Energetic responses to cold temperatures in rats lacking forebrain-caudal brain stem connections.
ABSTRACT Hypothalamic neurons are regarded as essential for integrating thermal afferent information from skin and core and issuing commands to autonomic and behavioral effectors that maintain core temperature (T(c)) during cold exposure and for the control of energy expenditure more generally. Caudal brain stem neurons are necessary elements of the hypothalamic effector pathway and also are directly driven by skin and brain cooling. To assess whether caudal brain stem processing of thermal afferent signals is sufficient to drive endemic effectors for thermogenesis, heart rate (HR), T(c), and activity responses of chronic decerebrate (CD) and control rats adapted to 23 degrees C were compared during cold exposure (4, 8, or 12 degrees C) for 6 h. Other CDs and controls were exposed to 4 or 23 degrees C for 2 h, and tissues were processed for norepinephrine turnover (NETO), a neurochemical measure of sympathetic drive. Controls maintained T(c) for all temperatures. CDs maintained T(c) for the 8 and 12 degrees C exposures, but T(c) declined 2 degrees C during the 4 degrees C exposure. Cold exposure elevated HR in CDs and controls alike. Tachycardia magnitude correlated with decreases in environmental temperature for controls, but not CDs. Cold increased NETO in brown adipose tissue, heart, and some white adipose tissue pads in CDs and controls compared with their respective room temperature controls. These data demonstrate that, in neural isolation from the hypothalamus, cold exposure drives caudal brain stem neuronal activity and engages local effectors that trigger sympathetic energetic and cardiac responses that are comparable in many, but not in all, respects to those seen in neurologically intact rats.
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ABSTRACT: Thermogenesis, the production of heat energy, is an essential component of the homeostatic repertoire to maintain body temperature during the challenge of low environmental temperature and plays a key role in elevating body temperature during the febrile response to infection. Mitochondrial oxidation in brown adipose tissue (BAT) is a significant source of neurally regulated metabolic heat production in many species from mouse to man. BAT thermogenesis is regulated by neural networks in the central nervous system which responds to feedforward afferent signals from cutaneous and core body thermoreceptors and to feedback signals from brain thermosensitive neurons to activate BAT sympathetic nerve activity. This review summarizes the research leading to a model of the feedforward reflex pathway through which environmental cold stimulates BAT thermogenesis and includes the influence on this thermoregulatory network of the pyrogenic mediator, prostaglandin E(2), to increase body temperature during fever. The cold thermal afferent circuit from cutaneous thermal receptors, through second-order thermosensory neurons in the dorsal horn of the spinal cord ascends to activate neurons in the lateral parabrachial nucleus which drive GABAergic interneurons in the preoptic area (POA) to inhibit warm-sensitive, inhibitory output neurons of the POA. The resulting disinhibition of BAT thermogenesis-promoting neurons in the dorsomedial hypothalamus activates BAT sympathetic premotor neurons in the rostral ventromedial medulla, including the rostral raphe pallidus, which provide excitatory, and possibly disinhibitory, inputs to spinal sympathetic circuits to drive BAT thermogenesis. Other recently recognized central sites influencing BAT thermogenesis and energy expenditure are also described.Frontiers in Endocrinology 01/2012; 3(5).
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ABSTRACT: White adipose tissue (WAT) is innervated by the sympathetic nervous system (SNS) and its activation is necessary for lipolysis. WAT parasympathetic innervation is not supported. Fully-executed SNS-norepinephrine (NE)-mediated WAT lipolysis is dependent on β-adrenoceptor stimulation ultimately hinging on hormone sensitive lipase and perilipin A phosphorylation. WAT sympathetic drive is appropriately measured by electrophysiological and neurochemical (NE turnover) in non-human animals and this drive is fat pad-specific preventing generalizations among WAT depots and non-WAT organs. Leptin-triggered SNS-mediated lipolysis is weakly supported, whereas insulin or adenosine inhibition of SNS/NE-mediated lipolysis is strongly supported. In addition to lipolysis control, increases or decreases in WAT SNS drive/NE inhibit and stimulate white adipocyte proliferation, respectively. WAT sensory nerves are of spinal-origin and sensitive to local leptin and increases in sympathetic drive, the latter implicating lipolysis. Transsynaptic viral tract tracer use revealed WAT central sympathetic and sensory circuits including SNS-sensory feedback loops that may control lipolysis.Frontiers in Neuroendocrinology 04/2014; · 7.99 Impact Factor
Chapter: Brown Adipose Tissue[Show abstract] [Hide abstract]
ABSTRACT: A constant body temperature can only be maintained when the rate of heat dissipation equals the rate of heat loss. Thermoregulatory heat production mechanisms compensating heat loss are classically categorized as shivering and non-shivering thermogenesis. Non-shivering thermogenesis occurs in brown adipose tissue, a unique heater organ only found in mammals. In brown adipose tissue mitochondria, the proton motive force across the inner membrane is dissipated as heat rather than converted to ATP. This tightly regulated process is catalyzed by the uncoupling protein 1. Non-shivering thermogenesis is elicited by the sympathetic innervation from hypothalamic and brain stem control regions which are activated by cold sensation. In a cold environment, up to half of the metabolic rate of rodents can be attributed to non-shivering thermogenesis in brown adipose tissue. The high thermogenic capacity of brown adipose tissue recruited in the defense of normothermia may also play a role in the regulation of energy balance in the face of hypercaloric nutrition. In this light, the recent discovery of significant amounts of metabolically active brown adipose tissue in healthy adult humans reintroduces an old player in human energy balance research and may enable new strategies to prevent excess body fat accumulation in man. KeywordsUncoupling protein 1-Brown adipose tissue-White adipose tissue-Adipocyte-Progenitor-Mitochondria-ATP synthesis-Non-shivering thermogenesis-Progenitor-Proliferation-Differentiation11/2011: pages 39-69;