Decerebration activates thermogenesis in the rat.

Rothwell, Nancy J.; Stock, Michael J.; Thexton, A.J.

doi:10.1113/jphysiol.1983.sp014836

Cited by 47 publications

(31 citation statements)

References 17 publications

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“…Following upon descriptions of the effects of transections of the neuraxis on BAT thermogenesis (5, 51, 57) and on the increases in BAT SNA produced by PGE 2 in POA (32, 47), we used transections of the neuraxis to obtain a similar, indirect assessment of descending inhibitory and excitatory influences on CVC neuronal activity. Transection of the neuraxis immediately caudal to the POA activates BAT thermogenesis (5,51), and a subsequent transection immediately caudal to the DMH reverses the increase in BAT SNA (32,47). To test the hypothesis that the pathways descending from or through the POA and the DMH influencing tail CVC neuronal activity are organized similarly to those that influence BAT thermogenesis, we determined the changes in tail CVC neuronal activity following transections caudal to POA and to DMH.…”

Section: Methodsmentioning

confidence: 99%

Central pathway for spontaneous and prostaglandin E₂-evoked cutaneous vasoconstriction

Rathner

Madden²,

Morrison³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

118

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Rathner JA, Madden CJ, Morrison SF. Central pathway for spontaneous and prostaglandin E2-evoked cutaneous vasoconstriction. Am J Physiol Regul Integr Comp Physiol 295: R343-R354, 2008. First published May 7, 2008 doi:10.1152/ajpregu.00115.2008.-A reduction of heat loss to the environment through increased cutaneous vasoconstrictor (CVC) sympathetic outflow contributes to elevated body temperature during fever. We determined the role of neurons in the dorsomedial hypothalamus (DMH) in increases in CVC sympathetic tone evoked by PGE2 into the preoptic area (POA) in chloralose/urethane-anesthetized rats. The frequency of axonal action potentials of CVC sympathetic ganglion cells recorded from the surface of the tail artery was increased by 1.8 Hz following nanoinjections of bicuculline (50 pmol) into the DMH. PGE2 nanoinjection into the POA elicited a similar excitation of tail CVC neurons (ϩ2.1 Hz). Subsequent to PGE2 into the POA, muscimol (400 pmol/side) into the DMH did not alter the activity of tail CVC neurons. Inhibition of neurons in the rostral raphé pallidus (rRPa) eliminated the spontaneous discharge of tail CVC neurons but only reduced the PGE2-evoked activity. Residual activity was abolished by subsequent muscimol into the rostral ventrolateral medulla. Transections through the neuraxis caudal to the POA increased the activity of tail CVC neurons, which were sustained through transections caudal to DMH. We conclude that while activation of neurons in the DMH is sufficient to activate tail CVC neurons, it is not necessary for their PGE2-evoked activity. These results support a CVC component of increased core temperature elicited by PGE2 in POA that arises from relief of a tonic inhibition from neurons in POA of CVC sympathetic premotor neurons in rRPa and is dependent on the excitation of CVC premotor neurons from a site caudal to DMH. rostral raphé pallidus; thermoregulation; fever; dorsomedial hypothalamus; preoptic hypothalamus IN BOTH HUMANS (19,20,43) and rats (53) cutaneous vasoconstrictor (CVC) tone regulates heat loss to the environment and contributes importantly to the maintenance of normal body temperature and to the development of fever. The essential role for the generation of PGE 2 in the preoptic area (POA) in the production of fever has led to the use of nanoinjections of PGE 2 into the POA to understand the neural pathways controlling thermoregulatory effectors during the febrile response. Similarly, observations of thermal effector responses elicited by changes in skin (T SK ) or core temperature (T C ) have provided important information on the central neural networks responsible for body temperature homeostasis. Such studies have been pursued most extensively with regard to the sympathetic neural regulation of non-shivering thermogenesis in rodent brown adipose tissue (BAT), a highly metabolic tissue in which heat production contributes significantly to the defense of body temperature in cold environments and to the elevation of body temperature during the febrile response. The neur...

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Section: Methodsmentioning

confidence: 99%

Central pathway for spontaneous and prostaglandin E₂-evoked cutaneous vasoconstriction

Rathner

Madden²,

Morrison³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

118

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“…Pontomedullary, but not postmammillary, transections of the neuraxis increase BAT temperature and core temperature (48,51), consistent with the existence of a tonically active inhibition of BAT thermogenesis located in the pontine retrorubral field (52). We sought to establish that pontomedullary transections increase BAT thermogenesis through stimulation of BAT SNA and to determine if the putative BAT sympathoinhibitory mechanism in the VLM would influence the activation of BAT SNA elicited by pontomedullary transection.…”

Section: Disinhibition Of Neurons In Vlm or In Nts Reversed The Incrementioning

confidence: 99%

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

Cao

Madden

Morrison

2010

American Journal of Physiology-Regulatory, Integrative and Comp

101

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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 CO 2. Disinhibition of neurons in either VLM or NTS with the GABA A receptor antagonist, bicuculline (30 pmol), reversed the increases in BAT SNA, BAT temperature, and end-expired CO 2 that were elicited 1) by cold defense; 2) during the febrile model of nanoinjection of prostaglandin E 2 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 -opioid receptor agonist fentanyl. Combined, but not separate, inhibitions of neurons in the VLM and in the NTS, with the GABA A receptor agonist, muscimol (120 pmol/site), produced increases in BAT SNA, BAT temperature, and expired CO 2, 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. chemoreceptor; fentanyl; raphe IN MEDIATING NONSHIVERING thermogenesis, brown adipose tissue (BAT) is a site of glucose utilization, lipid oxidation, and energy expenditure that plays an important role in the cold defense response of small mammals and infant primates, but which also contributes to diet-induced thermogenesis (47), and whose reduced function may be a factor in the overweight phenotype of obesity (59). The recent demonstration of significant, metabolically active BAT depots in adult humans (14,43,59) and the potential for dysregulation of BAT energy expenditure in human obesity (14,59) and in models of the wastage syndrome in cachexia (5) have focused interest on the central neural mechanism controlling BAT sympathetic outflow, the primary determinant of BAT thermogenesis and energy consumption (8). The principal pathways for the regulation of BAT thermogenic responses during cold defense and in response to central prostaglandin (PG) E 2 administration have been described (36). In particular, the rostral raphe pallidus (rRPa) is the principal site of BAT sympathetic premotor neurons, and BAT sympathetic outflow is markedly increased by antagonism of GABA A receptors in rRPa (37), presumably mediated by a disinhibition of BAT sympathetic premotor neurons in rRPa....

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“…High-level decerebration in the prepontine region produces dramatic increases in body temperature ( 3 4 " ) in several species (Bignall et al 1975;Chambers et al 1974;Rothwell et al 1983~). In the rat, this is associated with dramatic increases in metabolic rate (Rothwell et al 1983~) and blood flow to brown fat (Shibata et af. 1987), which are dependent on the sympathetic nervous system.…”

Section: Areas Of the Brain Controlling Batmentioning

confidence: 99%

Central control of brown adipose tissue

Rothwell

1989

Proc. Nutr. Soc.

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Thermogenesis is a term which can be used to describe any form of heat production, but is normally applied to adaptive or regulatory components of metabolic rate, namely non-shivering thermogenesis (NST) and diet-induced thermogenesis (DIT). NST and DIT are activated in response to physiological stimuli and are largely dependent on sympathetic activation of heat production in brown adipose tissue (BAT). The quantitative importance and thermogenic mechanisms of BAT will be reviewed by others participating in this symposium. The objective of the present review is to discuss our current knowledge of the central mechanisms involved in the control of BAT thermogenesis, and how they are affected by physiological or pathological conditions.Of all aspects of BAT thermogenesis it is the central control which is probably the least understood, partly as a result of its complexity, but also because it has received relatively little direct attention. Considerable information and insight into this area can, however, be gained from studies concerned with feeding behaviour and temperature regulation, both of which are closely related and show many common features with sympatheticallymediated thermogenesis. Over the past few years, our understanding of central thermogenic mechanisms has improved considerably, due mainly to studies specifically designed to investigate this problem. Areas of the brain controlling BATThe hypothalamus is the major area concerned with the control of autonomic functions, particularly feeding behaviour and thermoregulation, and has been the primary focus for studies on BAT thermogenesis. A close association between the ventromedial hypothalamus (VMH) and the regulation of body-weight or energy balance was first demonstrated almost 40 years ago, when destruction of the ventromedial nucleus was shown to result in hyperphagia and obesity. For a long time thereafter the VMH was referred to as a 'satiety' centre, acting reciprocally with the lateral hypothalamus (LH; known as the hunger centre) to control food intake (Stellar, 1954). However, obesity will develop in response to VMH lesions in the absence of hyperphagia, indicating that energy expenditure was simultaneously reduced (Han et al.

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Decerebration activates thermogenesis in the rat.

Cited by 47 publications

References 17 publications

Central pathway for spontaneous and prostaglandin E₂-evoked cutaneous vasoconstriction

Central pathway for spontaneous and prostaglandin E₂-evoked cutaneous vasoconstriction

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

Central control of brown adipose tissue

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