scholarly journals VGLUT2-expressing neurons in the vestibular nuclear complex mediate gravitational stress-induced hypothermia in mice

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Chikara Abe ◽  
Yusuke Yamaoka ◽  
Yui Maejima ◽  
Tomoe Mikami ◽  
Shigefumi Yokota ◽  
...  
Keyword(s):  
Plasma Catecholamines ◽  
Glutamate Transporter ◽  
Underlying Mechanism ◽  
Induced Hypothermia ◽  
Gamma Aminobutyric Acid ◽  
Interscapular Brown Adipose Tissue ◽  
Nuclear Complex ◽  
Brown Adipose ◽  
Gravitational Stress ◽  
Vestibular Nuclear Complex

AbstractThe vestibular system, which is essential for maintaining balance, contributes to the sympathetic response. Although this response is involved in hypergravity load-induced hypothermia in mice, the underlying mechanism remains unknown. This study showed that hypergravity (2g) decreased plasma catecholamines, which resulted in hypoactivity of the interscapular brown adipose tissue (iBAT). Hypothermia induced by 2g load was significantly suppressed by administration of beta-adrenergic receptor agonists, suggesting the involvement of decrease in iBAT activity through sympathoinhibition. Bilateral chemogenetic activation of vesicular glutamate transporter 2 (VGLUT2)-expressing neurons in the vestibular nuclear complex (VNC) induced hypothermia. The VGLUT2-expressing neurons contributed to 2g load-induced hypothermia, since their deletion suppressed hypothermia. Although activation of vesicular gamma-aminobutyric acid transporter-expressing neurons in the VNC induced slight hypothermia instead of hyperthermia, their deletion did not affect 2g load-induced hypothermia. Thus, we concluded that 2g load-induced hypothermia resulted from sympathoinhibition via the activation of VGLUT2-expressing neurons in the VNC.

scholarly journals Stimulation of the hypothalamic arcuate nucleus increases brown adipose tissue nerve activity via hypothalamic paraventricular and dorsomedial nuclei

2016 ◽  
Vol 311 (2) ◽  
pp. H433-H444 ◽  
Author(s):  
Vineet C. Chitravanshi ◽  
Kazumi Kawabe ◽  
Hreday N. Sapru
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Arcuate Nucleus ◽  
Glutamate Transporter ◽  
Nerve Activity ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Hypothalamic Arcuate Nucleus ◽  
Male Wistar Rats ◽  
Stimulation Of

Hypothalamic arcuate nucleus (ARCN) stimulation elicited increases in sympathetic nerve activity (IBATSNA) and temperature (TBAT) of interscapular brown adipose tissue (IBAT). The role of hypothalamic dorsomedial (DMN) and paraventricular (PVN) nuclei in mediating these responses was studied in urethane-anesthetized, artificially ventilated, male Wistar rats. In different groups of rats, inhibition of neurons in the DMN and PVN by microinjections of muscimol attenuated the increases in IBATSNA and TBAT elicited by microinjections of N-methyl-d-aspartic acid into the ipsilateral ARCN. In other groups of rats, blockade of ionotropic glutamate receptors by combined microinjections of D(-)-2-amino-7-phosphono-heptanoic acid (D-AP7) and NBQX into the DMN and PVN attenuated increases in IBATSNA and TBAT elicited by ARCN stimulation. Blockade of melanocortin 3/4 receptors in the DMN and PVN in other groups of rats resulted in attenuation of increases in IBATSNA and TBAT elicited by ipsilateral ARCN stimulation. Microinjections of Fluoro-Gold into the DMN resulted in retrograde labeling of cells in the ipsilateral ARCN, and some of these cells contained proopiomelanocortin (POMC), α-melanocyte-stimulating hormone (α-MSH), or vesicular glutamate transporter-3. Since similar projections from ARCN to the PVN have been reported by us and others, these results indicate that neurons containing POMC, α-MSH, and glutamate project from the ARCN to the DMN and PVN. Stimulation of ARCN results in the release of α-MSH and glutamate in the DMN and PVN which, in turn, cause increases in IBATSNA and TBAT.

scholarly journals Augmented Insulin and Leptin Resistance of High Fat Diet-Fed APPswe/PS1dE9 Transgenic Mice Exacerbate Obesity and Glycemic Dysregulation

2018 ◽  
Vol 19 (8) ◽  
pp. 2333 ◽  
Author(s):  
Yi-Heng Lee ◽  
Hao-Chieh Hsu ◽  
Pei-Chen Kao ◽  
Young-Ji Shiao ◽  
Skye Hsin-Hsien Yeh ◽  
...  
Keyword(s):  
Food Intake ◽  
Transgenic Mice ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Underlying Mechanism ◽  
Leptin Resistance ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Positron Emission ◽  
Brown Adipose

Alzheimer’s disease (AD), a progressive neurodegenerative disease is highly associated with metabolic syndromes. We previously demonstrated that glycemic dysregulation and obesity are augmented in high fat diet (HFD)-treated APPswe/PS1dE9 (APP/PS1) transgenic mice. In the current study, the underlying mechanism mediating exacerbated metabolic stresses in HFD APP/PS1 transgenic mice was further examined. APP/PS1 mice developed insulin resistance and, consequently, impaired glucose homeostasis after 10 weeks on HFD. [18F]-2-fluoro-2-deoxy-d-glucose ([18F]-FDG) positron emission tomography showed that interscapular brown adipose tissue is vulnerable to HFD and AD-related pathology. Chronic HFD induced hyperphagia, with limited effects on basal metabolic rates in APP/PS1 transgenic mice. Excessive food intake may be caused by impairment of leptin signaling in the hypothalamus because leptin failed to suppress the food intake of HFD APP/PS1 transgenic mice. Leptin-induced pSTAT3 signaling in the arcuate nucleus was attenuated. Dysregulated energy homeostasis including hyperphagia and exacerbated obesity was elicited prior to the presence of the amyloid pathology in the hypothalamus of HFD APP/PS1 transgenic mice; nevertheless, cortical neuroinflammation and the level of serum Aβ and IL-6 were significantly elevated. Our study demonstrates the pivotal role of AD-related pathology in augmenting HFD-induced insulin and leptin resistance and impairing hypothalamic regulation of energy homeostasis.

scholarly journals Differential Activation of the Sympathetic Innervation of Adipose Tissues by Melanocortin Receptor Stimulation

Endocrinology ◽  
2007 ◽  
Vol 148 (11) ◽  
pp. 5339-5347 ◽  
Author(s):  
Márcia N. Brito ◽  
Nilton A. Brito ◽  
Deborah J. Baro ◽  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Plasma Catecholamines ◽  
Melanocortin Receptor ◽  
Related Protein ◽  
Interscapular Brown Adipose Tissue ◽  
Lipid Mobilization ◽  
Brown Adipose ◽  
Induced Changes ◽  
Agouti Related Protein

Melanocortins are implicated in the control of energy intake/expenditure. Centrally administered melanotan II (MTII), a synthetic melanocortin 3/4-receptor agonist, decreases adiposity beyond that accountable by food intake decreases. Melanocortin-4 receptor (MC4-R) mRNA is expressed on sympathetic nervous system (SNS) outflow neurons to white adipose tissue (WAT) in Siberian hamsters, suggesting a role in lipid mobilization. Therefore, we tested whether third ventricular injections of MTII increased sympathetic drive to WAT and interscapular brown adipose tissue (IBAT) using norepinephrine turnover (NETO) as a measure of sympathetic drive. We also tested for MTII-induced changes in lipolysis-related WAT gene expression (β3-adrenoceptors, hormone sensitive lipase) and IBAT thermogenesis (β3-adrenoceptor, uncoupling protein-1). Finally, we tested whether third ventricularly injected MTII, a highly selective MC4-R agonist (cyclo[β-Ala-His-D-Phe-Arg-Trp-Glu]NH2) increased or agouti-related protein decreased IBAT temperature in hamsters implanted with sc IBAT temperature transponders. Centrally administered MTII provoked differential sympathetic drives to WAT and IBAT (increased inguinal WAT, dorsosubcutaneous WAT and IBAT NETO, but not epididymal WAT and retroperitoneal WAT NETO). MTII also increased circulating concentrations of the lipolytic products free fatty acids and glycerol but not plasma catecholamines, suggesting lipid mobilization via WAT SNS innervation and not via adrenal medullary catecholamines. WAT or IBAT gene expression was largely unaffected by acute MTII treatment, but IBAT temperature was increased by MTII and the MC4-R agonist and decreased by agouti-related protein. Collectively, this is the first demonstration of central melanocortin agonist stimulation of WAT lipolysis through the SNS and confirms melanocortin-induced changes in BAT thermogenesis.

scholarly journals Glucose transporter expression and glucose utilization in skeletal muscle and brown adipose tissue during starvation and re-feeding

1992 ◽  
Vol 282 (1) ◽  
pp. 231-235 ◽  
Author(s):  
D M Smith ◽  
S R Bloom ◽  
M C Sugden ◽  
M J Holness
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Tibialis Anterior ◽  
Glucose Transporter ◽  
Glucose Utilization ◽  
Interscapular Brown Adipose Tissue ◽  
Glut 4 ◽  
Mrna Concentration ◽  
Brown Adipose ◽  
Transporter Expression

Starvation (48 h) decreased the concentration of mRNA of the insulin-responsive glucose transporter isoform (GLUT 4) in interscapular brown adipose tissue (IBAT) (56%) and tibialis anterior (10%). Despite dramatic [7-fold (tibialis anterior) and 40-fold (IBAT)] increases in glucose utilization after 2 and 4 h of chow re-feeding, no significant changes in GLUT 4 mRNA concentration were observed in these tissues over this re-feeding period. The results exclude changes in GLUT 4 mRNA concentration in mediating the responses of glucose transport in these tissues to acute re-feeding after prolonged starvation.

scholarly journals Changes in β1- and β2-adrenergic receptor mRNA levels in brown adipose tissue and heart of hypothyroid rats

1991 ◽  
Vol 277 (3) ◽  
pp. 625-629 ◽  
Author(s):  
J P Revelli ◽  
R Pescini ◽  
P Muzzin ◽  
J Seydoux ◽  
M G Fitzgerald ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adrenergic Receptor ◽  
State Level ◽  
Total Density ◽  
Mrna Levels ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Displacement Experiments ◽  
Beta 2

The aim of the present work was to study the effect of hypothyroidism on the expression of the beta-adrenergic receptor (beta-AR) in interscapular brown adipose tissue and heart. The total density of plasma membrane beta-AR per tissue is decreased by 44% in hypothyroid rat interscapular brown adipose tissue and by 55% in hypothyroid rat heart compared with euthyroid controls. The effects of hypothyroidism on the density of both beta 1- and beta 2-AR subtypes were also determined in competition displacement experiments. The densities of beta 1- and beta 2-AR per tissue are decreased by 50% and 48% respectively in interscapular brown adipose tissue and by 52% and 54% in the heart. Northern blot analysis of poly(A)+ RNA from hypothyroid rat interscapular brown adipose tissue demonstrated that the levels of beta 1- and beta 2-AR mRNA per tissue are decreased by 73% and 58% respectively, whereas in hypothyroid heart, only the beta 1-AR mRNA is decreased, by 43%. The effect of hypothyroidism on the beta 1-AR mRNA is significantly more marked in the interscapular brown adipose tissue than in the heart. These results indicate that beta-AR mRNA levels are differentially regulated in rat interscapular brown adipose tissue and heart, and suggest that the decrease in beta-AR number in interscapular brown adipose tissue and heart of hypothyroid animals may in part be explained by a decreased steady-state level of beta-AR mRNA.

scholarly journals M146. NEUROCHEMICAL MODULATION OF AUDITORY CORTEX FUNCTIONAL CONNECTIVITY IN PATIENTS WITH AUDITORY VERBAL HALLUCINATIONS

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S191-S191
Author(s):  
Sarah Weber ◽  
Helene Hjelmervik ◽  
Alexander R Craven ◽  
Erik Johnsen ◽  
Rune Kroken ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Temporal Lobe ◽  
Superior Temporal Gyrus ◽  
Underlying Mechanism ◽  
Auditory Hallucinations ◽  
Anterior Cingulate ◽  
Gamma Aminobutyric Acid ◽  
Auditory Verbal Hallucinations ◽  
Left And Right ◽  
Neurochemical Correlates

Abstract Background Auditory hallucinations have been linked to aberrant functioning of the left superior temporal gyrus (STG) and are associated with impaired cognitive control regulated by areas in the prefrontal cortex. However, the mechanisms behind these dysfunctions are still unclear. Methods The current study combined resting state connectivity fMRI with MR spectroscopy (MRS) in a sample of 81 psychosis patients to explore how neurochemical correlates of auditory hallucinations modulate left STG functioning. The analyses were focused on glutamate (Glu) and gamma-aminobutyric acid (GABA), two neurotransmitters with excitatory and inhibitory functions, respectively, since these have previously been implicated in psychosis. Results Glu and GABA showed differential relationships with left STG connectivity in patients with and without hallucinations. Specifically, Glu concentration in the anterior cingulate cortex (ACC) was positively related to functional connectivity between the left and right temporal lobe in hallucinating patients only. In contrast, GABA concentration in the ACC was negatively related to connectivity between the left and right temporal lobe in non-hallucinating patients only. Discussion These findings support a recently proposed model of interhemispheric temporal lobe miscommunication in auditory hallucinations and indicate prefrontal neurochemical modulation as a potential underlying mechanism. The results can further be integrated with previously suggested excitatory/inhibitory imbalances as neurochemical modulators in AVH.

scholarly journals Evidence for increased thermogenesis in female C57BL/6J mice housed aboard the international space station

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Carmen P. Wong ◽  
Urszula T. Iwaniec ◽  
Russell T. Turner
Keyword(s):  
Adipose Tissue ◽  
Differential Expression ◽  
International Space Station ◽  
Space Station ◽  
Interscapular Brown Adipose Tissue ◽  
International Space ◽  
Expression Of Genes ◽  
Brown Adipose ◽  
Differential Expression Of Genes ◽  
Shivering Thermogenesis

AbstractSixteen-week-old female C57BL/6J mice were sacrificed aboard the International Space Station after 37 days of flight (RR-1 mission) and frozen carcasses returned to Earth. RNA was isolated from interscapular brown adipose tissue (BAT) and gonadal white adipose tissue (WAT). Spaceflight resulted in differential expression of genes in BAT consistent with increased non-shivering thermogenesis and differential expression of genes in WAT consistent with increased glucose uptake and metabolism, adipogenesis, and β-oxidation.

scholarly journals Stimulatory, but not anxiogenic, doses of caffeine act centrally to activate interscapular brown adipose tissue thermogenesis in anesthetized male rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
L. Van Schaik ◽  
C. Kettle ◽  
R. Green ◽  
W. Sievers ◽  
M. W. Hale ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Basolateral Amygdala ◽  
Free Breathing ◽  
Male Rats ◽  
Central Administration ◽  
Hypothalamic Area ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

AbstractThe role of central orexin in the sympathetic control of interscapular brown adipose tissue (iBAT) thermogenesis has been established in rodents. Stimulatory doses of caffeine activate orexin positive neurons in the lateral hypothalamus, a region of the brain implicated in stimulating BAT thermogenesis. This study tests the hypothesis that central administration of caffeine is sufficient to activate BAT. Low doses of caffeine administered either systemically (intravenous [IV]; 10 mg/kg) and centrally (intracerebroventricular [ICV]; 5–10 μg) increases BAT thermogenesis, in anaesthetised (1.5 g/kg urethane, IV) free breathing male rats. Cardiovascular function was monitored via an indwelling intra-arterial cannula and exhibited no response to the caffeine. Core temperature did not significantly differ after administration of caffeine via either route of administration. Caffeine administered both IV and ICV increased neuronal activity, as measured by c-Fos-immunoreactivity within subregions of the hypothalamic area, previously implicated in regulating BAT thermogenesis. Significantly, there appears to be no neural anxiety response to the low dose of caffeine as indicated by no change in activity in the basolateral amygdala. Having measured the physiological correlate of thermogenesis (heat production) we have not measured indirect molecular correlates of BAT activation. Nevertheless, our results demonstrate that caffeine, at stimulatory doses, acting via the central nervous system can increase thermogenesis, without adverse cardio-dynamic impact.

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