activity ◽  
Core Body Temperature ◽  
Central Administration ◽  
Dorsomedial Hypothalamus ◽  
Brown Adipose ◽  
Significant Difference ◽  
Raphe Pallidus ◽  
Core Body ◽  
The Brain ◽  
Cutaneous Vasoconstriction

Neurons in the dorsomedial hypothalamus (DMH) play key roles in physiological responses to exteroceptive (“emotional”) stress in rats, including tachycardia. Tachycardia evoked from the DMH or seen in experimental stress in rats is blocked by microinjection of the GABAA receptor agonist muscimol into the rostral raphe pallidus (rRP), an important thermoregulatory site in the brain stem, where disinhibition elicits sympathetically mediated activation of brown adipose tissue (BAT) and cutaneous vasoconstriction in the tail. Disinhibition of neurons in the DMH also elevates core temperature in conscious rats and sympathetic activity to least significant difference interscapular BAT (IBAT) and IBAT temperature in anesthetized preparations. The latter effects are blocked by microinjection of muscimol into the rRP, while microinjection of muscimol into either the rRP or DMH suppresses increases in sympathetic nerve activity to IBAT, IBAT temperature, and core body temperature elicited either by microinjection of PGE2 into the preoptic area (an experimental model for fever), or central administration of fentanyl. Neurons concentrated in the dorsal region of the DMH project directly to the rRP, a location corresponding to that of neurons transsynaptically labeled from IBAT. Thus these neurons control nonshivering thermogenesis in rats, and their activation signals its recruitment in diverse experimental paradigms. Evidence also points to a role for neurons in the DMH in thermoregulatory cutaneous vasoconstriction, shivering, and endocrine adjustments. These directions provide intriguing avenues for future exploration that may expand our understanding of the DMH as an important hypothalamic site for the integration of autonomic, endocrine, and behavioral responses to diverse challenges.

Engaging regularly with fiction influences connectivity in cortical areas for language and mentalizing

2017 ◽  
Author(s):  
Roel M. Willems ◽  
Franziska Hartung
Keyword(s):  
Functional Connectivity ◽  
Time Course ◽  
Language Skills ◽  
Brain Regions ◽  
Brain Areas ◽  
Daily Lives ◽  
Cortical Areas ◽  
Social Abilities ◽  
Behavioral Evidence ◽  
Amount Of Reading

Behavioral evidence suggests that engaging with fiction is positively correlated with social abilities. The rationale behind this link is that engaging with fictional narratives offers a ‘training modus’ for mentalizing and empathizing. We investigated the influence of the amount of reading that participants report doing in their daily lives, on connections between brain areas while they listened to literary narratives. Participants (N=57) listened to two literary narratives while brain activation was measured with fMRI. We computed time-course correlations between brain regions, and compared the correlation values from listening to narratives to listening to reversed speech. The between-region correlations were then related to the amount of fiction that participants read in their daily lives. Our results show that amount of fiction reading is related to functional connectivity in areas known to be involved in language and mentalizing. This suggests that reading fiction influences social cognition as well as language skills.

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