Procaine microinjection into the lower midbrain increases brown fat and body temperatures in anesthetized rats

Shibata, Masaaki; Iriki, Masami; Ai, Jun; Kiyohara, Toshikazu; Nakashima, Toshihiro; Miyata, Seiji; Matsukawa, Takashi

doi:10.1016/0006-8993(96)00040-6

Cited by 33 publications

(22 citation statements)

References 21 publications

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“…The efferent signals from the preoptic chiasma/anterior hypothalamic nuclei are the inhibitor of gamma-aminobutyric acids (GABA) to reach ventromedial hypothalamic nucleus [8]. The signal from the ventromedial hypothalamic nucleus reached the raphe nuclei through the lower midbrain and release GABA in this area [9,10]. The thermoregulatory signal is connected to the sympathetic chain.…”

Section: Discussionmentioning

confidence: 99%

Central Hyperthermia Treated With Baclofen for Patient With Pontine Hemorrhage

et al. 2014

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Central hyperthermia is a very rare disease; however, once it happens, it is associated with a poor prognosis and high mortality for patients with severe brainstem strokes. Following a pontine hemorrhage, a 46-years-old female developed prolonged hyperthermia. Work-ups to the fever gave no significant clues for the origin of fever, and hyperthermia did not respond to any empirical antibiotics or antipyretic agents. The patient's body temperature still fluctuated in a range of 37.5℃ to 39.2℃. Considering the lesion of hemorrhage, we suspected central hyperthermia rather than infectious diseases. We started with baclofen administration at a dose of 30 mg/day. The body temperature changed to a range of 36.6℃ to 38.2℃. We raised the dose of baclofen to 60 mg/day. The patient's body temperature finally dropped to a normal range. Central hyperthermia, caused by failures of thermoregulatory pathways in brainstem, following the pontine hemorrhage rarely occurs. Baclofen can be used to treat suspected central hyperthermia in a patient with pontine hemorrhage.

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Section: Discussionmentioning

confidence: 99%

Central Hyperthermia Treated With Baclofen for Patient With Pontine Hemorrhage

et al. 2014

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“…These areas also send descending projections to IBAT and have been linked to IBAT thermogenesis (52,56,58). For example, laboratory rats receiving procaine injections into the pedunculopontine tegmental nucleus or into the retrorubral field and rubrospinal tract increase T IBAT (51).…”

Section: Discussionmentioning

confidence: 99%

Anterograde transneuronal viral tract tracing reveals central sensory circuits from brown fat and sensory denervation alters its thermogenic responses

Vaughan

Bartness

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Vaughan CH, Bartness TJ. Anterograde transneuronal viral tract tracing reveals central sensory circuits from brown fat and sensory denervation alters its thermogenic responses. Am J Physiol Regul Integr Comp Physiol 302: R1049 -R1058, 2012. First published February 29, 2012 doi:10.1152/ajpregu.00640.2011.-Brown adipose tissue (BAT) thermogenic activity and growth are controlled by its sympathetic nervous system (SNS) innervation, but nerve fibers containing sensory-associated neuropeptides [substance P, calcitonin gene-related peptide (CGRP)] also suggest sensory innervation. The central nervous system (CNS) projections of BAT afferents are unknown. Therefore, we used the H129 strain of the herpes simplex virus-1 (HSV-1), an anterograde transneuronal viral tract tracer used to delineate sensory nerve circuits, to define these projections. HSV-1 was injected into interscapular BAT (IBAT) of Siberian hamsters and HSV-1 immunoreactivity (ir) was assessed 24, 48, 72, 96, and 114 h postinjection. The 96-and 114-h groups had the most HSV-1-ir neurons with marked infections in the hypothalamic paraventricular nucleus, periaqueductal gray, olivary areas, parabrachial nuclei, raphe nuclei, and reticular areas. These sites also are involved in sympathetic outflow to BAT suggesting possible BAT sensory-SNS thermogenesis feedback circuits. We tested the functional contribution of IBAT sensory innervation on thermogenic responses to an acute (24 h) cold exposure test by injecting the specific sensory nerve toxin capsaicin directly into IBAT pads and then measuring core (Tc) and IBAT (TIBAT) temperature responses. CGRP content was significantly decreased in capsaicin-treated IBAT demonstrating successful sensory nerve destruction. TIBAT and Tc were significantly decreased in capsaicin-treated hamsters compared with the saline controls at 2 h of cold exposure. Thus the central sensory circuits from IBAT have been delineated for the first time, and impairment of sensory feedback from BAT appears necessary for the appropriate, initial thermogenic response to acute cold exposure.herpes simplex virus-1; capsaicin; sensory afferents; iButton; body temperature; interscapular brown adipose tissue temperature; calcitonin gene-related peptide RECENT REPORTS of functional brown adipose tissue (BAT) in humans has sparked more interest in mapping the connections between BAT and the brain in the hope of increasing thermogenesis thereby enhancing energy expenditure and reversing or preventing obesity (18,59,61). BAT is the major effector tissue in rodent thermogenesis (for review see Ref. 10) controlled nearly exclusively by the sympathetic nervous system (SNS) drive to the tissue (for review see Ref. 5). Because of reports of sensory nerve-associated neuropeptides at the level of the BAT pad (23,24,43), the potential for reciprocal connections between BAT and the brain would thus create the possibility of SNS-sensory feedback loops to control the thermogenic activity of the tissue in response to varying environmental and physiological cha...

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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: 95%

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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Procaine microinjection into the lower midbrain increases brown fat and body temperatures in anesthetized rats

Cited by 33 publications

References 21 publications

Central Hyperthermia Treated With Baclofen for Patient With Pontine Hemorrhage

Central Hyperthermia Treated With Baclofen for Patient With Pontine Hemorrhage

Anterograde transneuronal viral tract tracing reveals central sensory circuits from brown fat and sensory denervation alters its thermogenic responses

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

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