Regulation of feeding behavior, gastric emptying, and sympathetic nerve activity to interscapular brown adipose tissue by galanin and enterostatin: the involvement of vagal-central nervous system interactions

2002 ◽  
Vol 37 (S14) ◽  
pp. 118-127 ◽  
Author(s):  
Hajime Nagase ◽  
Atsushi Nakajima ◽  
Hisahiko Sekihara ◽  
David A. York ◽  
George A. Bray
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Gastric Emptying ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose

Effect of beta-endorphin on sympathetic nerve activity to interscapular brown adipose tissue

1993 ◽  
Vol 264 (1) ◽  
pp. R109-R115 ◽  
Author(s):  
M. Egawa ◽  
H. Yoshimatsu ◽  
G. A. Bray
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Intracerebroventricular Injection ◽  
Nerve Activity ◽  
Reciprocal Effect ◽  
Interscapular Brown Adipose Tissue ◽  
Beta Endorphin ◽  
Brown Adipose

beta-Endorphin was injected into the third cerebroventricle to investigate its effects on sympathetic nerve activity to interscapular brown adipose tissue (IBAT) in rats. Multiunit discharges of sympathetic nerves to IBAT were recorded electrophysiologically in anesthetized rats. The intracerebroventricular injection of beta-endorphin (125, 250, and 500 pmol/rat in 10 microliters) suppressed sympathetic nerve activity in a dose-related fashion (-23.9 +/- 20.4, -38.7 +/- 7.1, and -66.7 +/- 7.6% 30 min after injection) compared with preinjection baseline. N-acetyl-beta-endorphin (250 pmol) had no effect on sympathetic nerve activity to IBAT. The intraperitoneal injection of naloxone (5.0 mg/rat) did not affect sympathetic nerve activity, but preinjection of naloxone inhibited the suppressive effect of intracerebroventricular injection of beta-endorphin (250 pmol). We conclude that the intracerebroventricular administration of beta-endorphin suppressed the sympathetic nerve activity to IBAT through opioid receptors. The results of this experiment are consistent with the hypothesis that beta-endorphin has a reciprocal effect on food intake and the sympathetic nervous system.

scholarly journals Identification of PACAP-Expressing Neurons in the Hypothalamic Origins of Sympathetic Outflow Tracts Terminating in Brown Adipose Tissue of Mice

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A541-A541
Author(s):  
Ekaterina Filatov ◽  
Alex P Rudecki ◽  
Alina-Geta Constantin ◽  
Sarah Louise Gray
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Cold Stress ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve ◽  
Energy Homeostasis ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Brown Adipose

Abstract Adaptive thermogenesis in brown adipose tissue is stimulated by the sympathetic nervous system (SNS) in response to cold stress. Using retrograde viral transneuronal tract tracers, previous studies have identified that the paraventricular nucleus (PVN), ventromedial hypothalamus (VMH), and median preoptic nucleus (MnPO) contain neurons that are part of sympathetic outflow tracts to brown adipose tissue, presumptively involved in SNS stimulation of interscapular brown adipose tissue (iBAT). Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) is a peptide hormone known to regulate energy homeostasis, acting in both the central (CNS) and peripheral nervous system (PNS). Mice lacking PACAP have impaired adrenergic-induced thermogenesis and a cold-sensitive phenotype. In the CNS, PACAP is highly expressed in the VMH, MnPO, and PVN of the hypothalamus. Injection of PACAP into the VMN increased core body temperature and sympathetic nerve activity to brown adipose tissue. While these studies show exogenous PACAP can activate sympathetic outflow tracts to brown adipose tissue, they do not confirm that endogenously expressed PACAP induces sympathetic nerve activity as an adaptive mechanism to cold stress, or if sympathetic outflow tracts originating in the hypothalamus express PACAP. We hypothesize that PACAP is expressed in neurons of sympathetic outflow tracts originating in the hypothalamus. To test this hypothesis, PACAP-eGFP transgenic mice were injected with the retrograde neural tracer, pseudorabies virus tagged with β-galactosidase (β-gal, PRV-BaBlu), in iBAT where postganglionic nerves innervate the tissue. Five-days post-infection, animals were culled, brains removed and cryosectioned. Neurons positive for green fluorescent protein (eGFP) and/or β-gal immunoreactivity (ir) were identified by immunohistochemistry in serial coronal and sagittal brain cryo-sections. Co-occurrence of eGFP-ir and β-gal-ir, inferred PACAP expressing neurons present in sympathetic outflow tracts (ImageJ). Co-occurrence was identified in several structures in the hypothalamus and thalamus. In conclusion, this study presents neuroanatomical evidence for populations of PACAPinergic neurons in the hypothalamus that are part of sympathetic outflow tracts to brown adipose tissue, providing further evidence of a central role for PACAP in regulating energy homeostasis.

Neuropeptide Y suppresses sympathetic activity to interscapular brown adipose tissue in rats

1991 ◽  
Vol 260 (2) ◽  
pp. R328-R334 ◽  
Author(s):  
M. Egawa ◽  
H. Yoshimatsu ◽  
G. A. Bray
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Hypothalamic Nucleus ◽  
Nerve Activity ◽  
Hypothalamic Area ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose

To investigate the effects of neuropeptide Y (NPY) on sympathetic nerve activity to interscapular brown adipose tissue (IBAT), we injected NPY into the third cerebroventricle (icv), medial preoptic area (MPOA), anterior hypothalamic area (AHA), paraventricular hypothalamic nucleus (PVN), ventromedial hypothalamic nucleus (VMN), and lateral hypothalamic area (LHA) of anesthetized rats. Multiunit discharges from sympathetic nerves to IBAT were recorded electrophysiologically. The icv injection of NPY suppressed sympathetic nerve activity in a dose-dependent manner, followed by a gradual recovery. The microinjection of NPY (25 pmol) unilaterally into the PVN also significantly suppressed the sympathetic nerve activity to IBAT. In contrast, microinjection of NPY into the MPOA significantly increased the sympathetic nerve activity. The injection of saline into either the PVN or MPOA had no significant effect on sympathetic nerve activity. The microinjection of NPY (25 pmol) into the AHA, VMN, or LHA did not change sympathetic nerve activity to IBAT. We conclude that central administration of NPY affects the sympathetic nerve activity to IBAT and that the suppressive effect of NPY, which may act in part through the PVN, is dominant to the stimulatory effect. The result is consistent with the hypothesis that NPY is a neurochemical modulator of the sympathetic nervous system which controls energy expenditure in IBAT.

scholarly journals Cardiovascular and Metabolic Crosstalk in the Brain: Leptin and Resistin

2021 ◽  
Vol 12 ◽  
Author(s):  
Emilio Badoer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Metabolic Complications ◽  
Brown Adipose ◽  
The Central Nervous System ◽  
The Brain

Leptin and resistin are cytokines whose plasma levels correlate with adiposity. Leptin is a hormone synthesised and released from adipocytes and can be transported into the brain. Resistin is produced in adipocytes in rodents and in macrophages in humans, particularly macrophages that have infiltrated adipose tissue. Both hormones can act within the brain to influence sympathetic nerve activity. Leptin appears to have a generalised sympatho-excitatory actions whilst resistin appears to increase sympathetic nerve activity affecting the cardiovascular system but inhibits sympathetic nerve activity to brown adipose tissue, which contrasts with leptin. Since both hormones can be elevated in conditions of metabolic dysfunction, interactions/crosstalk between these two hormones in the brain is a real possibility. This review describes the current knowledge regarding such crosstalk within the central nervous system. The evidence suggests that with respect to sympathetic nerve activity, crosstalk between leptin and resistin can elicit enhanced sympatho-excitatory responses to the kidneys. In contrast, with respect to food intake, resistin has weaker effects, but in regard to insulin secretion and thermogenesis, leptin and resistin have opposing actions. Thus, in conditions in which there is increased resistin and leptin levels, the result of crosstalk in the central nervous system could contribute to worse cardiovascular and metabolic complications.

scholarly journals Dual Regulatory Effects of Orexins on Sympathetic Nerve Activity Innervating Brown Adipose Tissue in Rats

Endocrinology ◽  
2005 ◽  
Vol 146 (6) ◽  
pp. 2744-2748 ◽  
Author(s):  
Tohru Yasuda ◽  
Takayuki Masaki ◽  
Tetsuya Kakuma ◽  
Masahide Hara ◽  
Tomoko Nawata ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Histidine Decarboxylase ◽  
Cerebral Ventricle ◽  
Induced Response ◽  
Nerve Activity ◽  
Orexin A ◽  
Brown Adipose

Abstract This study examined how orexin regulates the activity of the sympathetic nerves that innervate brown adipose tissue (BAT) in rats. Infusion of orexin A at a dose of 0.3 nmol into the third cerebral ventricle decreased BAT sympathetic nerve activity, compared with the effect of PBS (P < 0.05), whereas infusion of orexin B at the same dose caused a significant increase (P < 0.05). Pretreatment with a third cerebral ventricle injection of 2.24 μmol/kg α-fluoromethylhistidine, an irreversible inhibitor of the histamine-synthesizing enzyme histidine decarboxylase, attenuated the orexin B-induced response of BAT sympathetic nerve activity, but not that induced by orexin A. These results indicate that orexins may regulate both BAT energy expenditure and thermogenesis through their dual effects on sympathetic nerve activity. In particular, orexin B regulates BAT sympathetic nerve activity via neuronal histamine in the hypothalamus.

Effects of central injection of l-carnosine on sympathetic nerve activity innervating brown adipose tissue and body temperature in rats

2007 ◽  
Vol 144 (1-3) ◽  
pp. 62-71 ◽  
Author(s):  
Mamoru Tanida ◽  
Hitoshi Gotoh ◽  
Hiroyuki Taniguchi ◽  
Hiroto Otani ◽  
Jiao Shen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Brown Adipose
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