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1
Wilent, W. Bryan, Michael Y. Oh, Catherine Buetefisch, Julian E. Bailes, Diane Cantella, Cindy Angle, and Donald M. Whiting. "Mapping of microstimulation evoked responses and unit activity patterns in the lateral hypothalamic area recorded in awake humans." Journal of Neurosurgery 115, no. 2 (August 2011): 295–300. http://dx.doi.org/10.3171/2011.3.jns101574.
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Major contributions to the understanding of human brain function have come from detailed clinical reports of responses evoked by electrical stimulation and specific brain regions during neurosurgical procedures in awake humans. In this study, microstimulation evoked responses and extracellular unit recordings were obtained intraoperatively in 3 awake patients undergoing bilateral implantation of deep brain stimulation electrodes in the lateral hypothalamus. The microstimulation evoked responses exhibited a clear anatomical distribution. Anxiety was most reliably evoked by stimulation directed ventromedially within or adjacent to the ventromedial nucleus of the hypothalamus, nausea was most reliably evoked by stimulation directed at the center of the lateral hypothalamus, and paresthesias were most reliably evoked by stimulation at the border of the lateral hypothalamus and basal nuclei. Regarding the unit recordings, the firing rates of individual neurons did not have an anatomical distribution, but a small subpopulation of neurons located at the border of the lateral hypothalamus and basal nuclei exhibited a fast rhythmically bursting behavior with an intraburst frequency of 200–400 Hz and an interburst frequency of 10–20 Hz. Based on animal studies, the lateral hypothalamic area and surrounding hypothalamic nuclei are putatively involved with a variety of physiological, behavioral, and sensory functions. The lateral hypothalamus is situated to play a dynamic and complex role in human behavior and this report further shows that to be true. In addition, this report should serve as a valuable resource for future intracranial work in which accurate targeting within this region is required.
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Take, S., D. Uchimura, Y. Kanemitsu, T. Katafuchi, and T. Hori. "Interferon-alpha acts at the preoptic hypothalamus to reduce natural killer cytotoxicity in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 6 (June 1, 1995): R1406—R1410. http://dx.doi.org/10.1152/ajpregu.1995.268.6.r1406.
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We previously demonstrated that an intracerebroventricular injection of recombinant human interferon-alpha (rhIFN-alpha) reduced the cytotoxicity of splenic natural killer (NK) cells in rats and mice. In the present study, we investigated the brain sites at which rhIFN-alpha acts to suppress splenic NK activity in unanesthetized rats implanted unilaterally with a chronic hypothalamic cannula. A microinjection of 200 U of rhIFN-alpha into the medial part of the preoptic hypothalamus reduced NK activity to approximately 60% of control 30 min after the injection. Administration of 50 U of rhIFN-alpha also decreased NK activity to approximately 80%. The injection of 200 U of rhIFN-alpha into other hypothalamic areas (lateral preoptic hypothalamus, ventromedial hypothalamus, lateral hypothalamus, and paraventricular nucleus) had no effect. The medial preoptic hypothalamus-rhIFN-alpha-induced immunosuppression was completely blocked by splenic denervation, but not by adrenalectomy. These results suggest that IFN-alpha suppresses splenic NK activity predominantly through the medial preoptic hypothalamus-sympathetic pathway.
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Yuan, C. S., and W. D. Barber. "Interactions of gastric vagal and peripheral nerves on single neurons of lateral hypothalamus in the cat." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 5 (November 1, 1996): G858—G865. http://dx.doi.org/10.1152/ajpgi.1996.271.5.g858.
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Extracellularly recorded unitary responses in the lateral hypothalamus were evaluated in anesthetized cats during electrical stimulation of the gastric branches of the ventral and dorsal vagal trunks, the T9 intercostal nerve, and the common peroneal nerve (L6-S2). These nerves were stimulated with single or paired (10-ms interval) pulses of 300–500 microA for 0.3 ms at a frequency of 0.5 Hz. The latency of the evoked lateral hypothalamic responses after stimulation of the gastric vagal branches (373 +/- 39.8 ms; means +/- SD) was significantly longer than the latencies after intercostal nerve (62 +/- 17.0 ms) or common peroneal nerve (109 +/- 29.3 ms) stimulation. Convergence of gastric vagal input from the proximal stomach and peripheral nerves (PNs) on single neurons in the lateral hypothalamus was observed. Ninety-two percent of the lateral hypothalamic neurons tested that responded to gastric vagal stimulation also received inputs from the T9 intercostal nerve. Seventy-seven percent of the lateral hypothalamic gastric vagally evoked unitary responses received convergent inputs from the intercostal nerve and the common peroneal nerve. A condition-test paradigm was applied to determine the time course of convergent gastric and PN input on single lateral hypothalamic neurons. The test revealed that stimulation of the T9 intercostal nerve had a more pronounced effect than common peroneal nerve stimulation on the lateral hypothalamic neurons that receive gastric vagal input. The results demonstrated that gastric vagal afferent and PN inputs converge onto single lateral hypothalamic neurons and suggested that the central processing of visceral input from the stomach can be substantially affected by peripheral nerve stimulation.
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Gutterman, D. D., A. C. Bonham, G. F. Gebhart, M. L. Marcus, and M. J. Brody. "Connections between hypothalamus and medullary reticular formation mediate coronary vasoconstriction." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 3 (September 1, 1990): H917—H924. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h917.
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We have recently identified discrete sites within the lateral hypothalamus and medullary reticular formation that, when stimulated electrically, produce neurally mediated coronary vasoconstriction. This study examined whether these sites are part of the same coronary vasomotor pathway. The neuronal tracing dye fast blue was injected in cats into the coronary vasoconstrictor site within medullary reticular formation. Fluorescence microscopy revealed major afferent projections originating from within the same region of midbrain ventrolateral periaqueductal gray that receives projections from lateral hypothalamus. To determine the functional importance of the proposed connections between the hypothalamic and medullary sites, anesthetized cats were prepared for continuous hemodynamic measurements. Constant current electrical stimulation within lateral hypothalamus produced significant increases in heart rate (21 +/- 6%), arterial pressure (11 +/- 3%), and femoral (36 +/- 18%) and coronary resistances (14 +/- 9%) with no change in coronary flow velocity (-1.1 +/- 2.5%). After beta-adrenoreceptor blockade, significantly greater increases in arterial pressure (35 +/- 8%) and coronary resistance (39 +/- 5%) with transient decreases in coronary flow velocity (21 +/- 6%) were seen. Microinjections of lidocaine into the medullary site blocked coronary constriction produced by lateral hypothalamic stimulation (39 +/- 5% increase in coronary resistance to electrical stimulation before and 2.4 +/- 2% increase after lidocaine in medullary reticular formation). These data provide evidence that specific regions of lateral hypothalamus and medullary reticular formation are part of a common central vasomotor projection that mediates coronary vasoconstriction in addition to other hemodynamic effects.
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Yuan, C. S., and W. D. Barber. "Hypothalamic unitary responses to gastric vagal input from the proximal stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 1 (January 1, 1992): G74—G80. http://dx.doi.org/10.1152/ajpgi.1992.262.1.g74.
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Gastric vagally evoked extracellular unitary responses were recorded in the hypothalamus of anesthetized cats. The evoked unitary responses were localized in the paraventricular dorsomedial region, ventromedial nucleus, and lateral hypothalamus. The mean latency of the gastric vagally evoked hypothalamic neuronal responses in these three areas ranged from 368 +/- 39.8 to 371 +/- 45.2 (SD) ms. The majority (82%) of the gastric vagally evoked hypothalamic responses consisted of one to five spikes, while the remaining 18% were tonically active units. The vagal effect was inhibitory in 78% of the tonically active hypothalamic units responding to gastric vagal input. Convergence of gastric vagal input on single hypothalamic units from afferents in the dorsal and ventral vagal trunks was observed. Units were identified in the hypothalamus that responded to activation of mechanoreceptors in the proximal stomach by an intragastric balloon. This study provided new direct evidence of the density, localization, and characteristics of neuronal processing of gastric vagal input from the proximal stomach in the hypothalamus. The reciprocal connections between these areas of the hypothalamus and nucleus tractus solitarius in the caudal brain stem suggest that the hypothalamus may serve an important role in modulating the input of primary vagal afferent input from the proximal stomach.
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Shimizu, Toru, Kevin Cox, Harvey J. Karten, and Luiz R. G. Britto. "Cholera toxin mapping of retinal projections in pigeons (Columba livia), with emphasis on retinohypothalamic connections." Visual Neuroscience 11, no. 3 (May 1994): 441–46. http://dx.doi.org/10.1017/s0952523800002376.
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AbstractAnterograde transport of cholera toxin subunit B (CTb) was used to study the retinal projections in birds, with an emphasis on retinohypothalamic connections. Pigeons (Columba livia) were deeply anesthetized and received unilateral intraocular injections of CTb. In addition to known contralateral retinorecipient regions, CTb-immunoreactive fibers and presumptive terminals were found in several ipsilateral regions, such as the nucleus of the basal optic root, ventral lateral geniculate nucleus, intergeniculate leaflet, nucleus lateralis anterior, area pretectalis, and nucleus pretectalis diffusus. In the hypothalamus, CTb-immunoreactive fibers were observed in at least two contralateral cell groups, a medial hypothalamic retinorecipient nucleus, and a lateral hypothalamic retinorecipient nucleus. To compare retinorecipient hypothalamic nuclei in pigeons with the mammalian suprachiasmatic nucleus, double-label experiments were conducted to study the existence of neurophysin-like immunoreactivity in the retinorecipient avian hypothalamus. The results showed that only cell bodies in the medial hypothalamic nucleus contained neurophysin-like immunoreactivity. The results demonstrate CTb to be a sensitive anterograde tracer and provide further anatomical information on the avian equivalent of the mammalian suprachiasmatic nucleus.
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Bonham, A. C., D. D. Gutterman, J. M. Arthur, M. L. Marcus, G. F. Gebhart, and M. J. Brody. "Electrical stimulation in perifornical lateral hypothalamus decreases coronary blood flow in cats." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 3 (March 1, 1987): H474—H484. http://dx.doi.org/10.1152/ajpheart.1987.252.3.h474.
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Based on evidence implicating the central nervous system in the regulation of coronary vascular resistance and the knowledge that the hypothalamus is a central site for integration of cardiovascular control, studies were undertaken to determine if electrical stimulation in the hypothalamus produced coronary vasoconstriction. In anesthetized cats, following beta-adrenergic receptor blockade, stimulation in perifornical lateral hypothalamus produced a transient decrease in coronary blood flow velocity (30 +/- 5%), a small pressor effect (7 +/- 2 mmHg), and an initial decrease in hindquarter blood flow velocity (51 +/- 5%). The decrease in coronary flow velocity, which had an onset latency of 1-3 s and a duration of 5-15 s, was abolished by ipsilateral stellate ganglionectomy and by intravenous and intracoronary prazosin. The coronary vasoconstriction produced by hypothalamic stimulation was not different from that produced by cardioaccelerator nerve stimulation. These results suggest that electrical stimulation of a hypothalamic site produces an alpha-adrenergic receptor-mediated decrease in coronary blood flow that is unmasked by beta-adrenergic receptor blockade, requires the integrity of ipsilateral cardiac sympathetic innervation, and mimics the coronary response to cardioaccelerator nerve stimulation.
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Meylakh, Noemi, Kasia K. Marciszewski, Flavia Di Pietro, Vaughan G. Macefield, Paul M. Macey, and Luke A. Henderson. "Altered regional cerebral blood flow and hypothalamic connectivity immediately prior to a migraine headache." Cephalalgia 40, no. 5 (March 12, 2020): 448–60. http://dx.doi.org/10.1177/0333102420911623.
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Background There is evidence of altered resting hypothalamic activity patterns and connectivity prior to a migraine, however it remains unknown if these changes are driven by changes in overall hypothalamic activity levels. If they are, it would corroborate the idea that changes in hypothalamic function result in alteration in brainstem pain processing sensitivity, which either triggers a migraine headache itself or allows an external trigger to initiate a migraine headache. We hypothesise that hypothalamic activity increases immediately prior to a migraine headache and this is accompanied by altered functional connectivity to pain processing sites in the brainstem. Methods In 34 migraineurs and 26 healthy controls, we collected a series comprising 108 pseudo-continuous arterial spin labelling images and 180 gradient-echo echo planar resting-state functional magnetic resonance volumes to measure resting regional cerebral blood flow and functional connectivity respectively. Images were pre-processed and analysed using custom SPM12 and Matlab software. Results Our results reflect that immediately prior to a migraine headache, resting regional cerebral blood flow decreases in the lateral hypothalamus. In addition, resting functional connectivity strength decreased between the lateral hypothalamus and important regions of the pain processing pathway, such as the midbrain periaqueductal gray, dorsal pons, rostral ventromedial medulla and cingulate cortex, only during this critical period before a migraine headache. Conclusion These data suggest altered hypothalamic function and connectivity in the period immediately prior to a migraine headache and supports the hypothesis that the hypothalamus is involved in migraine initiation.
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Mondal, Muhtashan S., Masamitsu Nakazato, and Shigeru Matsukura. "Orexins (hypocretins): novel hypothalamic peptides with divergent functions." Biochemistry and Cell Biology 78, no. 3 (April 2, 2000): 299–305. http://dx.doi.org/10.1139/o00-022.
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The hypothalamus is the most important region in the control of food intake and body weight. The ventromedial "satiety center" and lateral hypothalamic "feeding center" have been implicated in the regulation of feeding and energy homeostasis by various studies of brain lesions. The discovery of orexin peptides, whose neurons are localized in the lateral hypothalamus and adjacent areas, has given us new insight into the regulation of feeding. Dense fiber projections are found throughout the brain, especially in the raphe nucleus, locus coeruleus, paraventricular thalamic nucleus, arcuate nucleus, and central gray. Orexins mainly stimulate food intake, but by the virtue of wide immunoreactive projections throughout the brain and spinal cord, orexins interact with various neuronal pathways to potentate divergent functions. In this review, we summarize recent progress in the physiological, neuroanatomical, and molecular studies of the novel neuropeptide orexins (hypocretins).Key words: orexins (hypocretins), hypothalamus, lateral hypothalamus, feeding behavior, energy homeostasis, neurons.
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Ishii, Yuko, and Sebastien G. Bouret. "Embryonic Birthdate of Hypothalamic Leptin-Activated Neurons in Mice." Endocrinology 153, no. 8 (May 23, 2012): 3657–67. http://dx.doi.org/10.1210/en.2012-1328.
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The hypothalamus plays a critical role in the regulation of energy balance. Neuroanatomical and mouse genetic data have defined a core circuitry in the hypothalamus that mediates many of the effects of leptin on feeding and energy balance regulation. The present study used 5-bromo-2′-deoxyuridine (a marker of dividing cells) and a neuronal marker to systematically examine neurogenesis in the mouse embryonic hypothalamus, particularly the birth of neurons that relay leptin signaling. The vast majority of neurons in hypothalamic nuclei known to control energy balance is generated between embryonic days (E) 12 and E16, with a sharp peak of neurogenesis occurring on E12. Neurons in the dorsomedial and paraventricular nuclei and the lateral hypothalamic area are born between E12 and E14. The arcuate and ventromedial nuclei exhibit a relatively longer neurogenic period. Many neurons in these nuclei are born on E12, but some neurons are generated as late as E16. We also examined the birth of leptin-activated cells by coupling the 5-bromo-2′-deoxyuridine staining with cFos immunohistochemistry. Remarkably, the majority of leptin-activated cells in the adult hypothalamus were also born during a discrete developmental window on E12. These results provide new insight into the development of hypothalamic neurons that control feeding and identify important developmental periods when alterations in the intrauterine environment may affect hypothalamic neurogenesis and produce long-term consequences on hypothalamic cell numbers.
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Uchoa, Ernane Torres, Paula Beatriz Marangon, Rodrigo Rorato, Silvia Graciela Ruginsk, Lucas Kniess Debarba, Jose Antunes-Rodrigues, and Lucila L. K. Elias. "Adrenalectomy impairs insulin-induced hypophagia and related hypothalamic changes." Journal of Endocrinology 242, no. 2 (August 2019): 125–38. http://dx.doi.org/10.1530/joe-19-0217.
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Adrenalectomy (ADX) induces hypophagia and glucocorticoids counter-regulate the peripheral metabolic effects of insulin. This study evaluated the effects of ADX on ICV (lateral ventricle) injection of insulin-induced changes on food intake, mRNA expression of hypothalamic neuropeptides (insulin receptor (InsR), proopiomelanocortin, cocaine and amphetamine-regulated transcript (Cart), agouti-related protein, neuropeptide Y (Npy) in the arcuate nucleus of the hypothalamus (ARC), corticotrophin-releasing factor in the paraventricular nucleus of the hypothalamus) and hypothalamic protein content of insulin signaling-related molecules (insulin receptor substrate (IRS) 1, protein kinase B (AKT), extracellular-signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK), protein tyrosine phosphatase-1B (PTP1B) and T cell protein tyrosine phosphatase (TCPTP)) Compared with sham animals, ADX increased the hypothalamic content of pJNK/JNK, PTP1B and TCPTP, as well as decreased mRNA expression of InsR, and corticosterone (B) treatment reversed these effects. Insulin central injection enhanced hypothalamic content of pAKT/AKT and Cart mRNA expression, decreased Npy mRNA expression and food intake only in sham rats, without effects in ADX and ADX + B rats. Insulin did not alter the hypothalamic phosphorylation of IRS1 and ERK1/2 in the three experimental groups. These data demonstrate that ADX reduces the expression of InsR and increases insulin counter-regulators in the hypothalamus, as well as ADX abolishes hypophagia, activation of hypothalamic AKT pathway and changes in Cart and Npy mRNA expression in the ARC induced by insulin. Thus, the higher levels of insulin counter-regulatory proteins and lower expression of InsR in the hypothalamus are likely to underlie impaired insulin-induced hypophagia and responses in the hypothalamus after ADX.
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Simpson, Katherine Anne, Niamh M. Martin, and Stephen R. Bloom. "Hypothalamic regulation of food intake and clinical therapeutic applications." Arquivos Brasileiros de Endocrinologia & Metabologia 53, no. 2 (March 2009): 120–28. http://dx.doi.org/10.1590/s0004-27302009000200002.
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Current estimates suggest that over 1 billion people are overweight and over 300 million people are obese. Weight gain is due to an imbalance between energy expenditure and dietary intake. This review discusses the hypothalamic control of appetite and highlights key developments in research that have furthered our understanding of the complex pathways involved. Nuclei within the hypothalamus integrate peripheral signals such as adiposity and caloric intake to regulate important pathways within the central nervous system controlling food intake and energy expenditure. Firmly established pathways involve the orexigenic NPY/AgRP and the anorexigenic POMC/CART neurons in the arcuate nucleus (ARC) of the hypothalamus. These project from the ARC to other important hypothalamic nuclei, including the paraventricular, dorsomedial, ventromedial and lateral hypothalamic nuclei. In addition there are many projections to and from the brainstem, cortical areas and reward pathways, which modulate food intake.
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Diano, Sabrina, Balazs Horvath, Henryk F. Urbanski, Peter Sotonyi, and Tamas L. Horvath. "Fasting Activates the Nonhuman Primate Hypocretin (Orexin) System and Its Postsynaptic Targets." Endocrinology 144, no. 9 (September 1, 2003): 3774–78. http://dx.doi.org/10.1210/en.2003-0274.
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Abstract In rodents, hypocretin (HCRT, also called orexin) influences a variety of endocrine, autonomic, and metabolic functions. The present study was undertaken to determine whether the HCRT-producing circuit is involved in the hypothalamic regulation of homeostasis in primates as well. We studied female monkeys (Cercopithecus aethiops) that were either fed or fasted for 24 h. Immunocytochemistry revealed HCRT-producing perikarya exclusively in the lateral hypothalamus-perifornical region and dorsomedial hypothalamus of the monkey brain. HCRT axons and axon terminals were present in different parts of the hypothalamus and adjacent forebrain and thalamic nuclei. The 24-h fast resulted in an approximately 50% decline in circulating leptin levels and significantly elevated c-fos expression in the perifornical region; in the dorsomedial, ventromedial, and arcuate nuclei; and in the medial preoptic area. In the dorsomedial nucleus and perifornical region of fasted monkeys, three times more HCRT-neurons expressed nuclear c-fos than those of the normally fed controls. Neurons in different parts of the hypothalamus and basal forebrain that expressed c-fos, but did not contain HCRT, were targets of HCRT-immunopositive boutons establishing asymmetric synapses. In the arcuate nucleus, subsets of these HCRT-targeted c-fos-expressing cells contained neuropeptide Y. The present study provides the first experimental evidence to implicate HCRT in the hypothalamic regulation of homeostasis in primates. The fact that these lateral hypothalamic cells have leptin receptors and can be activated by a metabolic challenge and that they innervate diverse brain regions indicates that the HCRT system may be a key integrator of environmental cues in their regulation of diverse brain activity.
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Sakaguchi, T., M. Takahashi, and G. A. Bray. "Lateral hypothalamus and sympathetic firing rate." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 3 (September 1, 1988): R507—R512. http://dx.doi.org/10.1152/ajpregu.1988.255.3.r507.
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Measurements of sympathetic firing rate have been made after the acute microinjection of glucose or insulin into the lateral hypothalamic area as well as after ablation of this area with locally injected gold thioglucose. Injection of glucose into the lateral hypothalamus (LH) produced a small but significant and dose-dependent reduction in the firing rate of efferent sympathetic nerves to interscapular brown adipose tissue. Injection of insulin into the same region produced a very short-lived increase in efferent sympathetic firing rate. Bilateral lesions in the lateral hypothalamus produced by microinjection and gold thioglucose lowered body weight more than sham injections into the LH of control animals. There was an increase in basal sympathetic firing rate at 3, 9, and 24 h after LH lesions. There was also an increase in firing rate at 1 and 3 days, but by 7 days firing rate had returned to control levels. The data support the hypothesis that LH lesions enhance sympathetic activity but show only very limited modulation by glucose or insulin.
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Boundy, Virginia A., and Anthony H. Cincotta. "Hypothalamic adrenergic receptor changes in the metabolic syndrome of genetically obese (ob/ob) mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 2 (August 1, 2000): R505—R514. http://dx.doi.org/10.1152/ajpregu.2000.279.2.r505.
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The genetically, seasonally, and diet-induced obese, glucose-intolerant states in rodents, including ob/ ob mice, have each been associated with elevated hypothalamic levels of norepinephrine (NE). With the use of quantitative autoradiography on brain slices of 6-wk-old obese ( ob/ ob) and lean mice, the adrenergic receptor populations in several hypothalamic nuclei were examined. The binding of [125I]iodocyanopindolol to β1- and β2-adrenergic receptors in ob/ ob mice was significantly increased in the paraventricular hypothalamic nucleus (PVN) by 30 and 38%, in the ventromedial hypothalamus (VMH) by 23 and 72%, and in the lateral hypothalamus (LH) by 10 and 15%, respectively, relative to lean controls. The binding of [125I]iodo-4-hydroxyphenyl-ethyl-aminomethyl-tetralone to α1-adrenergic receptors was also significantly increased in the PVN (26%), VMH (67%), and LH (21%) of ob/ ob mice. In contrast, the binding of [125I]paraiodoclonidine to α2-adrenergic receptors in ob/ ob mice was significantly decreased in the VMH (38%) and the dorsomedial hypothalamus (17%) relative to lean controls. This decrease was evident in the α2A- but not the α2BC-receptor subtype. Scatchard analysis confirmed this decreased density of α2-receptors in ob/ ob mice. Together with earlier studies, these changes in hypothalamic adrenergic receptors support a role for increased hypothalamic NE activity in the development of the metabolic syndrome of ob/ obmice.
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Barber, W. D., and C. S. Yuan. "Gastric vagal-evoked and greater splanchnic-evoked unitary responses in the hypothalamus." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 6 (June 1, 1993): G1133—G1141. http://dx.doi.org/10.1152/ajpgi.1993.264.6.g1133.
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Gastric vagal and greater splanchnic nerve fibers were electrically stimulated to localize and characterize neuronal interactions in the hypothalamus of anesthetized cats. Extracellular recordings from 635 hypothalamic units were identified that responded to electrical stimulation of the left greater splanchnic nerve or gastric vagal fibers serving the proximal stomach. A total of 504 hypothalamic units in this group received input from both gastric vagal and greater splanchnic nerves. The gastric vagal-evoked hypothalamic (GVeH) and greater splanchnic-evoked hypothalamic (SeH) responses were widely distributed in the medial, paraventricular, and dorsomedial nuclei and lateral hypothalamus. The conduction velocity of the SeH response was significantly greater than the GVeH response. The latency of the SeH response showed two peaks [58 +/- 15.7 (SD) ms and 136 +/- 18.3 (SD) ms] indicating that the splanchnic input terminated on two different groups or populations of hypothalamic neurons. It also suggested that different pathways or fiber diameters in the pathway may be involved in the transmission of splanchnic input to the hypothalamus. The majority of the GVeH and SeH unitary responses were multiple spikes or short trains of action potentials. Excitatory and inhibitory responses were observed in tonically active hypothalamic units that responded to gastric vagal or greater splanchnic input. The duration of decreased excitability to gastric vagal or greater splanchnic input was significantly greater than the period of increased excitability. The condition-test paradigm was used to determine the time course of convergent gastric vagal-greater splanchnic input on single hypothalamic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
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Campbell, Erin J., Mitchell KRI Hill, Xavier J. Maddern, Shubo Jin, Terence Y. Pang, and Andrew J. Lawrence. "Orexin-1 receptor signaling within the lateral hypothalamus, but not bed nucleus of the stria terminalis, mediates context-induced relapse to alcohol seeking." Journal of Psychopharmacology 34, no. 11 (October 16, 2020): 1261–70. http://dx.doi.org/10.1177/0269881120959638.
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Background: The lateral hypothalamic orexin (hypocretin) system has a well-established role in the motivation for reward. This has particular relevance to substance use disorders since orexin-1 receptors play a critical role in alcohol-seeking behavior, acting at multiple nodes in relapse-associated networks. Aims: This study aimed to further our understanding of the role of orexin-1 receptor signaling within the lateral hypothalamus and bed nucleus of the stria terminalis, specifically in context-induced relapse to alcohol-seeking following punishment-imposed abstinence. Methods: We trained inbred male alcohol-preferring rats to self-administer alcohol in one environment or context (Context A) and subsequently punished their alcohol-reinforced lever presses in a different environment (Context B) using contingent foot shock punishment. Finally, we tested rats for relapse-like behavior in either context following systemic, intra-lateral hypothalamus or intra-bed nucleus of the stria terminalis orexin-1 receptor antagonism with SB-334867. Results/outcomes: We found that systemic orexin-1 receptor antagonism significantly reduced alcohol-seeking in both contexts. Intra-lateral hypothalamus orexin-1 receptor antagonism significantly reduced alcohol-seeking in Context A whereas intra-bed nucleus of the stria terminalis orexin-1 receptor antagonism had no effect on alcohol-seeking behavior. Conclusions/interpretation: Our results suggest a role for the orexin-1 receptor system in context-induced relapse to alcohol-seeking. Specifically, intra-lateral hypothalamus orexin microcircuits contribute to alcohol-seeking.
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You, Yaqian, Chung Yoh Kim, Gen Yan, and Jin Seo Park. "Surface models and true-color sectioned images of hypothalamic nuclei and its neighboring structures." Technology and Health Care 30 (February 25, 2022): 27–36. http://dx.doi.org/10.3233/thc-228003.
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BACKGROUND: Knowledge regarding the hypothalamic nuclei is essential for understanding neuroanatomy and has substantial clinical relevance. OBJECTIVE: The aim was to contribute to elucidate the complex hypothalamic architecture for research and provide an anatomical basis for clinical brain operation. METHODS: In this research, high-resolution and true-color sectioned images from Visible Korean were employed for hypothalamic nuclei and neighboring structures surface modeling, and a high-resolution three-dimensional atlas of the hypothalamus was created. RESULTS: Surface models of 26 structures including the hypothalamic nuclei and its neighboring structures were produced, which contained 5 anterior hypothalamic areas’ nuclei, 4 intermediate hypothalamic areas’ nuclei, 3 lateral hypothalamic areas’ nuclei, and 2 posterior hypothalamic areas’ nuclei, as well as 12 hypothalamic neighboring structures. CONCLUSIONS: The study evaluated the topographical anatomy of the hypothalamic nuclei and its neighboring structures based on true-color and highresolution sectioned images of Visible Korean.
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Gujar, Amit D., Baher A. Ibrahim, Pratistha Tamrakar, Ajeesh Koshy Cherian, and Karen P. Briski. "Hindbrain lactostasis regulates hypothalamic AMPK activity and metabolic neurotransmitter mRNA and protein responses to hypoglycemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 306, no. 7 (April 1, 2014): R457—R469. http://dx.doi.org/10.1152/ajpregu.00151.2013.
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Nerve cell metabolic activity is monitored in multiple brain regions, including the hypothalamus and hindbrain dorsal vagal complex (DVC), but it is unclear if individual metabolosensory loci operate autonomously or interact to coordinate central nervous system (CNS) reactivity to energy imbalance. This research addressed the hypothesis that hypoglycemia-associated DVC lactoprivation stimulates hypothalamic AMPK activity and metabolic neurotransmitter expression. As DVC catecholaminergic neurons express biomarkers for metabolic monitoring, we investigated whether these cells are a source of lactate deficit signaling to the hypothalamus. Caudal fourth ventricle (CV4) infusion of the glucose metabolite l-lactate during insulin-induced hypoglycemia reversed changes in DVC A2 noradrenergic, arcuate neuropeptide Y (NPY) and pro-opiomelanocortin (POMC), and lateral hypothalamic orexin-A (ORX) neuronal AMPK activity, coincident with exacerbation of hypoglycemia. Hindbrain lactate repletion also blunted hypoglycemic upregulation of arcuate NPY mRNA and protein. This treatment did not alter hypoglycemic paraventricular oxytocin (OT) and lateral hypothalamic ORX mRNA profiles, but exacerbated or reversed adjustments in OT and ORX neuropeptide synthesis, respectively. CV4 delivery of the monocarboxylate transporter inhibitor, 4-CIN, increased A2 phosphoAMPK (pAMPK), elevated circulating glucose, and stimulated feeding, responses that were attenuated by 6-hydroxydopamine pretreatment. 4-CIN-infused rats exhibited increased (NPY, ORX neurons) or decreased (POMC neurons) pAMPK concurrent with hyperglycemia. These data show that hindbrain lactoprivic signaling regulates hypothalamic AMPK and key effector neurotransmitter responses to hypoglycemia. Evidence that A2 AMPK activity is lactate-dependent, and that DVC catecholamine cells are critical for lactoprivic control of glucose, feeding, and hypothalamic AMPK, implies A2 derivation of this metabolic regulatory stimulus.
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Kinote, Andrezza, Juliana A. Faria, Erika A. Roman, Carina Solon, Daniela S. Razolli, Letícia M. Ignacio-Souza, Carolina S. Sollon, et al. "Fructose-Induced Hypothalamic AMPK Activation Stimulates Hepatic PEPCK and Gluconeogenesis due to Increased Corticosterone Levels." Endocrinology 153, no. 8 (May 14, 2012): 3633–45. http://dx.doi.org/10.1210/en.2012-1341.
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Fructose consumption causes insulin resistance and favors hepatic gluconeogenesis through mechanisms that are not completely understood. Recent studies demonstrated that the activation of hypothalamic 5′-AMP-activated protein kinase (AMPK) controls dynamic fluctuations in hepatic glucose production. Thus, the present study was designed to investigate whether hypothalamic AMPK activation by fructose would mediate increased gluconeogenesis. Both ip and intracerebroventricular (icv) fructose treatment stimulated hypothalamic AMPK and acetyl-CoA carboxylase phosphorylation, in parallel with increased hepatic phosphoenolpyruvate carboxy kinase (PEPCK) and gluconeogenesis. An increase in AMPK phosphorylation by icv fructose was observed in the lateral hypothalamus as well as in the paraventricular nucleus and the arcuate nucleus. These effects were mimicked by icv 5-amino-imidazole-4-carboxamide-1-β-d-ribofuranoside treatment. Hypothalamic AMPK inhibition with icv injection of compound C or with injection of a small interfering RNA targeted to AMPKα2 in the mediobasal hypothalamus (MBH) suppressed the hepatic effects of ip fructose. We also found that fructose increased corticosterone levels through a mechanism that is dependent on hypothalamic AMPK activation. Concomitantly, fructose-stimulated gluconeogenesis, hepatic PEPCK expression, and glucocorticoid receptor binding to the PEPCK gene were suppressed by pharmacological glucocorticoid receptor blockage. Altogether the data presented herein support the hypothesis that fructose-induced hypothalamic AMPK activation stimulates hepatic gluconeogenesis by increasing corticosterone levels.
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Yu, Hui, and Malcolm James Low. "Single Nucleus RNA-Sequencing Reveals Overall Conservation of Hypothalamic Cell Identities but Differential Expression of Specific Genes in the Magel2 Null Mouse Model of Prader-Willi Syndrome." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A509. http://dx.doi.org/10.1210/jendso/bvab048.1041.
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Abstract Prader-Willi syndrome (PWS) is a genetic disorder affecting 1 in 10,000 to 30,000 live births. Diagnostic features of PWS including insatiable appetite and obesity are well-defined and many are associated with disruption of hypothalamic function. PWS is caused by sporadic or inherited loss of expression from the paternal allele of one or more maternally imprinted/silenced genes located in chromosomal region 15q11-q13 that encompasses five protein coding genes Mkrn3, Magel2, Necdin and Snurf-Snprn and a family of snoRNAs. Seminal studies have indicated that isolated Magel2 gene silencing plays a pivotal role in the development of many, but not all, clinical features of PWS. Magel2 is highly expressed in the hypothalamus and loss of function studies revealed substantial cellular and molecular changes in hypothalamic neurons located in the suprachiasmatic, paraventricular, supraoptic and arcuate nuclei and the lateral hypothalamus. In addition to neuronal alterations, loss of MAGEL2 increases the density and activation of microglia in adult hypothalamus. In the current study, we characterized global changes in hypothalamic gene expression and searched for novel cell populations associated with loss of Magel2 expression using single nucleus RNA sequencing. Single cell nuclei were isolated in two technical replicates per group from hypothalami of adult male and female Magel2-null (C57BL/6-Magel2tm1Stw/J) and wild type sibling mice for the 10X genomics scRNA-seq pipeline. A total of 63,470 cells divided approximately equally by sex and Magel2 genotype were analyzed. Unsupervised cell clustering identified 19 distinct clusters in males (10 neuronal and 9 non-neuronal) and 21 clusters in females (11 neuronal and 10 non-neuronal) based on their transcriptional profiles of signature genes. The percentages of total cells and the transcriptional profiles of each defined cluster from all four combinations of genotype and sex were nearly identical, indicating that loss-of-function of Magel2 does not alter overall cell cluster identities in the hypothalamus. However, a quantitative analysis of gene expression profiles from all individual clusters demonstrated upregulation of a set of genes including Fkbp5, Zbtb16, Htra1, 2900097C17Rik and 1700030F04Rik predominantly in oligodendrocytes and astrocytes in both sexes of Magel2 null mice. In contrast, the majority of down-regulated genes were found in neuronal cell clusters in both sexes of Magel2 null mice. Our current study is the first to characterize cellular and genetic changes in the whole hypothalamus due to the lack of MAGEL2. The data provide a valuable resource for elucidating the regulatory mechanisms of MAGEL2 for the pathogenesis of PWS and shed light on the discovery of new candidate targets for the potential treatment of PWS. This study is supported by the Foundation for Prader-Willi Research and NIH grant R01DK068400.
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Schoenknecht, P., A. Anwander, F. Petzold, S. Schindler, T. Knoesche, U. Hegerl, R. Turner, and S. Geyer. "FC12-03 - DTI-based in vivo mapping of subregions within the human hypothalamus." European Psychiatry 26, S2 (March 2011): 1878. http://dx.doi.org/10.1016/s0924-9338(11)73582-9.
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IntroductionThe hypothalamus is involved in many aspects of behavioral responses but parcellations of hypothalamic subnuclei have only been feasible in post-mortem brains. Thus it would be-from a clinical point of view-highly desirable if hypothalamic subnuclei could be delineated also noninvasively in living subjects. This study is a first step in this direction: We exploited the directionality information inherent in high-resolution DTI data to map subregions of the hypothalamus in healthy volunteers.directionality information using DTI data to map subregions of the hypothalamus.MethodsWe scanned 10 subjects with a Siemens 3 T scanner, acquired DTI and T1 scans. We computed the similarity of fiber orientations between all voxels and subjects, and clustered the similarity matrix in 3 regions using a k-means algorithm.ResultsThe diffusion images showed anisotropic tissue orientation within the hypothalamus which was consistent across subjects. The clustering in 3 regions resulted in an anatomically coherent arrangement of clusters across hemispheres and subjects. In each ROI, we found an anterior, a posteromedial, and a lateral subdivision with consistent microscopic tissue orientations across subjects.ConclusionThis is to our best knowledge the first study that demonstrates the fine-grained microstructural organization within the human hypothalamus noninvasively in living subjects.
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Wu, Z., E. R. Kim, H. Sun, Y. Xu, L. R. Mangieri, D. P. Li, H. L. Pan, Y. Xu, B. R. Arenkiel, and Q. Tong. "GABAergic Projections from Lateral Hypothalamus to Paraventricular Hypothalamic Nucleus Promote Feeding." Journal of Neuroscience 35, no. 8 (February 25, 2015): 3312–18. http://dx.doi.org/10.1523/jneurosci.3720-14.2015.
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Ruiter, Marieke, Patricia Duffy, Steven Simasko, and Robert C. Ritter. "Increased Hypothalamic Signal Transducer and Activator of Transcription 3 Phosphorylation after Hindbrain Leptin Injection." Endocrinology 151, no. 4 (February 25, 2010): 1509–19. http://dx.doi.org/10.1210/en.2009-0854.
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Reduction of food intake and body weight by leptin is attributed largely to its action in the hypothalamus. However, the signaling splice variant of the leptin receptor, LRb, also is expressed in the hindbrain, and leptin injections into the fourth cerebral ventricle or dorsal vagal complex are associated with reductions of feeding and body weight comparable to those induced by forebrain leptin administration. Although these observations suggest direct hindbrain action of leptin on feeding and body weight, the possibility that hindbrain leptin administration also activates the Janus kinase/signal transducer and activator of transcription 3 (STAT3) signaling in the hypothalamus has not been investigated. Confirming earlier work, we found that leptin produced comparable reductions of feeding and body weight when injected into the lateral ventricle or the fourth ventricle. We also found that lateral and fourth ventricle leptin injections produced comparable increases of STAT3 phosphorylation in both the hindbrain and the hypothalamus. Moreover, injection of 50 ng of leptin directly into the nucleus of the solitary tract also increased STAT3 phosphorylation in the hypothalamic arcuate and ventromedial nuclei. Increased hypothalamic STAT3 phosphorylation was not due to elevation of blood leptin concentrations and the pattern of STAT3 phosphorylation did not overlap distribution of the retrograde tracer, fluorogold, injected via the same cannula. Our observations indicate that even small leptin doses administered to the hindbrain can trigger leptin-related signaling in the forebrain, and raise the possibility that STAT3 phosphorylation in the hypothalamus may contribute to behavioral and metabolic changes observed after hindbrain leptin injections.
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Douglas, R. M., C. O. Trouth, S. D. James, L. M. Sexcius, P. Kc, O. Dehkordi, E. R. Valladares, and J. C. McKenzie. "Decreased CSF pH at ventral brain stem induces widespread c-Fos immunoreactivity in rat brain neurons." Journal of Applied Physiology 90, no. 2 (February 1, 2001): 475–85. http://dx.doi.org/10.1152/jappl.2001.90.2.475.
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Physiological evidence has indicated that central respiratory chemosensitivity may be ascribed to neurons located at the ventral medullary surface (VMS); however, in recent years, multiple sites have been proposed. Because c-Fos immunoreactivity is presumed to identify primary cells as well as second- and third-order cells that are activated by a particular stimulus, we hypothesized that activation of VMS cells using a known adequate respiratory stimulus, H+, would induce production of c-Fos in cells that participate in the central pH-sensitive respiratory chemoreflex loop. In this study, stimulation of rostral and caudal VMS respiratory chemosensitive sites in chloralose-urethane-anesthetized rats with acidic (pH 7.2) mock cerebrospinal fluid induced c-Fos protein immunoreactivity in widespread brain sites, such as VMS, ventral pontine surface, retrotrapezoid, medial and lateral parabrachial, lateral reticular nuclei, cranial nerves VII and X nuclei, A1 and C1 areas, area postrema, locus coeruleus, and paragigantocellular nuclei. At the hypothalamus, the c-Fos reaction product was seen in the dorsomedial, lateral hypothalamic, supraoptic, and periventricular nuclei. These results suggest that 1) multiple c-Fos-positive brain stem and hypothalamic structures may represent part of a neuronal network responsive to cerebrospinal fluid pH changes at the VMS, and 2) VMS pH-sensitive neurons project to widespread regions in the brain stem and hypothalamus that include respiratory and cardiovascular control sites.
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Remmers, Floor, Linda A. W. Verhagen, Roger A. H. Adan, and Henriette A. Delemarre-van de Waal. "Hypothalamic Neuropeptide Expression of Juvenile and Middle-Aged Rats after Early Postnatal Food Restriction." Endocrinology 149, no. 7 (March 27, 2008): 3617–25. http://dx.doi.org/10.1210/en.2007-1388.
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Rats subjected to early postnatal food restriction (FR) show persistent changes in energy balance. The hypothalamus plays a major role in the regulation of energy balance. Therefore, we hypothesized that early postnatal food restriction induces developmental programming of hypothalamic gene expression of neuropeptides involved in this regulation. In the hypothalamus of juvenile and middle-aged rats that were raised in control (10 pups) or FR litters (20 pups), gene expression was investigated for neuropeptide Y (NPY), agouti-related protein (AgRP), proopiomelanocortin (POMC), and cocaine- and amphetamine-regulated transcript (CART) in the arcuate nucleus (ARC); CRH and TRH in the paraventricular nucleus; and melanin-concentrating hormone (MCH) and orexin in the lateral hypothalamic area. Early postnatal FR acutely and persistently reduced body size. Juvenile FR rats had significantly reduced CART gene expression and increased MCH expression. In middle-aged FR rats, POMC and CART mRNA levels were significantly reduced. The ratio between expression of the ARC orexigenic peptides (NPY and AgRP) and anorexigenic peptides (POMC and CART) was increased in juvenile, but not in middle-aged, FR rats. These results suggest that in neonatal rats, FR already triggers the ARC, and to a lesser extent the lateral hypothalamic area, but not the paraventricular nucleus, to increase expression of orexigenic relative to anorexigenic peptides. In addition, with enduring small body size and normalized hypothalamic gene expression, the adult FR rats appeared to have accepted this smaller body size as normal. This suggests that the body weight set-point was differently programmed in animals with early postnatal FR.
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Takahashi, Akira, Eiko Kishi, Hirohisa Ishimaru, Yasushi Ikarashi, and Yuji Maruyama. "Stimulation of rat hypothalamus by microdialysis with K+: increase of ACh release elevates plasma glucose." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 5 (November 1, 1998): R1647—R1653. http://dx.doi.org/10.1152/ajpregu.1998.275.5.r1647.
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The effects of stimulation of the ventromedial hypothalamus (VMH) or lateral hypothalamus (LH) with potassium chloride through a microdialysis probe were studied. The concentrations of ACh and norepinephrine (NE) in the dialysate obtained from the hypothalamic nuclei and plasma glucose concentration were measured. Stimulation of the hypothalamic nuclei, VMH and LH, with potassium increased the plasma glucose level as well as the extracellular concentrations of ACh and choline. Addition of atropine, a muscarinic ACh receptor antagonist, into the potassium solution reduced the increase in the level of plasma glucose. Cholinergic stimulation of these nuclei with neostigmine increased the extracellular concentrations of ACh and plasma glucose. Stimulation of the nuclei with potassium also increased the release of NE. However, stimulation of the VMH or LH with NE and/or pargyline, a monoamine oxidase inhibitor, through the dialysis probe membrane did not significantly increase the plasma glucose concentration. These results suggest that activation of the muscarinic cholinergic or ACh-receptive neurons in the hypothalamic nuclei, VMH and LH, contribute to the elevation of plasma glucose level.
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Lawrence, Catherine B., Torrie Williams, and Simon M. Luckman. "Intracerebroventricular Galanin-Like Peptide Induces Different Brain Activation Compared with Galanin." Endocrinology 144, no. 9 (September 1, 2003): 3977–84. http://dx.doi.org/10.1210/en.2003-0391.
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Abstract Like galanin, the 60-amino-acid peptide, galanin-like peptide (GALP), has orexigenic actions, demonstrated by an acute increase in feeding after central injection in rodents. However, in contrast to galanin, GALP causes a prolonged rise in core body temperature and a reduction in body weight over 24 h. In an attempt to identify potential explanations for the observed differences between GALP and galanin, this study examined which brain areas were activated by these peptides. Intracerebroventricular injection of GALP into conscious rats significantly stimulated feeding over 0–1 h, increased core body temperature, but reduced body weight gain over 24 h. Immunohistochemistry to detect c-fos demonstrated that intracerebroventricular injection of GALP or galanin activated several brain regions in common, including the dorsomedial nucleus of the hypothalamus, lateral hypothalamus, and nucleus tractus solitarius of the brainstem. However, GALP also induced c-fos expression in the periventricular hypothalamic region and supraoptic hypothalamic nucleus. Cell activation induced by GALP in the supraoptic hypothalamic nucleus and nucleus tractus solitarius was dependent on food intake but independent of food consumption in all other brain regions. Double immunohistochemistry indicated that small cells expressing c-fos in the periventricular hypothalamic region after GALP were astrocytes and not microglia.
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Mori, Rosana CT, Regina B. Guimarães, Cláudia MO Nascimento, and Eliane B. Ribeiro. "Lateral hypothalamic serotonergic responsiveness to food intake in rat obesity as measured by microdialysis." Canadian Journal of Physiology and Pharmacology 77, no. 4 (April 1, 1999): 286–92. http://dx.doi.org/10.1139/y99-024.
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The hypothalamic serotonergic system is involved in the regulation of food ingestion and energy metabolism. Since disturbances of both energy intake and expenditure can contribute to obesity, the objective of the present study was to evaluate the serotonergic response stimulated by food ingestion in two different models of obesity: the hyperphagic Zucker and the hypophagic and hypometabolic, monosodium glutamate (MSG) obese Wistar rat. For this we used microdialysis to examine the release of 5-hydroxytryptamine (serotonin, 5HT) and 5-hydroxyindoleacetic acid (5HIAA) in the lateral hypothalamus. Daily intake of MSG-obese rats was 40% lower while that of Zucker obese rats was 60% higher than that of the respective lean controls. In overnight-fasted animals, 20-min microdialysate samples were collected before (basal release) and during a 2-h period of access to a balanced palatable food mash. The animals began to eat during the first 20 min of food access, and food consumption was similar among the four groups in all six individual 20-min periods recorded. Ingestion of food increased 5HT release in all groups. In MSG-obese and lean Wistar rats, 5HT levels were similarly elevated during the whole experimental period. In the Zucker strain, 5HT increments of basal release tended to be higher in obese than in lean rats at 20 and 40 min, and a significantly higher increment was observed at 60 min after food access (40 and 135% for lean and obese, respectively). The area under the curve relating serotonin levels to the 120 min of food availability was significantly higher in Zucker obese (246.7 ± 23.3) than MSG-obese (152.7 ± 13.4), lean Wistar (151.9 ± 11.1), and lean Zucker (173.5 ± 24.0) rats. The present observation, of a food-induced serotonin release in the lateral hypothalamus of lean Wistar and Zucker rats, evidences that 5HT in the lateral hypothalamus is important in the normal response to feeding. In obese animals, the serotonin response was similar to (in the hypophagic-hypometabolic MSG model) or even higher than (in the hyperphagic Zucker model) that seen in the respective lean controls. This result indicates that the energy homeostasis disturbances of both these obesity models may not be ascribed to an impairment of the acute lateral hypothalamic serotonin response to a dietary stimulus.Key words: serotonin, food intake, brain microdialysis, lateral hypothalamus, monosodium glutamate obesity, Zucker obesity.
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Takaki, A., S. Aou, Y. Oomura, E. Okada, and T. Hori. "Feeding suppression elicited by electrical and chemical stimulations of monkey hypothalamus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, no. 4 (April 1, 1992): R586—R594. http://dx.doi.org/10.1152/ajpregu.1992.262.4.r586.
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The effects of electrical (ES) and chemical stimulations of the hypothalamus were investigated in monkeys during bar-press feeding. ES elicited both prolonged and nonprolonged types of suppression of bar-press feeding in hungry animals. Prolonged type suppression persisted for greater than 1 min beyond one or more post-ES trials and was found after ES of the dorsomedial hypothalamus (DMH), the ventromedial hypothalamus (VMH), and the ventromedial part of the lateral hypothalamic area (LHA). Non-prolonged type suppression was observed only during ES at some sites of both in hypothalamic and extrahypothalamic areas. A microinjection of glutamate into the VMH and the DMH, but not into the LHA, was able to reproduce the ES-induced prolonged type suppression. In contrast, the ES of the LHA, but not the VMH and DMH, in a satiated state provoked feeding. The results, together with the previous findings, suggest that the neuronal inhibitory mechanism of feeding exists in the VMH and DMH, while both the neuronal facilitatory and axonal inhibitory mechanisms in the LHA are involved in the feeding regulation, and these mechanisms of the LHA are affected by the hunger/satiety state.
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Pena-Leon, Veronica, Cintia Folgueira, Silvia Barja-Fernández, Raquel Pérez-Lois, Natália Da Silva Lima, Marion Martin, Violeta Heras, et al. "Prolonged breastfeeding protects from obesity by hypothalamic action of hepatic FGF21." Nature Metabolism 4, no. 7 (July 2022): 901–17. http://dx.doi.org/10.1038/s42255-022-00602-z.
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AbstractEarly-life determinants are thought to be a major factor in the rapid increase of obesity. However, while maternal nutrition has been extensively studied, the effects of breastfeeding by the infant on the reprogramming of energy balance in childhood and throughout adulthood remain largely unknown. Here we show that delayed weaning in rat pups protects them against diet-induced obesity in adulthood, through enhanced brown adipose tissue thermogenesis and energy expenditure. In-depth metabolic phenotyping in this rat model as well as in transgenic mice reveals that the effects of prolonged suckling are mediated by increased hepatic fibroblast growth factor 21 (FGF21) production and tanycyte-controlled access to the hypothalamus in adulthood. Specifically, FGF21 activates GABA-containing neurons expressing dopamine receptor 2 in the lateral hypothalamic area and zona incerta. Prolonged breastfeeding thus constitutes a protective mechanism against obesity by affecting long-lasting physiological changes in liver-to-hypothalamus communication and hypothalamic metabolic regulation.
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Wright, Chadwick L., Penny W. Burgoon, Georgia A. Bishop, and Jack A. Boulant. "Cyclic GMP alters the firing rate and thermosensitivity of hypothalamic neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 5 (May 2008): R1704—R1715. http://dx.doi.org/10.1152/ajpregu.00714.2007.
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The rostral hypothalamus, especially the preoptic-anterior hypothalamus (POAH), contains temperature-sensitive and -insensitive neurons that form synaptic networks to control thermoregulatory responses. Previous studies suggest that the cyclic nucleotide cGMP is an important mediator in this neuronal network, since hypothalamic microinjections of cGMP analogs produce hypothermia in several species. In the present study, immunohistochemisty showed that rostral hypothalamic neurons contain cGMP, guanylate cyclase (necessary for cGMP synthesis), and CNG A2 (an important cyclic nucleotide-gated channel). Extracellular electrophysiological activity was recorded from different types of neurons in rat hypothalamic tissue slices. Each recorded neuron was classified according to its thermosensitivity as well as its firing rate response to 2–100 μM 8-bromo-cGMP (a membrane-permeable cGMP analog). cGMP has specific effects on different neurons in the rostral hypothalamus. In the POAH, the cGMP analog decreased the spontaneous firing rate in 45% of temperature-sensitive and -insensitive neurons, an effect that is likely due to cGMP-enhanced hyperpolarizing K+ currents. This decreased POAH activity could attenuate thermoregulatory responses and produce hypothermia during exposures to cool or neutral ambient temperatures. Although 8-bromo-cGMP did not affect the thermosensitivity of most POAH neurons, it did increase the warm sensitivity of neurons in other hypothalamic regions located dorsal, lateral, and posterior to the POAH. This increased thermosensitivity may be due to pacemaker currents that are facilitated by cyclic nucleotides. If some of these non-POAH thermosensitive neurons promote heat loss or inhibit heat production, then their increased thermosensitivity could contribute to cGMP-induced decreases in body temperature.
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Elias, Carol F., Clifford B. Saper, Eleftheria Maratos-Flier, Nicholas A. Tritos, Charlotte Lee, Joseph Kelly, Jeffrey B. Tatro, et al. "Chemically defined projections linking the mediobasal hypothalamus and the lateral hypothalamic area." Journal of Comparative Neurology 402, no. 4 (December 28, 1998): 442–59. http://dx.doi.org/10.1002/(sici)1096-9861(19981228)402:4<442::aid-cne2>3.0.co;2-r.
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Kudriavova, A. S., V. Meskenaite, V. I. Mikhailov, M. Schesny, E. A. Korneva, Y. V. Gavrilov, and P. O. Valko. "PRESERVED NUMBER OF OREXIN NEURONS IN POSTMORTEM HYPOTHALAMIC TISSUE OF CHRONIC ALCOHOLICS." Medical academic journal 19, no. 1S (December 15, 2019): 91–92. http://dx.doi.org/10.17816/maj191s191-92.
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The hypothalamic orexin system is critically involved in addiction, including chronic alcohol abuse. Microinjection of orexin into the lateral hypothalamus increases alcohol intake in rats, while reduced immunoreactivity of orexin neurons is associated with decreased alcohol drinking. Recently, the numbers of orexin neurons were found to be increased in opiate addiction in humans [4] and cocaine addiction in rats [2], but the integrity of orexin neurons has not yet been studied in human alcoholics. We examined the hypothalamus of 9 patients of chronic alcoholism and 10 subjects without a history of alcoholism or any other neurological or psychiatric disorder. We performed immunohistochemistry for orexin A, followed by stereological quantification. The hypothalamic tissue of chronic alcoholics exhibited a slightly increased number (9%) of orexin-containing neurons compared to the control group (123’087 ± 18’536 and 110’431 ± 14’439, p = 0.11). Mean Gundersen’s coefficient of error was 0.06 ± 0.01. The number of orexin neurons was similar in chronic alcoholics and control subjects without a history of alcoholism. Further examination of alcohol-induced hypothalamic damage is needed to understand, whether a neuroplastic increase in orexin neurons counterbalances a concurrent alcohol-toxic damage to these neurons.
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Bertelli, Daniela F., Eliana P. Araújo, Maristela Cesquini, Graziela R. Stoppa, Miriam Gasparotto-Contessotto, Marcos H. Toyama, Jorge V. C. Felix, et al. "Phosphoinositide-Specific Inositol Polyphosphate 5-Phosphatase IV Inhibits Inositide Trisphosphate Accumulation in Hypothalamus and Regulates Food Intake and Body Weight." Endocrinology 147, no. 11 (November 1, 2006): 5385–99. http://dx.doi.org/10.1210/en.2006-0280.
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The enzyme phosphatidylinositol 3-kinase (PI3-kinase) exerts an important role in the transduction of the anorexigenic and thermogenic signals delivered by insulin and leptin to first-order neurons of the arcuate nucleus in the hypothalamus. The termination of the intracellular signals generated by the activation of PI3-kinase depends on the coordinated activity of specific inositol phosphatases. Here we show that phosphoinositide-specific inositol polyphosphate 5-phosphatase IV (5ptase IV) is highly expressed in neurons of the arcuate and lateral nuclei of the hypothalamus. Upon intracerebroventricular (ICV) treatment with insulin, 5ptase IV undergoes a time-dependent tyrosine phosphorylation, which follows the same patterns of canonical insulin signaling through the insulin receptor, insulin receptor substrate-2, and PI3-kinase. To evaluate the participation of 5ptase IV in insulin action in hypothalamus, we used a phosphorthioate-modified antisense oligonucleotide specific for this enzyme. The treatment of rats with this oligonucleotide for 4 d reduced the hypothalamic expression of 5ptase IV by approximately 80%. This was accompanied by an approximately 70% reduction of insulin-induced tyrosine phosphorylation of 5ptase IV and an increase in basal accumulation of phosphorylated inositols in the hypothalamus. Finally, inhibition of hypothalamic 5ptase IV expression by the antisense approach resulted in reduced daily food intake and body weight loss. Thus, 5ptase IV is a powerful regulator of signaling through PI3-kinase in hypothalamus and may become an interesting target for therapeutics of obesity and related disorders.
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Gong, Ningping, Elisabeth Jönsson, and Björn Thrandur Björnsson. "Acute anorexigenic action of leptin in rainbow trout is mediated by the hypothalamic Pi3k pathway." Journal of Molecular Endocrinology 56, no. 3 (April 2016): 227–38. http://dx.doi.org/10.1530/jme-15-0279.
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Leptin (Lep) is an anorexigenic hormone and regulates appetite-related neuropeptides in mammals. A number of neuropeptides have also been linked to appetite regulation in teleost fish, but Lep signaling activation and effects on appetite-regulating neurons are poorly elucidated in early vertebrates. This study uses cellular, tissue and organismal approaches to elucidate the acute, central Lep action in rainbow trout. The results demonstrate that Lep activates phosphorylation of protein kinase B (Akt) and signal transducer and activator of transcription 3 in rainbow trout hypothalamus-derived cells, and that the phosphatidylinositol-3-kinase (Pi3k) inhibitor LY294002 can suppress the Lep-induced Akt phosphorylation. Intracerebroventricular (ICV) Lep administration strongly suppresses food intake at the doses of 0.05 and 0.5 µg Lep fish−1. At low dose, Lep stimulates hypothalamic transcription of anorexigenic cocaine- and amphetamine-regulated transcript (Cart) and orexigenic neuropeptide Y. At high dose, Lep stimulates hypothalamic transcription of anorexigenic proopiomelanocortin (Pomc) A1, A2, and B, while coinjection with LY294002 reverses this upregulation. The data suggest that the anorexigenic action of Lep in rainbow trout is mediated through stimulation of the anorexigenic neuropeptides Pomc and Cart. Furthermore, ICV Lep treatment increases phosphor–Akt-immunoreactive cells in the nucleus lateralis tuberis, periventricular zone along infundibulum, and lateral recess surrounded by nucleus anterior tuberis, while LY294002 inhibits this effect. Lep receptor-immunoreactive cells are also predominant in these regions. These results demonstrate that Lep activates the Pi3k-Akt pathway in the lateral tuberal hypothalamus of rainbow trout for acute appetite regulation, indicating the conservation of anorexigenic Lep action in the mediobasal hypothalamus.
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Bencze, János, Krisztina Pocsai, Balázs Murnyák, Péter Attila Gergely, Béla Juhász, Zoltán Szilvássy, and Tibor Hortobágyi. "The melanin-concentrating hormone system in human, rodent and avian brain." Open Medicine 13, no. 1 (July 6, 2018): 264–69. http://dx.doi.org/10.1515/med-2018-0040.
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AbstractMelanin-concentrating hormone (MCH) is a cyclic 19 amino acid orexigenic hypothalamic peptide. MCH is located in the lateral and dorsal hypothalamus, as well as in the zona incerta. In mammals MCH increases food intake, contributes to regulation of energy balance, temperature, reproductive function, endocrine homeostasis and biological rhythms. Several studies have proved the significance of MCH in obesity, diabetes and depression.Although the peptide is well-characterized in mouse models, much less is known about its functions in avians. In birds the MCH system especially in the lateral and basal hypothalamus has important connections to the limbic system and it coordinates the vegetative and endocrine functions, as well as the emotional behaviour. Pharmacological modulation of MCH system could contribute to the therapy of eating disorders and improve agricultural efficiency regarding avians. Reviewing the current knowledge on MCH system in human, rodents and avians may stimulate a new wave of studies in the field.
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Franzini, Angelo, Paolo Ferroli, Massimo Leone, and Giovanni Broggi. "Stimulation of the Posterior Hypothalamus for Treatment of Chronic Intractable Cluster Headaches: First Reported Series." Neurosurgery 52, no. 5 (May 1, 2003): 1095–101. http://dx.doi.org/10.1093/neurosurgery/52.5.1095.
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Abstract OBJECTIVE To describe the results of deep brain stimulation of the ipsilateral posterior hypothalamus for the treatment of drug-resistant chronic cluster headaches (CHs). A technique for electrode placement is reported. METHODS Because recent functional studies suggested hypothalamic dysfunction as the cause of CH bouts, we explored the therapeutic effectiveness of posterior hypothalamic stimulation for the treatment of CHs. Five patients with intractable chronic CHs were treated with long-term, high-frequency, electrical stimulation of the posterior hypothalamus. Electrodes were stereotactically implanted in the following position: 3 mm behind the midcommissural point, 5 mm below the midcommissural point, and 2 mm lateral to the midline. RESULTS Since this treatment, all five patients continue to be pain-free after 2 to 22 months of follow-up monitoring. Two of the five patients have remained pain-free without any medication, whereas three of the five required low doses of methysergide (two patients) or verapamil (one patient). No adverse side effects of chronic, high-frequency, hypothalamic stimulation have been observed, and we have not encountered any acute complications resulting from the implant procedure. There have been no tolerance phenomena. CONCLUSION These preliminary results indicate a role for posterior hypothalamic stimulation, which was demonstrated to be safe and effective, in the treatment of drug-resistant chronic CHs. These data point to a central pathogenesis for chronic CHs.
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Schick, R. R., S. Samsami, J. P. Zimmermann, T. Eberl, C. Endres, V. Schusdziarra, and M. Classen. "Effect of galanin on food intake in rats: involvement of lateral and ventromedial hypothalamic sites." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 2 (February 1, 1993): R355—R361. http://dx.doi.org/10.1152/ajpregu.1993.264.2.r355.
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Galanin has previously been reported to elicit feeding in satiated animals when injected into the hypothalamic paraventricular nucleus. It is not known, however, 1) whether this action is due to activation of feeding signals or suppression of satiety signals or both or 2) whether other hypothalamic regions such as the lateral hypothalamus (LH) or the ventromedial hypothalamus (VMH) are involved in this action. The effects of galanin on food intake were therefore examined in satiated and in fasted rats both after intracerebroventricular injection (0.1, 1, and 10 micrograms/10 microliters) and after microinjection (1 and 5 micrograms/0.5 microliters) into the LH and VMH. Twenty minutes after intracerebroventricular injection, galanin significantly and dose dependently augmented food intake by up to sevenfold in freely feeding rats and by up to 79% in fasted animals. The galanin-induced augmentation of cumulative food intake up to 2 h after injection was due to the initial increase in food consumption during the 0 to 20-min interval. This suggests that galanin acts by activation of feeding behavior and not by suppression of satiety signals in these fasted animals, in which satiety signals are presumably not initially operative. Twenty minutes after intrahypothalamic injections into both the LH and VMH, galanin (5 micrograms) significantly increased food consumption, fivefold in freely feeding rats and 30-35% in fasted rats. Thus stimulation of feeding by centrally injected galanin also involves loci within the LH and VMH.
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Florent, Vincent, Marc Baroncini, Patrice Jissendi-Tchofo, Renaud Lopes, Matthieu Vanhoutte, Sowmyalakshmi Rasika, Jean-Pierre Pruvo, et al. "Hypothalamic Structural and Functional Imbalances in Anorexia Nervosa." Neuroendocrinology 110, no. 6 (September 5, 2019): 552–62. http://dx.doi.org/10.1159/000503147.
Full textAbstract:
The hypothalamus contains integrative systems that support life, including physiological processes such as food intake, energy expenditure, and reproduction. Here, we show that anorexia nervosa (AN) patients, contrary to normal weight and constitutionally lean individuals, respond with a paradoxical reduction in hypothalamic levels of glutamate/glutamine (Glx) upon feeding. This reversal of the Glx response is associated with decreased wiring in the arcuate nucleus and increased connectivity in the lateral hypothalamic area, which are involved in the regulation on a variety of physiological and behavioral functions including the control of food intake and energy balance. The identification of distinct hypothalamic neurochemical dysfunctions and associated structural variations in AN paves the way for the development of new diagnostic and treatment strategies in conditions associated with abnormal body mass index and a maladaptive response to negative energy balance.
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Date, Yukari, Muhtashan S. Mondal, Haruaki Kageyama, Masoud Ghamari-Langroudi, Fumiko Takenoya, Hideki Yamaguchi, Yukio Shimomura, et al. "Neuropeptide W: An Anorectic Peptide Regulated by Leptin and Metabolic State." Endocrinology 151, no. 5 (February 26, 2010): 2200–2210. http://dx.doi.org/10.1210/en.2009-1153.
Full textAbstract:
Neuropeptide W (NPW) is an anorectic peptide produced in the brain. Here, we showed that NPW was present in several hypothalamic nuclei, including the paraventricular hypothalamic nucleus, ventromedial hypothalamic nucleus, lateral hypothalamus, and hypothalamic arcuate nucleus. NPW expression was significantly up-regulated in leptin-deficient ob/ob and leptin receptor-deficient db/db mice. The increase in NPW expression in ob/ob mice was abrogated to control levels after leptin replacement. Leptin induced suppressors of cytokine signaling-3 after phosphorylation of signal transducer and activator of transcription-3 in NPW-expressing neurons. In addition, we demonstrated that NPW reduces feeding via the melanocortin-4-receptor signaling pathway. We also showed that NPW activates proopiomelanocortin and inhibits neuropeptide Y neurons using loose-patch extracellular recording of these neurons identified by promoter-driven green fluorescent protein expression. This study indicates that NPW may play an important role in the regulation of feeding and energy metabolism under the conditions of leptin insufficiency.
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Sanz, Carmen, Isabel Roncero, Patricia Vázquez, M. Angeles Navas, and Enrique Blázquez. "Effects of glucose and insulin on glucokinase activity in rat hypothalamus." Journal of Endocrinology 193, no. 2 (May 2007): 259–67. http://dx.doi.org/10.1677/joe-06-0146.
Full textAbstract:
In an attempt to study the role of glucokinase (GK) and the effects of glucose and peptides on GK gene expression and on the activity of this enzyme in the hypothalamus, we used two kinds of biological models: hypothalamic GT1-7 cells and rat hypothalamic slices. The expression of the GK gene in GT1-7 cells was reduced by insulin (INS) and was not modified by different glucose concentrations, while GK enzyme activities were significantly reduced by the different peptides. Interestingly, a distinctive pattern of GK activities between the ventromedial hypothalamus (VMH) and lateral hypothalamus (LH) were found, with higher enzyme activities in the VMH as the glucose concentrations rose, while LH enzyme activities decreased at 2.8 and 20 mM glucose, the latter effect being prevented by incubation with INS. These effects were produced only by d-glucose and the modifications found were due to GK, but not to other hexokinases. In addition, GK activities in the VMH and the LH were reduced by glucagon-like peptide 1, leptin, orexin B, INS, and neuropeptide Y (NPY), but this effect was only statistically significant for NPY in LH. Our results indicate that the effects of both glucose and peptides occur on GK enzyme activities rather than on GK gene transcription. Moreover, the effects of glucose and INS on GK activity suggest that in the brain GK behaves in a manner opposite to that in the liver, which might facilitate its role in glucose sensing. Finally, hypothalamic slices seem to offer a good physiological model to discriminate the effects between different areas.
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Sarruf, David A., Fang Yu, Hong T. Nguyen, Diana L. Williams, Richard L. Printz, Kevin D. Niswender, and Michael W. Schwartz. "Expression of Peroxisome Proliferator-Activated Receptor-γ in Key Neuronal Subsets Regulating Glucose Metabolism and Energy Homeostasis." Endocrinology 150, no. 2 (February 1, 2009): 707–12. http://dx.doi.org/10.1210/en.2008-0899.
Full textAbstract:
In addition to increasing insulin sensitivity and adipogenesis, peroxisome proliferator-activated receptor (PPAR)-γ agonists cause weight gain and hyperphagia. Given the central role of the brain in the control of energy homeostasis, we sought to determine whether PPARγ is expressed in key brain areas involved in metabolic regulation. Using immunohistochemistry, PPARγ distribution and its colocalization with neuron-specific protein markers were investigated in rat and mouse brain sections spanning the hypothalamus, the ventral tegmental area, and the nucleus tractus solitarius. In several brain areas, nuclear PPARγ immunoreactivity was detected in cells that costained for neuronal nuclei, a neuronal marker. In the hypothalamus, PPARγ immunoreactivity was observed in a majority of neurons in the arcuate (including both agouti related protein and α-MSH containing cells) and ventromedial hypothalamic nuclei and was also present in the hypothalamic paraventricular nucleus, the lateral hypothalamic area, and tyrosine hydroxylase-containing neurons in the ventral tegmental area but was not expressed in the nucleus tractus solitarius. To validate and extend these histochemical findings, we generated mice with neuron-specific PPARγ deletion using nestin cre-LoxP technology. Compared with littermate controls, neuron-specific PPARγ knockout mice exhibited dramatic reductions of both hypothalamic PPARγ mRNA levels and PPARγ immunoreactivity but showed no differences in food intake or body weight over a 4-wk study period. We conclude that: 1) PPARγ mRNA and protein are expressed in the hypothalamus, 2) neurons are the predominant source of PPARγ in the central nervous system, although it is likely expressed by nonneuronal cell types as well, and 3) arcuate nucleus neurons that control energy homeostasis and glucose metabolism are among those in which PPARγ is expressed. Peroxisome proliferator-activated receptor-γ, a key regulator of adipogenesis and insulin sensitivity in peripheral tissues, is also expressed in neurons involved in body weight control.
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Toshinai, Koji, Yukari Date, Noboru Murakami, Mitsushi Shimada, Muhtashan S. Mondal, Takuya Shimbara, Jian-Lian Guan, et al. "Ghrelin-Induced Food Intake Is Mediated via the Orexin Pathway." Endocrinology 144, no. 4 (April 1, 2003): 1506–12. http://dx.doi.org/10.1210/en.2002-220788.
Full textAbstract:
Abstract The hypothalamus regulates energy intake by integrating the degree of starvation or satiation with the status of the environment through a variety of neuronal and blood-derived signals. Ghrelin, a peptide produced in the stomach and hypothalamus, stimulates feeding and GH secretion. Centrally administered ghrelin exerts an orexigenic activity through the neuropeptide Y (NPY) and agouti-related protein systems. The interaction between ghrelin and other hypothalamic orexigenic peptides, however, has not been clarified. Here, we investigated the anatomical interactions and functional relationship between ghrelin and two orexigenic peptides, orexin and melanin-concentrating hormone (MCH), present in the lateral hypothalamus. Ghrelin-immunoreactive axonal terminals made direct synaptic contacts with orexin-producing neurons. Intracerebroventricular administration of ghrelin induced Fos expression, a marker of neuronal activation, in orexin-producing neurons but not in MCH-producing neurons. Ghrelin remained competent to induce Fos expression in orexin-producing neurons following pretreatment with anti-NPY IgG. Pretreatment with anti-orexin-A IgG and anti-orexin-B IgG, but not anti-MCH IgG, attenuated ghrelin-induced feeding. Administration of NPY receptor antagonist further attenuated ghrelin-induced feeding in rats treated with anti-orexin-IgGs. Ghrelin-induced feeding was also suppressed in orexin knockout mice. This study identifies a novel hypothalamic pathway that links ghrelin and orexin in the regulation of feeding behavior and energy homeostasis.
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Wittmann, Gabor, Surbhi Gahlot, Malcolm James Low, and Ronald M. Lechan. "Rax Expression Identifies a Novel Cell Type in the Adult Mouse Hypothalamus." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A42. http://dx.doi.org/10.1210/jendso/bvab048.082.
Full textAbstract:
Abstract Hypothalamic tanycytes are radial glia-like ependymal cells lining the ventrolateral walls and floor of the third ventricle. Recent data show that tanycytes are adult neural stem/progenitor cells, capable of generating neurons that populate the adjacent hypothalamic nuclei involved in the regulation of feeding and energy balance. Thus, the genetic fate mapping of tanycytes has become an invaluable tool to identify and study tanycyte-derived adult-born hypothalamic neurons. Perhaps the most selective tanycyte marker identified to date is the retina and anterior neural fold homeobox (Rax), that has been used as a tanycyte marker in multiple single-cell transcriptomic studies. By using in situ hybridization and immunofluorescence, we show that Rax mRNA and RAX protein are also expressed in a minor but significant population of parenchymal cells that are concentrated in the caudal arcuate nucleus. RAX-positive nuclei in the parenchyma were often observed in pairs, suggesting recent cell divisions. The morphology of these cells was studied in tamoxifen-treated Rax-CreERT2; Ai34(RCL-Syp/tdT)-D mice, in which the synaptophysin-tdTomato fusion protein permanently labels Rax-expressing cells and their progeny. While some parenchymal RAX-positive cells had tanycyte-like morphology indicative of tanycyte migration into the parenchyma, the majority had a very different morphology with extensive local processes that often encircled adjacent neurons (termed “frizzy cells”). The tdTomato labeling also revealed numerous frizzy cells that were negative for RAX, indicating downregulation of endogenous Rax expression subsequent to the induction of synaptophysin-tdTomato reporter expression. Many of these cells were distributed outside the caudal arcuate nucleus, including the rostral lateral arcuate nucleus, ventromedial and dorsomedial hypothalamic nuclei and lateral hypothalamus. RAX-negative frizzy cells were also conspicuous in the paraventricular nucleus, and occasionally observed in the preoptic region and bed nucleus of the stria terminalis. Frizzy cells were negative for the tanycyte-enriched proteins vimentin, monocarboxylate transporter 8 (MCT8) or glial fibrillary acidic protein (GFAP). These results identify a novel Rax-expressing cell type in the adult hypothalamus that differs from tanycytes in location, morphology and gene expression characteristics. Future studies are required to determine whether frizzy cells are derived from tanycytes or constitute a separate cell lineage, and whether they represent a migratory form of neural precursor cells in the adult hypothalamus.
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Schick, R. R., T. L. Yaksh, D. R. Roddy, and V. L. Go. "Release of hypothalamic cholecystokinin in cats: effects of nutrient and volume loading." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 1 (January 1, 1989): R248—R254. http://dx.doi.org/10.1152/ajpregu.1989.256.1.r248.
Full textAbstract:
Systemic cholecystokinin (CCK) suppresses food intake in various species and has therefore been proposed to act as a satiety factor. Because CCK is also present in the hypothalamus and furthermore meets neurotransmitter criteria, the hypothesis was tested whether CCK participates in the transmission of satiety messages at the lateral hypothalamic (LH) level. The results of this study demonstrate that in halothane-anesthetized cats, neurons located in the LH will indeed release CCK-like material after a carbohydrate-protein meal in a time-dependent fashion. This release, as water loads demonstrate, is most likely due to volumetric distension rather than to the nutrient content. The releasable CCK does not originate from peripheral sources, since intravenously infused CCK octapeptide (CCK-8) does not appear in the perfusate. The release occurs only in discrete neurons and is not universal to CCK-releasing systems within the LH, and also, CCK-releasing systems are not present at all locations. The molecular form of CCK in feline hypothalamus is the COOH-terminal octapeptide (CCK-8) as shown by high-performance liquid chromatography. No gastrin-17 is present. CCK-8 is also the predominant form found in meal-induced as well as in KCl-induced CCK released from hypothalamic neurons. These results suggest a correlated role for hypothalamic CCK in the termination of food intake.
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Zheng, Huiyuan, Michele Corkern, Irina Stoyanova, Laurel M. Patterson, Rui Tian, and Hans-Rudolf Berthoud. "Appetite-inducing accumbens manipulation activates hypothalamic orexin neurons and inhibits POMC neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 6 (June 1, 2003): R1436—R1444. http://dx.doi.org/10.1152/ajpregu.00781.2002.
Full textAbstract:
Corticolimbic circuits involving the prefrontal cortex, amygdala, and ventral striatum determine the reward value of food and might play a role in environmentally induced obesity. Chemical manipulation of the nucleus accumbens shell (AcbSh) has been shown to elicit robust feeding and Fos expression in the hypothalamus and other brain areas of satiated rats. To determine the neurochemical phenotype of hypothalamic neurons receiving input from the AcbSh, we carried out c-Fos/peptide double-labeling immunohistochemistry in various hypothalamic areas known to contain feeding peptides, from rats that exhibited a significant feeding response after AcbSh microinjection of the GABAA agonist muscimol. In the perifornical area, a significantly higher percentage of orexin neurons expressed Fos after muscimol compared with saline injection. In contrast, Fos expression was not induced in melanin-concentrating hormone and cocaine-amphetamine-related transcript (CART) neurons. In the arcuate nucleus, Fos activation was significantly lower in neurons coexpressing CART and proopiomelanocortin, and there was a tendency for higher Fos expression in neuropeptide Y neurons. In the paraventricular nucleus, no significant activation of oxytocin and CART neurons was found. Thus AcbSh manipulation may elicit food intake through coordinated stimulation of hypothalamic neurons expressing orexigenic peptides and suppression of neurons expressing anorexigenic peptides. However, activation of many neurons not expressing these peptides suggests that additional peptides/transmitters in the lateral hypothalamus and accumbens projections to other brain areas might also be involved.
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MATTEAU, ISABELLE, DENIS BOIRE, and MAURICE PTITO. "Retinal projections in the cat: A cholera toxin B subunit study." Visual Neuroscience 20, no. 5 (September 2003): 481–93. http://dx.doi.org/10.1017/s0952523803205022.
Full textAbstract:
The B fragment of cholera toxin (CTb) is a highly sensitive anterograde tracer for the labelling of retinal axons. It can reveal dense retinofugal projections to well-known retinorecipient nuclei along with sparse but distinct input to target areas that are not commonly recognized. Following a unilateral injection of CTb into the vitreous chamber of seven adult cats, we localized the toxin immunohistochemically in order to identify direct retinal projections in these animals. Consistent with previous findings, the strongest projections were observed in the superficial layers of the superior colliculus, the dorsal and ventral lateral geniculate nuclei, the pretectal nuclei, the accessory optic nuclei, and the suprachiasmatic nucleus of the hypothalamus. However, we also found labelled terminals in several other brain areas, including the zona incerta, the medial geniculate nucleus, the lateral posterior-pulvinar complex, the lateral habenular nucleus, and the anterior and lateral hypothalamic regions. The morphological characteristics of the retinal axon terminals in most of the identified novel target sites are described.
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Scheurink, A. J., A. B. Steffens, and R. P. Gaykema. "Hypothalamic adrenoceptors mediate sympathoadrenal activity in exercising rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 3 (September 1, 1990): R470—R477. http://dx.doi.org/10.1152/ajpregu.1990.259.3.r470.
Full textAbstract:
The role of hypothalamic adrenoceptors in the exercise-induced alterations of plasma norepinephrine (NE), epinephrine (E), and corticosterone concentrations was investigated in rats. Exercise consisted of strenuous swimming against a counter-current for 15 min. Before, during, and after swimming, blood samples were withdrawn through a permanent heart catheter for determination of E, NE, and corticosterone. In control rats E, NE, and corticosterone levels were all increased during exercise. Infusion of the alpha-adrenoceptor antagonist phentolamine through permanent bilateral cannulas into the ventromedial hypothalamus (VMH) immediately before exercise reduced the exercise-induced increase in plasma E without affecting NE. Infusion of the beta-adrenoceptor antagonist timolol into the VMH enhanced plasma E and attenuated plasma NE increases. Infusion of phentolamine into the lateral hypothalamic area (LHA) led to enhanced NE and unchanged E concentrations, whereas infusion of timolol into the LHA caused a potentiation of the increase in plasma E without an effect on NE. Plasma corticosterone concentrations were not affected. The results suggest that 1) alpha- and beta-adrenoceptors in the hypothalamus influence peripheral catecholamine release, and 2) E and NE responses to exercise can be dissociated by interference of the central nervous system.
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Van Dijk, G., T. E. Thiele, J. C. Donahey, L. A. Campfield, F. J. Smith, P. Burn, I. L. Bernstein, S. C. Woods, and R. J. Seeley. "Central infusions of leptin and GLP-1-(7-36) amide differentially stimulate c-FLI in the rat brain." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 4 (October 1, 1996): R1096—R1100. http://dx.doi.org/10.1152/ajpregu.1996.271.4.r1096.
Full textAbstract:
Recently, glucagon-like peptide-1-(7-36) amide (GLP-1) and leptin have been implicated in the regulation of food intake. In the present study, we compared the effects of third ventricular administration (i3vt) of leptin (3.5 micrograms) and GLP-1 (10.0 micrograms) on short-term food intake and c-Fos-like immunoreactivity (c-FLI) in hypothalamic, limbic, and hindbrain areas in the rat. Relative to controls, infusion of leptin or GLP-1 (3 h before lights off) significantly reduced food intake over the first 2 h in the dark phase (53 and 63%, respectively). In different rats, infusion of leptin or GLP-1 elevated c-FLI in the paraventricular hypothalamus and central amygdala. Furthermore, leptin selectively elevated c-FLI in the dorsomedial hypothalamus, whereas GLP-1 selectively elevated c-FLI in the nucleus of the solitary tract, area postrema, lateral parabrachial nucleus, and arcuate hypothalamic nucleus. The fact that most of the c-FLI after leptin or GLP-1 administration was observed in separate regions within the central nervous system (CNS) suggests different roles for leptin and GLP-1 in the CNS regulation of food intake and body weight.