Vestibular-mediated increase in central serotonin plays an important role in hypergravity-induced hypophagia in rats

2010 ◽  
Vol 109 (6) ◽  
pp. 1635-1643 ◽  
Author(s):  
Chikara Abe ◽  
Kunihiko Tanaka ◽  
Chihiro Iwata ◽  
Hironobu Morita
Keyword(s):  
Area Postrema ◽  
Vestibular Nucleus ◽  
Central Nucleus ◽  
Medial Vestibular Nucleus ◽  
Hypothalamic Nucleus ◽  
Solitary Tract ◽  
Afferent Pathway ◽  
Vestibular Input ◽  
Paraventricular Hypothalamic Nucleus ◽  
Fos Expression

Exposure to a hypergravity environment induces acute transient hypophagia, which is partially restored by a vestibular lesion (VL), suggesting that the vestibular system is involved in the afferent pathway of hypergravity-induced hypophagia. When rats were placed in a 3-G environment for 14 days, Fos-containing cells increased in the paraventricular hypothalamic nucleus, the central nucleus of the amygdala, the medial vestibular nucleus, the raphe nucleus, the nucleus of the solitary tract, and the area postrema. The increase in Fos expression was completely abolished or significantly suppressed by VL. Therefore, these regions may be critical for the initiation and integration of hypophagia. Because the vestibular nucleus contains serotonergic neurons and because serotonin (5-HT) is a key neurotransmitter in hypophagia, with possible involvement in motion sickness, we hypothesized that central 5-HT increases during hypergravity and induces hypophagia. To examine this proposition, the 5-HT concentrations in the cerebrospinal fluid were measured when rats were reared in a 3-G environment for 14 days. The 5-HT concentrations increased in the hypergravity environment, and these increases were completely abolished in rats with VL. Furthermore, a 5-HT2A antagonist (ketanserin) significantly reduced 3-G (120 min) load-induced Fos expression in the medial vestibular nucleus, and chronically administered ketanserin ameliorated hypergravity-induced hypophagia. These results indicate that hypergravity induces an increase in central 5-HT via the vestibular input and that this increase plays a significant role in hypergravity-induced hypophagia. The 5-HT2A receptor is involved in the signal transduction of hypergravity stress in the vestibular nucleus.

Effect of vagal and splanchnic nerve section on Fos expression in ferret brain stem after emetic stimuli

1996 ◽  
Vol 271 (1) ◽  
pp. R228-R236 ◽  
Author(s):  
F. M. Boissonade ◽  
J. S. Davison
Keyword(s):  
Vagus Nerve ◽  
Brain Stem ◽  
Area Postrema ◽  
Splanchnic Nerve ◽  
Vagal Afferents ◽  
Sham Operation ◽  
Relative Importance ◽  
Solitary Tract ◽  
Nerve Section ◽  
Fos Expression

Previous studies have demonstrated that intraduodenal hypertonic saline (IHS) induces dense Fos expression within two regions of the ferret dorsal vagal complex (DVC): the area postrema (AP) and the medial subnucleus of the nucleus of the solitary tract (mn). The aims of the present experiments were to determine the peripheral pathways involved in excitation of DVC neurons after IHS and the relative importance of mn and AP excitation in the emetic response to this stimulus. The emetic response and the distribution of Fos were examined after IHS in animals that had received either vagotomy alone, vagotomy and splanchnic nerve section, or sham operation. The emetic response was studied in both awake and anesthetized animals, and Fos induction was studied in anesthetized animals. Vagotomy alone or combined with splanchnic nerve section abolished the emetic response and the area of dense labeling within the mn and reduced but did not abolish the labeling in the AP. It was concluded that both the emetic reflex and the dense expression of Fos within the mn after IHS are dependent on an intact vagus nerve. The excitation of neurons in the AP after IHS is partially dependent on vagal afferents, and the residual labeling that is present in the AP of neurectomized animals may be mediated via a blood-borne route.

Duodenal nutrient infusions differentially affect sham feeding and Fos expression in rat brain stem

1998 ◽  
Vol 274 (6) ◽  
pp. R1725-R1733 ◽  
Author(s):  
Curtis B. Phifer ◽  
Hans-Rudolf Berthoud
Keyword(s):  
Amino Acids ◽  
Linoleic Acid ◽  
Area Postrema ◽  
Gastric Distension ◽  
Acid Mixture ◽  
Neural Pathways ◽  
Solitary Tract ◽  
Sham Feeding ◽  
Caloric Value ◽  
Fos Expression

Duodenal infusions of macronutrients inhibit sham and normal feeding. Neural substrates of this response were studied by infusing glucose, linoleic acid, an amino acid mixture, saline, or water into the duodenum of unanesthetized rats and then measuring sham feeding of 30% sucrose or Fos expression in the dorsal vagal complex. Linoleic acid and amino acids (both 1.5 kcal) and glucose (4.5 kcal) suppressed sham feeding relative to control infusions, and all three macronutrients triggered Fos expression in the nucleus of the solitary tract and area postrema. Although there were significant quantitative differences, the subnuclear distribution pattern of Fos-expressing neurons was not different for the three macronutrients and was largely localized to the medial, dorsomedial, and commissural subnuclei of the nucleus of the solitary tract and the area postrema. Linoleic acid suppressed intake and stimulated Fos expression similarly to glucose infusions of three times the caloric value. Amino acids strongly suppressed sham feeding but triggered relatively little Fos expression. These results indicate that the intake-suppressing potency of duodenal macronutrients is dependent on nutrient type, rather than simply caloric value, and that amino acids, although potent inducers of satiety, affect ingestion by processes different from those subserving lipids and carbohydrates. Furthermore, the similar patterns of neuronal activation after different duodenal infusions may indicate a large degree of convergence at the level of primary and second-order sensory neurons, whereas the distinctly different pattern obtained earlier with gastric distension indicates partially separate neural pathways for satiety signals generated by duodenal nutrients and gastric mechanoreceptors.

scholarly journals Dysfunctions of the paraventricular hypothalamic nucleus induce hypersomnia in mice

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Chang-Rui Chen ◽  
Yu-Heng Zhong ◽  
Shan Jiang ◽  
Wei Xu ◽  
Lei Xiao ◽  
...  
Keyword(s):  
Glutamate Transporter ◽  
Neural Circuitry ◽  
Lateral Septum ◽  
Hypothalamic Nucleus ◽  
Active Period ◽  
Vesicular Glutamate Transporter ◽  
Paraventricular Hypothalamic Nucleus ◽  
Electrophysiological Recordings ◽  
Inactive Period ◽  
Fos Expression

Hypersomnolence disorder (HD) is characterized by excessive sleep, which is a common sequela following stroke, infection or tumorigenesis. HD is traditionally thought to be associated with lesions of wake-promoting nuclei. However, lesions of a single wake-promoting nucleus, or even two simultaneously, did not exert serious HD. Therefore, the specific nucleus and neural circuitry for HD remain unknown. Here, we observed that the paraventricular nucleus of the hypothalamus (PVH) exhibited higher c-fos expression during the active period (23:00) than during the inactive period (11:00) in mice. Therefore, we speculated that the PVH, in which most neurons are glutamatergic, may represent one of the key arousal-controlling centers. By using vesicular glutamate transporter 2 (vglut2Cre) mice together with fiber photometry, multichannel electrophysiological recordings, and genetic approaches, we found that PVHvglut2 neurons were most active during wakefulness. Chemogenetic activation of PVHvglut2 neurons induced wakefulness for 9 h, and photostimulation of PVHvglut2→parabrachial complex/ventral lateral septum circuits immediately drove transitions from sleep to wakefulness. Moreover, lesioning or chemogenetic inhibition of PVHvglut2 neurons dramatically decreased wakefulness. These results indicate that the PVH is critical for arousal promotion and maintenance.

Plasma hormone levels and central c-Fos expression in ferrets after systemic administration of cholecystokinin

2001 ◽  
Vol 281 (4) ◽  
pp. R1243-R1255 ◽  
Author(s):  
I. Billig ◽  
B. J. Yates ◽  
L. Rinaman
Keyword(s):  
Brain Stem ◽  
Area Postrema ◽  
Hormone Secretion ◽  
Early Gene ◽  
Central Nucleus ◽  
Ventrolateral Medulla ◽  
Pituitary Hormone ◽  
Bed Nucleus ◽  
Fos Expression ◽  
Glucagon Like Peptide 1

Posterior pituitary hormone secretion and central neural expression of the immediate-early gene product c-Fos was examined in adult ferrets after intravenous administration of CCK octapeptide. Pharmacological doses of CCK (1, 5, 10, or 50 μg/kg) did not induce emesis, but elicited behavioral signs of nausea and dose-related increases in plasma vasopressin (AVP) levels without significant increases in plasma oxytocin (OT) levels. CCK activated neuronal c-Fos expression in several brain stem viscerosensory regions, including a dose-related activation of neurons in the dorsal vagal complex (DVC). Activated brain stem neurons included catecholaminergic and glucagon-like peptide-1-positive cells in the DVC and ventrolateral medulla. In the forebrain, activated neurons were prevalent in the paraventricular and supraoptic nuclei of the hypothalamus and also were observed in the central nucleus of the amygdala and bed nucleus of the stria terminalis. Activated hypothalamic neurons included cells that were immunoreactive for AVP, OT, and corticotropin-releasing factor. Comparable patterns of brain stem and forebrain c-Fos activation were observed in ferrets after intraperitoneal injection of lithium chloride (LiCl; 86 mg/kg), a classic emetic agent. However, LiCl activated more neurons in the area postrema and fewer neurons in the nucleus of the solitary tract compared with CCK. Together with results from previous studies in rodents, our findings support the view that nauseogenic treatments activate similar central neural circuits in emetic and nonemetic species, despite differences in treatment-induced emesis and pituitary hormone secretion.

The anorectic hormone amylin contributes to feeding-related changes of neuronal activity in key structures of the gut-brain axis

2004 ◽  
Vol 286 (1) ◽  
pp. R114-R122 ◽  
Author(s):  
T. Riediger ◽  
D. Zuend ◽  
C. Becskei ◽  
T. A. Lutz
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Peptide Hormone ◽  
Central Nucleus ◽  
Circumventricular Organ ◽  
Hypothalamic Area ◽  
Physiological Concentration ◽  
Lateral Parabrachial Nucleus ◽  
Neuronal Mechanisms ◽  
Fos Expression

Amylin is a peptide hormone that is cosecreted with insulin from the pancreas during and after food intake. Peripherally injected amylin potently inhibits feeding by acting on the area postrema (AP), a circumventricular organ lacking a functional blood-brain barrier. We recently demonstrated that AP neurons are excited by a near physiological concentration of amylin. However, the subsequent neuronal mechanisms and the relevance of endogenously released amylin for the regulation of food intake are poorly understood. Therefore, we investigated 1) amylin's contribution to feeding-induced c-Fos expression in the rat AP and its ascending projection sites, and 2) amylin's ability to reverse fasting-induced c-Fos expression in the lateral hypothalamic area (LHA). Similar to amylin (20 μg/kg sc), refeeding of 24-h food-deprived rats induced c-Fos expression in the AP, the nucleus of the solitary tract, the lateral parabrachial nucleus, and the central nucleus of the amygdala. In AP-lesioned rats, the amylin-induced c-Fos expression in each of these sites was blunted, indicating an AP-mediated activation of these structures. Pretreatment with the amylin antagonist AC-187 (1 mg/kg sc) inhibited feeding-induced c-Fos expression in the AP. Food deprivation activated LHA neurons, a response known to be associated with hunger. This effect was reversed within 2 h after refeeding and also in nonrefed animals that received amylin. In summary, our data provide the first evidence that feeding-induced amylin release activates AP neurons projecting to subsequent relay stations known to transmit meal-related signals to the forebrain. Activation of this pathway seems to coincide with an inhibition of LHA neurons.

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