The caudal periaqueductal gray participates in the activation of brown adipose tissue in rats

Chen, Xiaoming; Nishi, Maiko; Taniguchi, Aki; Nagashima, Kei; Shibata, Masaaki; Kanosue, Kazuyuki

doi:10.1016/s0304-3940(02)00757-7

Cited by 41 publications

(39 citation statements)

References 14 publications

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“…That we did not observe a significant change in MAP or HR with 7 % CO 2 may be attributable to this level of CO 2 being insufficient to promote sympatho-excitation. Regarding PAG participation in thermoregulation, there is evidence that electrical and chemical stimulations, particularly in caudal regions, stimulate brown adipose tissue (BAT) thermogenesis in rodents [16]. We did not find any differences between lesioned and control animals, suggesting that the PAG does not play a role in Tb regulation under euthermic conditions.…”

Section: Discussioncontrasting

confidence: 54%

Periaqueductal gray matter modulates the hypercapnic ventilatory response

Tenorio‐Lopes

Patrone

Bícego

et al. 2012

Pflugers Arch - Eur J Physiol

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The periaqueductal gray (PAG) is a midbrain structure directly involved in the modulation of defensive behaviors. It has direct projections to several central nuclei that are involved in cardiorespiratory control. Although PAG stimulation is known to elicit respiratory responses, the role of the PAG in the CO(2)-drive to breathe is still unknown. The present study assessed the effect of chemical lesion of the dorsolateral and dorsomedial and ventrolateral/lateral PAG (dlPAG, dmPAG, and vPAG, respectively) on cardiorespiratory and thermal responses to hypercapnia. Ibotenic acid (IBO) or vehicle (PBS, Sham group) was injected into the dlPAG, dmPAG, or vPAG of male Wistar rats. Rats with lesions outside the dlPAG, dmPAG, or vPAG were considered as negative controls (NC). Pulmonary ventilation (VE: ), mean arterial pressure (MAP), heart rate (HR), and body temperature (Tb) were measured in unanesthetized rats during normocapnia and hypercapnic exposure (5, 15, 30 min, 7 % CO(2)). IBO lesioning of the dlPAG/dmPAG caused 31 % and 26.5 % reductions of the respiratory response to CO(2) (1,094.3 ± 115 mL/kg/min) compared with Sham (1,589.5 ± 88.1 mL/kg/min) and NC groups (1,488.2 ± 47.7 mL/kg/min), respectively. IBO lesioning of the vPAG caused 26.6 % and 21 % reductions of CO(2) hyperpnea (1,215.3 ± 108.6 mL/kg/min) compared with Sham (1,657.3 ± 173.9 mL/kg/min) and NC groups (1,537.6 ± 59.3). Basal VE: , MAP, HR, and Tb were not affected by dlPAG, dmPAG, or vPAG lesioning. The results suggest that dlPAG, dmPAG, and vPAG modulate hypercapnic ventilatory responses in rats but do not affect MAP, HR, or Tb regulation in resting conditions or during hypercapnia.

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Section: Discussioncontrasting

confidence: 54%

Periaqueductal gray matter modulates the hypercapnic ventilatory response

Tenorio‐Lopes

Patrone

Bícego

et al. 2012

Pflugers Arch - Eur J Physiol

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“…For instance, catecholaminergic neurons in the ventrolateral medulla, also located in the brainstem, inhibit rRPa BAT premotor neurons through activation of α2 adrenergic receptors probably regulating a hypothermic process [134], [145]. The lateral parabrachial nucleus, periaqueductal gray, and locus coeruleus have also been linked to the control of thermogenesis [146], [147], [148], [149], [150], their exact role remains unclear.…”

Section: Next Stop: the Brainstemmentioning

confidence: 99%

Traveling from the hypothalamus to the adipose tissue: The thermogenic pathway

et al. 2017

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Brown adipose tissue (BAT) is a specialized tissue critical for non-shivering thermogenesis producing heat through mitochondrial uncoupling; whereas white adipose tissue (WAT) is responsible of energy storage in the form of triglycerides. Another type of fat has been described, the beige adipose tissue; this tissue emerges in existing WAT depots but with thermogenic ability, a phenomenon known as browning. Several peripheral signals relaying information about energy status act in the brain, particularly the hypothalamus, to regulate thermogenesis in BAT and browning of WAT. Different hypothalamic areas have the capacity to regulate the thermogenic process in brown and beige adipocytes through the sympathetic nervous system (SNS). This review discusses important concepts and discoveries about the central control of thermogenesis as a trip that starts in the hypothalamus, and taking the sympathetic roads to reach brown and beige fat to modulate thermogenic functions.

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“…Excitation of cPAG neurons increases T bat (60), although this excitation does not play a role in the skin cooling-evoked stimulation of BAT thermogenesis (241). In addition to the evidence for a direct monosynaptic pathway from the DMH/DA to the rRPa, both anatomical and physiological evidence suggest a role for neurons in the PAG in determining the level of BAT thermogenesis, potentially by influencing the output from the DMH/DA.…”

Section: Brain Regions That Modulate Cold-defensive Bat Thermogenesismentioning

confidence: 99%

Central Nervous System Regulation of Brown Adipose Tissue

Morrison

Madden

2014

Comprehensive Physiology

124

103

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Thermogenesis, the production of heat energy, in brown adipose tissue is a significant component of the homeostatic repertoire to maintain body temperature during the challenge of low environmental temperature in many species from mouse to man and plays a key role in elevating body temperature during the febrile response to infection. The sympathetic neural outflow determining brown adipose tissue (BAT) thermogenesis is regulated by neural networks in the CNS which increase BAT sympathetic nerve activity in response to cutaneous and deep body thermoreceptor signals. Many behavioral states, including wakefulness, immunologic responses, and stress, are characterized by elevations in core body temperature to which central command-driven BAT activation makes a significant contribution. Since energy consumption during BAT thermogenesis involves oxidation of lipid and glucose fuel molecules, the CNS network driving cold-defensive and behavioral state-related BAT activation is strongly influenced by signals reflecting the short and long-term availability of the fuel molecules essential for BAT metabolism and, in turn, the regulation of BAT thermogenesis in response to metabolic signals can contribute to energy balance, regulation of body adipose stores and glucose utilization. This review summarizes our understanding of the functional organization and neurochemical influences within the CNS networks that modulate the level of BAT sympathetic nerve activity to produce the thermoregulatory and metabolic alterations in BAT thermogenesis and BAT energy expenditure that contribute to overall energy homeostasis and the autonomic support of behavior.

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The caudal periaqueductal gray participates in the activation of brown adipose tissue in rats

Cited by 41 publications

References 14 publications

Periaqueductal gray matter modulates the hypercapnic ventilatory response

Periaqueductal gray matter modulates the hypercapnic ventilatory response

Traveling from the hypothalamus to the adipose tissue: The thermogenic pathway

Central Nervous System Regulation of Brown Adipose Tissue

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