Activation of brown adipose tissue thermogenesis by chemical stimulation of the hypothalamic supraoptic nucleus

Amir, Shimon; Blasio, Emma De

doi:10.1016/0006-8993(91)91561-e

Cited by 15 publications

(3 citation statements)

References 30 publications

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“…Abundant experimental evidence suggests that the central control of the sympathetic outflow to IBAT in the rat is exerted mainly by the hypothalamus, which is the major brain area involved in thermoregulation and feeding behavior. Alterations in IBAT temperature, lipid turnover, or firing rate of sympathetic efferents to IBAT have been reported after electrical or chemical stimulation of several hypothalamic nuclei, such as VMH (Perkins et al, 1981; Takahashi and Shimazu, 1981; Amir, 1990b), lateral hypothalamic area (LH; Sakaguchi et al, 1988c; Yoshimatsu et al, 1992), paraventricular hypothalamic nucleus (PVH; Amir, 1990c), supraoptic nucleus (Amir and De Blasio, 1991), suprachiasmatic nucleus (SCh; Amir et al, 1989), and posterior hypothalamus (PH; Amir, 1990a). Studies using discrete lesions have corroborated the involvement of some of these nuclei in the control of IBAT thermogenesis (Saito et al, 1985; Sakaguchi et al, 1988a, b; Monda et al, 1996, 1997).…”

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confidence: 99%

Anatomical substrates for the central control of sympathetic outflow to interscapular adipose tissue during cold exposure

Cano

Passerin

Schiltz

et al. 2003

J of Comparative Neurology

296

333

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The thermogenic activity of interscapular brown adipose tissue (IBAT) in response to physiologic stimuli, such as cold exposure, is controlled by its sympathetic innervation. To determine which brain regions might be involved in the regulation of cold-evoked increases in sympathetic outflow to IBAT, the present study compared central nervous system (CNS) areas activated by cold exposure with brain regions anatomically linked to the sympathetic innervation of IBAT. Immunocytochemical localization of Fos was examined in the brains of rats exposed to 4 degrees C for 4 hours. In a separate group of rats, the neural circuit involved in IBAT control, including the location of sympathetic preganglionic neurons in the spinal cord, was characterized with pseudorabies virus, a retrograde transynaptic tracer. Central noradrenergic and serotonergic groups related to the sympathetic outflow to IBAT also were identified. Localization of viral antigens at different survival times (66-96 hours) revealed infection in circumscribed CNS populations, but only a subset of the regions comprising this circuitry showed cold-evoked Fos expression. The raphe pallidus and the ventromedial parvicellular subdivision of the paraventricular hypothalamic nucleus (PVH), both infected at early survival times, were the main areas containing sympathetic premotor neurons activated by cold exposure. Major cold-sensitive areas projecting to spinal interneurons or to regions containing sympathetic premotor neurons, which became infected at intermediate intervals, included lateral hypothalamic, perifornical, and retrochiasmatic areas, anterior and posterior PVH, ventrolateral periaqueductal gray, and Barrington's nucleus. Areas infected later, most likely related to reception of cold-related signals, comprised the lateral preoptic area, parastrial nucleus, dorsomedial hypothalamic nucleus, lateral parabrachial nucleus, and nucleus of the solitary tract. These interconnected areas, identified by combining functional and retrograde anatomic approaches, likely constitute the central circuitry responsible for the increase in sympathetic outflow to IBAT during cold-evoked thermogenesis.

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mentioning

confidence: 99%

Anatomical substrates for the central control of sympathetic outflow to interscapular adipose tissue during cold exposure

Cano

Passerin

Schiltz

et al. 2003

J of Comparative Neurology

296

333

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“…Cholinomimetics have been shown to excite a portion of the cells in SON [6,10]. The neuronal networks of osmoregulatory systems including SON overlap with the body temperature regulation mechanism [1]. It has been reported that electrical stimulation of SON [13] and glutamate microinjection into SON [1] increase body temperature.…”

Section: Introductionmentioning

confidence: 99%

“…The neuronal networks of osmoregulatory systems including SON overlap with the body temperature regulation mechanism [1]. It has been reported that electrical stimulation of SON [13] and glutamate microinjection into SON [1] increase body temperature. On the other hand, it has also been reported that hypothalamic injection of cholinomimetics induces hypothermia [14,17,31].…”

Section: Introductionmentioning

confidence: 99%

Cholinergic input to the supraoptic nucleus increases Fos expression and body temperature in rats

Takahashi

Ishimaru

Ikarashi

et al. 2001

Pflügers Arch - Eur J Physiol

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To examine the role played by cholinergic input and processes in the supraoptic nucleus (SON) in the control of body temperature and water intake in rats, we used microdialysis to stimulate and analyze SON without disturbing the behavior of unanesthetized rats. After microdialysis, we also investigated immunoreactivity for c-Fos protein in the brain as an index of neuronal activation. Stimulation with neostigmine, an acetylcholine esterase inhibitor, through the microdialysis probe increased the extracellular concentration of acetylcholine in the SON. This cholinergic stimulation dose-dependently increased body temperature but did not significantly change the water intake. The stimulation markedly increased c-Fos-like immunoreactivity (Fos-IR) in the SON and certain hypothalamic areas, including the paraventricular nucleus (PVN) and median preoptic nucleus (MnPO). Fos-IR was also evident in certain regions of the pons and brainstem, including the locus ceruleus (LC), area postrema (AP), and nucleus of the solitary tract (NTS). Addition of atropine, a muscarinic receptor antagonist, to the dialysis medium containing neostigmine attenuated the increase of Fos-IR and suppressed the neostigmine-induced responses in body temperature. These results suggest that cholinergic input and activation of the muscarinic cholinoceptive neurons in the SON contribute to the regulation of body temperature. Activation of noradrenergic pathways in the brainstem including LC and NTS may be involved in the thermoregulation mechanism.

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Endocrinological and Metabolic Responses to Acute and Chronic Heat Exposures

Francesconi

1996

Comprehensive Physiology

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Activation of brown adipose tissue thermogenesis by chemical stimulation of the hypothalamic supraoptic nucleus

Cited by 15 publications

References 30 publications

Anatomical substrates for the central control of sympathetic outflow to interscapular adipose tissue during cold exposure

Anatomical substrates for the central control of sympathetic outflow to interscapular adipose tissue during cold exposure

Cholinergic input to the supraoptic nucleus increases Fos expression and body temperature in rats

Endocrinological and Metabolic Responses to Acute and Chronic Heat Exposures

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