Activation of brain areas in rat following warm and cold ambient exposure
Semmelweis University, Budapeŝto, Budapest, Hungary Neuroscience
(Impact Factor: 3.36).
02/2004; 127(2):385-97. DOI: 10.1016/j.neuroscience.2004.05.016
Environmental thermal stimuli result in specific and coordinated thermoregulatory response in homeothermic animals. Warm exposure activates numerous brain areas within the cortex, hypothalamus, pons and medulla oblongata. We identified these thermosensitive cell groups in the medulla and pons that were suggested but not outlined by previous physiological studies. Using Fos immunohistochemistry, we localized all the nuclei and cell groups in the rat brain that were activated by warm and cold ambient exposure. These neurons located in the hypothalamus and the brainstem, are part of a network responsible for the thermospecific response elicited by thermal stress. Comparison of the distribution of Fos-immunoreactive cells throughout the rat brain revealed topographical differences between the patterns of activated cells following warm and cold environmental exposure. Among several brain regions, warm exposure elicited c-fos expression specifically in the ventrolateral part of the medial preoptic area, the central subdivision of the lateral parabrachial nucleus and the caudal part of the peritrigeminal nucleus, whereas cold stress resulted in c-fos expression in the ventromedial part of the medial preoptic area, the external subdivision of the lateral parabrachial nucleus and the rostral part of the peritrigeminal nucleus. These neurons are part of a network coordinating specific response to warm or cold exposure. The topographical differences suggest that well-defined cell groups and subdivisions of nuclei are responsible for the specific physiological (endocrine, autonomic and behavioral) changes observed in different thermal environment.
Available from: Domenico Tupone
- "thermogenesis is driven, not by the spinothalamocortical pathway mediating perception, localization and discrimination of cutaneous thermal stimuli, but rather by a spinoparabrachiopreoptic pathway, in which collateral axons of spinothalamic and trigeminothalamic lamina I dorsal horn neurons (Hylden et al., 1989; Li et al., 2006) activate lateral parabrachial nucleus (LPB) neurons projecting to thermoregulatory networks in the preoptic area (POA). Specifically, neurons in the external lateral subnucleus (LPBel) of the lateral parabrachial nucleus (LPB) and projecting to the median subnucleus (MnPO) of the POA are glutamatergically activated following cold exposure (Bratincsak and Palkovits, 2004; Nakamura and Morrison, 2008b), and thirdorder warm sensory neurons in the dorsal subnucleus (LPBd) are activated in response to skin warming (Bratincsak and Palkovits, 2004; Nakamura and Morrison, 2010). Although nociceptive inputs play only a minor role (Nakamura and Morrison, 2008b), there may be other non-thermal signals that are integrated with cutaneous thermal afferent inputs to LPB neurons in the afferent pathway contributing to regulate BAT thermogenesis. "
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ABSTRACT: From mouse to man, brown adipose tissue (BAT) is a significant source of thermogenesis contributing to the maintenance of the body temperature homeostasis during the challenge of low environmental temperature. In rodents, BAT thermogenesis also contributes to the febrile increase in core temperature during the immune response. BAT sympathetic nerve activity controlling BAT thermogenesis is regulated by CNS neural networks which respond reflexively to thermal afferent signals from cutaneous and body core thermoreceptors, as well as to alterations in the discharge of central neurons with intrinsic thermosensitivity. Superimposed on the core thermoregulatory circuit for the activation of BAT thermogenesis, is the permissive, modulatory influence of central neural networks controlling metabolic aspects of energy homeostasis. The recent confirmation of the presence of BAT in human and its function as an energy consuming organ have stimulated interest in the potential for the pharmacological activation of BAT to reduce adiposity in the obese. In contrast, the inhibition of BAT thermogenesis could facilitate the induction of therapeutic hypothermia for fever reduction or to improve outcomes in stroke or cardiac ischemia by reducing infarct size through a lowering of metabolic oxygen demand. This review summarizes the central circuits for the autonomic control of BAT thermogenesis and highlights the potential clinical relevance of the pharmacological inhibition or activation of BAT thermogenesis.
Frontiers in Neuroscience 02/2014; 8(8):14. DOI:10.3389/fnins.2014.00014 · 3.66 Impact Factor
Available from: Miklós Palkovits
- "In agreement with these findings, medial paralemniscal and possibly also posterior intralaminar TIP39 neurons have afferent neuronal connections with the primary auditory cortex and the external cortex of the inferior colliculus (Varga et al., 2008) providing the anatomical basis for an auditory influence on the CRH neurons in the PVN. Cold exposure but not warm ambient temperature induced cfos in some PVG neurons (Kiyohara et al., 1995; Miyata et al., 1995; Baffi and Palkovits, 2000; Bratincsak and Palkovits, 2004) providing the possibility that TIP39 neurons in this region could be activated by cold exposure leading to both stress responses and temperature regulation. It has also been reported that the cfos expression in the PVG significantly outlasts the cold exposure (Miyata et al., 1995), suggesting that it may have a role in the maintenance of homeostasis during adaptation to cold stress (Baffi and Palkovits, 2000). "
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ABSTRACT: The G-protein coupled parathyroid hormone 2 receptor (PTH2R) is concentrated in endocrine and limbic regions in the forebrain. Its endogenous ligand, tuberoinfundibular peptide of 39 residues (TIP39), is synthesized in only two brain regions, within the posterior thalamus and the lateral pons. TIP39-expressing neurons have a widespread projection pattern, which matches the PTH2R distribution in the brain. Neuroendocrine centers including the preoptic area, the periventricular, paraventricular, and arcuate nuclei contain the highest density of PTH2R-positive networks. The administration of TIP39 and an antagonist of the PTH2R as well as the investigation of mice that lack functional TIP39 and PTH2R revealed the involvement of the PTH2R in a variety of neural and neuroendocrine functions. TIP39 acting via the PTH2R modulates several aspects of the stress response. It evokes corticosterone release by activating corticotropin-releasing hormone-containing neurons in the hypothalamic paraventricular nucleus. Block of TIP39 signaling elevates the anxiety state of animals and their fear response, and increases stress-induced analgesia. TIP39 has also been suggested to affect the release of additional pituitary hormones including arginine-vasopressin and growth hormone. A role of the TIP39-PTH2R system in thermoregulation was also identified. TIP39 may play a role in maintaining body temperature in a cold environment via descending excitatory pathways from the preoptic area. Anatomical and functional studies also implicated the TIP39-PTH2R system in nociceptive information processing. Finally, TIP39 induced in postpartum dams may play a role in the release of prolactin during lactation. Potential mechanisms leading to the activation of TIP39 neurons and how they influence the neuroendocrine system are also described. The unique TIP39-PTH2R neuromodulator system provides the possibility for developing drugs with a novel mechanism of action to control neuroendocrine disorders.
Frontiers in Endocrinology 10/2012; 3:121. DOI:10.3389/fendo.2012.00121
Available from: Christopher John Madden
- "Neurons in the external lateral subnucleus (LPBel) of the LPB and projecting to the median subnucleus (MnPO) of the POA are activated following cold exposure (Bratincsak and Palkovits, 2004; Nakamura and Morrison, 2008b), while those in the dorsal subnucleus (LPBd) are activated in response to skin warming (Bratincsak and Palkovits, 2004; Nakamura and Morrison, 2010). The discharge rate of single, MnPO-projecting LPBel neurons recorded in vivo increased markedly in response to skin cooling in a manner paralleling the skin cooling-evoked increases in BAT SNA (Nakamura and Morrison, 2008b). "
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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). DOI:10.3389/fendo.2012.00005
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