Neuropeptides in interscapular and perirenal brown adipose tissue in the rat: a plurality of innervation

Norman, David; Mukherjee, Sagarika; Symons, Deborah; Jung, R. T.; Lever, J. D.

doi:10.1007/bf01187853

Cited by 64 publications

(28 citation statements)

References 20 publications

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“…One possibility is that it comes from other BAT deposits around the body, since iBAT cannot account for more than 40% of all BAT deposits (24). However, there is no evidence to suggest that BAT deposits could be activated separately (8,22,26,27). The other possibility is that it comes from non-BAT tissues.…”

Section: Discussionmentioning

confidence: 99%

Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat

Marks¹,

Vianna²,

Carrive³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Marks A, Vianna DM, Carrive P. Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat. Am J Physiol Regul Integr Comp Physiol 296: R1239 -R1247, 2009. First published February 11, 2009 doi:10.1152/ajpregu.90723.2008.-As with other forms of psychological stress, conditioned fear causes an increase in body temperature. The mechanisms underlying this stress-induced hyperthermia are not well understood, but previous research suggests that nonshivering thermogenesis might contribute, as it does during cold exposure. The major source of nonshivering thermogenesis in the rat is brown adipose tissue (BAT), and the largest BAT deposit in that species is in the interscapular area just below the skin. BAT is also under sympathetic control via ␤-adrenoceptors. If BAT contributes to fear-induced hyperthermia, then the interscapular skin should warm up faster than other skin areas, and this response should be suppressed by the ␤-adrenoceptor antagonist, propranolol. We tested this noninvasively by infrared thermography. In conscious rats, 30 min of contextual fear caused hyperthermia (as indicated by a ϩ1.5°C increase in lumbar back skin temperature) and increased the difference in temperature between interscapular and lumbar back skin (TiScap Ϫ TBack) by ϩ1°C. Propranolol (10 mg/kg ip) completely abolished this hyperthermia; however, the TiScap-TBack increase was not reduced. In contrast, exposure to cold air (4°C) induced a ϩ2.7°C increase in TiScap-TBack, which was reduced to ϩ1°C after propranolol. The results show that conditioned fear-induced hyperthermia is of nonshivering origin and mediated by ␤-adrenoceptors, but interscapular BAT does not contribute to it and does not appear to be activated, either. stress hyperthermia; thermoregulation; tail skin; freezing; sympathetic responses MANY PSYCHOLOGICAL STRESSORS can cause an increase in body temperature (2,11,25,29), an effect also known as stress hyperthermia (2, 18). There are two ways in which body temperature can be elevated, either by reducing heat loss or by increasing heat production. The most effective way of reducing heat loss in the animal is through skin vasoconstriction (13). Increased heat production or thermogenesis can be achieved via two mechanisms: shivering thermogenesis if the heat comes from contracting skeletal muscles (15) or nonshivering thermogenesis if it comes from elsewhere (13, 17). The best studied effector of nonshivering thermogenesis is brown adipose tissue (BAT), which is under sympathetic control (4, 20). Only present in mammals, BAT is classically called into action during cold exposure. It is most often found in newborns, small mammals, and hibernating species, which are the ones who are most prone to suffer from cold stress, but it might also be functional in adult humans (6,20). Moreover, it is the only site where cold adaptation, that is, the development of increased recruitable thermogenic capacity in response to chronic cold exposure, occurs (4, 9, 12). In rats and ...

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Section: Discussionmentioning

confidence: 99%

Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat

Marks¹,

Vianna²,

Carrive³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…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 challenges (for review see Ref. 6).…”

mentioning

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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“…However, the failure of NPY to modulate the cAMP production, oxygen consumption and also ERK activation suggests that functional NPY receptors are lacking in brown adipocytes. Therefore, it is unlikely that NPY directly controls basal and NE-regulated thermogenesis in a short period of time, even if some sympathetic nerves carrying both NE and NPY innervate brown adipocytes [23,28,38].…”

Section: Discussionmentioning

confidence: 99%

“…The co-existence of sympathetic and peptidergic innervation has been demonstrated in BAT [5,11,23,28,38]. Among peptidergic neurotransmitters, neuropeptide Y (NPY) levels in the BAT are significantly decreased and increased by surgical excision of the sympathetic nerves to the BAT and putting an animal into a cold environment, respectively [30].…”

Section: Introductionmentioning

confidence: 99%

“…Similarly, it is suggested that NPY co-localizes with tyrosine hydroxylase in noradrenergic neurons, but only in the perivascular nerve fiber network [11]. However, other studies showed that NE-and NPY-positive fibers were also found around parenchymal brown adipocytes in mice [38] and rats [23,28]. 4 NPY exhibits its physiological effects through at least four receptors known as Y1, Y2, Y4, and Y5.…”

Section: Introductionmentioning

confidence: 99%

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Neuropeptide Y activates phosphorylation of ERK and STAT3 in stromal vascular cells from brown adipose tissue, but fails to affect thermogenic function of brown adipocytes

et al. 2012

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Neuropeptides in interscapular and perirenal brown adipose tissue in the rat: a plurality of innervation

Cited by 64 publications

References 20 publications

Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat

Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat

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

Neuropeptide Y activates phosphorylation of ERK and STAT3 in stromal vascular cells from brown adipose tissue, but fails to affect thermogenic function of brown adipocytes

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