Intraduodenal infusion of lipids induces c-fos expression in the locus coeruleus, area postrema, nucleus os the solitary tract and paraventricular nucleus of the hypothalamus via CCK-A receptors and capsaicin-sensitive vagal pathways

1996 ◽  
Vol 64 (1-3) ◽  
pp. 130
Keyword(s):  
Locus Coeruleus ◽  
Paraventricular Nucleus ◽  
Area Postrema ◽  
Solitary Tract ◽  
Intraduodenal Infusion ◽  
Fos Expression

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.

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.

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.

Intragastric hypertonic saline increases vasopressin and central Fos immunoreactivity in conscious rats

1997 ◽  
Vol 272 (3) ◽  
pp. R750-R758 ◽  
Author(s):  
S. H. Carlson ◽  
A. Beitz ◽  
J. W. Osborn
Keyword(s):  
Hypertonic Saline ◽  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Area Postrema ◽  
Parabrachial Nucleus ◽  
Solitary Tract ◽  
Plasma Osmolarity ◽  
Systemic Blood ◽  
Conscious Rats ◽  
Lateral Parabrachial Nucleus

Although experimental evidence supports peripheral osmoreceptor modulation of arginine vasopressin (AVP) release, a local osmotic signal required for osmoreceptor activation has yet to be identified using physiological sodium loads. Additionally, the central pathway involved in peripheral control of AVP has not been clearly established. Experiments were conducted to examine the effect of intragastric saline on portal venous osmolarity, plasma AVP (P(AVP)), and Fos immunoreactivity. In anesthetized rats, intragastric infusion (2.9 ml) of hypertonic (600 mosM) saline significantly increased portal venous osmolarity while systemic blood osmolarity remained constant. In conscious rats, intragastric hypertonic saline significantly elevated P(AVP) (3.6 +/- 1.3 to 5.8 +/- 1.9 pg/ml), whereas no changes were observed in plasma osmolarity in either the isotonic (296.2 +/- 1.4 to 297.6 +/- 1.1 mosM) or hypertonic (291.7 +/- 1.7 to 291.4 +/- 1.8 mosM) group. Finally, intragastric hypertonic saline significantly increased Fos immunoreactivity in the nucleus of the solitary tract (NTS), area postrema (AP), lateral parabrachial nucleus (LPBN), supraoptic nucleus (SON), and paraventricular nucleus (PVN). These results indicate that intragastric hypertonic saline produces a portal venous osmotic signal that triggers peripheral osmoreceptors to stimulate AVP release while activating the NTS, AP, and LPBN in addition to the SON and PVN.

Central leptin modulates behavioral and neural responsivity to CCK

1999 ◽  
Vol 276 (5) ◽  
pp. R1545-R1549 ◽  
Author(s):  
Michael Emond ◽  
Gary J. Schwartz ◽  
Ellen E. Ladenheim ◽  
Timothy H. Moran
Keyword(s):  
Food Intake ◽  
Paraventricular Nucleus ◽  
Area Postrema ◽  
Protein Product ◽  
Liquid Diet ◽  
Solitary Tract ◽  
Ob Gene ◽  
Medial Nucleus

The mechanisms through which leptin, the protein product of the ob gene, affects food intake remain to be determined. To assess whether the actions of leptin depend on modulation of within-meal satiety signals, we measured the effect of third ventricular leptin administration on the satiety actions of CCK. Leptin (10 μg) administered 1 h before 30-min access to a liquid diet had no effect on intake when administered alone, but doses of 3.5 or 10 μg dose dependently increased the suppression of intake produced by 1 nmol/kg CCK. Examination of patterns of c-Fos activation induced by 3.5 μg leptin and 1 nmol/kg CCK revealed that the combination produced significant c-Fos activation within the area postrema and the caudal and medial nucleus of the solitary tract (NST) compared with either leptin or CCK treatments alone. The leptin-CCK combination also resulted in increased c-Fos activation within the paraventricular nucleus of the hypothalamus above that produced by leptin alone. These data suggest that the actions of leptin in food intake are mediated through its ability to modulate responsivity to within-meal satiety signals.

Fos expression in ferret dorsal vagal complex after peripheral emetic stimuli

1994 ◽  
Vol 266 (4) ◽  
pp. R1118-R1126 ◽  
Author(s):  
F. M. Boissonade ◽  
K. A. Sharkey ◽  
J. S. Davison
Keyword(s):  
Electrical Stimulation ◽  
Hypertonic Saline ◽  
Area Postrema ◽  
Dorsal Vagal Complex ◽  
Solitary Tract ◽  
Communicating Branch ◽  
Nuclear Phosphoprotein ◽  
Fos Expression ◽  
Hypertonic Saline Injection ◽  
Stimulation Of

The aim of this study was to investigate neuronal activation in the dorsal vagal complex of the halothane-anesthetized ferret after peripheral emetic stimuli. Neuronal activity was studied by examining the distribution of the nuclear phosphoprotein Fos using immunohistochemistry. The emetic stimuli used were electrical stimulation of the supradiaphragmatic vagal communicating branch (SVCB) or intraduodenal injection of hypertonic saline. Electrical stimulation of the SVCB induced the densest Fos expression within the medial subnucleus of the nucleus of the solitary tract. After hypertonic saline injection, the greatest density of Fos-positive nuclei was observed within the area postrema and also in the medial subnucleus of the nucleus of the solitary tract. It was concluded that the emetic response to hypertonic saline involves neurons in both the area postrema and the nucleus of the solitary tract, especially the medial subnucleus, and that the medial subnucleus is important in the emetic response to SVCB stimulation.

Noradrenergic neurons of the area postrema mediate amylin's hypophagic action

2010 ◽  
Vol 299 (2) ◽  
pp. R623-R631 ◽  
Author(s):  
Catarina S. Potes ◽  
Victoria F. Turek ◽  
Rebecca L. Cole ◽  
Calvin Vu ◽  
Barbara L. Roland ◽  
...  
Keyword(s):  
Food Intake ◽  
Low Dose ◽  
Area Postrema ◽  
Solitary Tract ◽  
Noradrenergic Neurons ◽  
Neuronal Activation ◽  
Fos Protein ◽  
Noradrenaline Synthesis ◽  
Fos Expression

Circulating amylin inhibits food intake via activation of the area postrema (AP). The aim of this study was to identify the neurochemical phenotype of the neurons mediating amylin's hypophagic action by immunohistochemical and feeding studies in rats. Expression of c-Fos protein was used as a marker for neuronal activation and dopamine-β-hydroxylase (DBH), the enzyme-catalyzing noradrenaline synthesis, as a marker for noradrenergic neurons. We found that ∼50% of amylin-activated AP neurons are noradrenergic. To clarify the functional role of these neurons in amylin's effect on eating, noradrenaline-containing neurons in the AP were lesioned using a saporin conjugated to an antibody against DBH. Amylin (5 or 20 μg/kg sc)-induced anorexia was observed in sham-lesioned rats with both amylin doses. Rats with a lesion of > 50% of the noradrenaline neurons were unresponsive to the low dose of amylin (5 μg/kg) and only displayed a reduction in food intake 60 min after injection of the high amylin dose (20 μg/kg). In a terminal experiment, the same rats received amylin (20 μg/kg) or saline. The AP and nucleus of the solitary tract (NTS) were stained for DBH to assess noradrenaline lesion success and for c-Fos expression to evaluate amylin-induced neuronal activation. In contrast to sham-lesioned animals, noradrenaline-lesioned rats did not show a significant increase in amylin-induced c-Fos expression in the AP and NTS. We conclude that the noradrenergic neurons in the AP mediate at least part of amylin's hypophagic effect.

Trigeminal Nociception-Induced Cerebral Fos Expression in the Conscious Rat

Cephalalgia ◽  
2001 ◽  
Vol 21 (10) ◽  
pp. 963-975 ◽  
Author(s):  
GJ Ter Horst ◽  
WJ Meijler ◽  
J Korf ◽  
RHA Kemper
Keyword(s):  
Locus Coeruleus ◽  
Area Postrema ◽  
Brain Activity ◽  
Dorsal Raphe ◽  
Reticular Nucleus ◽  
Conscious Rat ◽  
Trigeminal Stimulation ◽  
Trigeminal Nociception ◽  
Fos Expression ◽  
Dorsal Raphé

Little is known about trigeminal nociception-induced cerebral activity and involvement of cerebral structures in pathogenesis of trigeminovascular headaches such as migraine. Neuroimaging has demonstrated cortical, hypothalamic and brainstem activation during the attack and after abolition with sumatriptan. This has led to the conclusion that the dorsal raphe and locus coeruleus may initiate events that generate migraneous headache. Using a conscious rat model of trigeminal nociception and cerebral Fos expression as histochemical markers of neuronal activity, we characterized the pattern of brain activity after noxious trigeminal stimulation with capsaicin (250 and 1000 nm). A significantly increased Fos immunoreactivity was found in the trigeminal nucleus caudalis (layers I and II), the area postrema, the nucleus of the solitary tract, the parvicellular reticular nucleus, the locus coeruleus, the parabrachial nucleus and the raphe nuclei. In addition, the ventrolateral periaqueductal grey, the intralaminar thalamic and various hypothalamic areas, showed an enhanced Fos expression after the intracisternal administration of capsaicin. Other responding areas were the amygdala, the upper lip and forelimb regions of the primary somatosensory cortex, and the insula. Many of these areas participate in (anti)-nociception, although we cannot exclude the possibility that in conscious animals the pain-associated physiological and behavioural responses that are an intrinsic and necessary part of coping with pain have generated the increased Fos expression. Trigeminal stimulation-induced locus coeruleus, dorsal raphe and hypothalamic activation are opposed to a suggested pathogenic role of these nuclei in migraine and cluster headache, respectively.

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