c-Fos Expression in Rat Brain and Brainstem Nuclei in Response to Treatments That Alter Food Intake and Gastric Motility

Olson, Beatriz R.; Freilino, Maria L.; Hoffman, Gloria E.; Stricker, Edward M.; Sved, Alan F.; Verbalis, Joseph G.

doi:10.1006/mcne.1993.1011

Cited by 153 publications

(90 citation statements)

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“…In rodents, vagal neurons contain Y2 receptors [21], peripheral administration of PYY (3-36) stimulates vagal afferent nerve activity [21], and vagal denervation blocks the anorexic response to peripheral administration of PYY in rats [1,21], but not mice [19]. Our findings extend these results by showing that systemic administration of an anorexigenic dose of PYY(3-36) activated neurons in hindbrain areas (cmNTS, gNTS, and AP) that receive and integrate incoming meal-related satiety signals transmitted by vagal sensory neurons from the gut [17,26,32,38]. These sites are similar to those activated by peripheral administration of the prototypic satiety peptide CCK-8, which is also postulated to inhibit food intake by activating vagal sensory nerves [7,31].…”

Section: Discussionsupporting

confidence: 71%

“…In rodents, IP injection of PYY (3-36) decreases NPY mRNA expression in the ARC [9], either has no effect [5] or increases POMC mRNA expression in the ARC [9], causes a nearly 2-fold increase in number of Fos (+) cells in the ARC [5], and produces a 13% [20] to 260% increase in Fos (+) POMC neurons in the ARC [5]. Furthermore, direct administration of Y2 agonists PYY and Ac-[Leu28,Leu31] NPY (24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36) into the ARC dose-dependently inhibits food intake in rats [5], while PYY(3-36) administration into cerebral ventricles either has no effect or potently increases food intake [36]. Thus, Batterham et al [5] initially postulated that the anorexigenic response to circulating PYY(3-36) is mediated by a Y2 receptor-mediated mechanism in the ARC.…”

Section: Discussionmentioning

confidence: 99%

“…Vagal neurons have Y2 receptors [21], peripheral administration of PYY stimulates vagal afferent nerve activity [21], and vagal denervation has been reported to block the anorexic response to peripheral administration of PYY in rats [1,21] but not mice [19]. Rinaman and colleagues [30,31] have provided evidence that the prototypical intestinal satiety peptide cholecystokinin inhibits food intake by a mechanism involving downstream catecholaminergic neurons in the caudal NTS, an area that receives and integrates incoming meal-related satiety signals transmitted by vagal sensory neurons from the gut [17,26,32,38]. It remains to be determined whether PYY(3-36) acts in part through a similar mechanism.…”

Section: Introductionmentioning

confidence: 99%

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PYY(3–36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats

et al. 2008

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Peptide YY ] inhibits feeding in rodents, nonhuman primates and humans, yet the neural circuits underlying this action remain to be determined. Here we assessed whether PYY(3-36) inhibits feeding by activating neurons in forebrain and hindbrain sites containing Y2 receptors and linked to control of food intake, or in hindbrain sites immediately downstream of vagal afferent neurons. Rats received an anorexigenic dose of PYY(3-36), and the number of neurons expressing Fos, an indicator of neural activation, was determined in anterior hypothalamus (AH), arcuate nucleus (ARC), dorsomedial hypothalamus (DMH), lateral hypothalamus (LH), ventromedial hypothalamus (VMH), central nucleus of the amygdala (CeA), area postrema (AP), and caudal medial nucleus tractus solitarius (cmNTS), commissural NTS (cNTS), and gelatinosus NTS (gNTS). Expression of tyrosine hydroxylase (TH), an indicator of catecholamine synthesis, was also measured in the cmNTS. PYY(3-36) increased Fos in ARC, cmNTS, gNTS and AP. Approximately 10% of Fos (+) neurons in the cmNTS were TH (+). These results suggest that PYY(3-36) inhibits feeding through direct activation of ARC neurons, and direct and/or indirect activation via vagal afferent nerves of cmNTS, gNTS and AP, including some catecholaminergic neurons in the cmNTS.

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Section: Discussionsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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PYY(3–36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats

et al. 2008

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“…In previous studies, however, using intact adult [10,11] and young [12] male rats, c-Fos expression was not found in the paraventricular nucleus (PVN) and the nucleus of the solitary tract (NTS) after 15-, 22-, 24-, 27-or 48-h fasting. Moreover, there are only a few reports concerning androgen-dependent potentiation of neuronal c-…”

Section: Introductionmentioning

confidence: 99%

Effect of Fasting on c-Fos Expression in the Hypothalamic Nuclei and Nucleus of the Solitary Tract in Male Rats: Time Course Study and the Role of Testosterone.

Reyes

Yamada

Estacio

et al. 2001

Journal of Reproduction and Development

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Abstract.We have shown that 48-h fasting suppresses luteinizing hormone (LH) secretion in female rats which is enhanced by an estrogenic milieu and mediated by noradrenergic neurons. A similar fasting protocol yielded a suppression of LH secretion in male rats in a testosterone-dependent manner. In this experiment, we intended to identify specific nuclei in the hypothalamus and caudal brainstem that are activated during fasting for 6, 24, 30 or 48 h in castrated male rats with or without chronic testosterone treatment. Fasting started at 1300 h (lights-off at 1900 h). In testosterone-treated castrates, Fos-like-immunoreactive (FL-ir) cells were significantly increased in the paraventricular nucleus, A2 region of the nucleus of the solitary tract, supraoptic nucleus and amygdala 6 h after the onset of fasting but not 24, 30 or 48 h after the onset. On the other hand, FL-ir cells were not significantly different in those areas among fasted castrates compared with unfasted controls. In the A2 region of testosterone-treated castrates, tyrosine hydroxylase-and dopamine-β-hydroxylaseimmunoreactive (TH-ir, DBH-ir) cells did not exhibit Fos-like immunoreactivity (FLI). Our results suggest that the absence of food may activate neurons in discrete hypothalamic and brainstem nuclei in male rats at the beginning of fasting and this activation requires an androgenic milieu. The absence of FLI in TH-or DBH-ir cells in the A2 region would indicate that transmitter systems other than catecholaminergic neurons may be involved during the very early stage of 48-h fasting-induced suppression of LH secretion. Key words: c-Fos, Fasting, Paraventricular nucleus, Nucleus of the solitary tract, Testosterone (J. Reprod. Dev. 47: [53][54][55][56][57][58][59][60][61][62] 2001) asting is known to inhibit gonadal function by suppressing gonadotropin secretion in humans [1] and animals [2][3][4][5]. We have previously reported that 48-h fasting suppresses pulsatile luteinizing hormone (LH) secretion in female rats in an estrogen-dependent manner [6,7]. Using the same fasting conditions in male rats, 48-h fasting inhibits LH release in a testosterone-dependent manner [8]. These studies suggest that the cascade of events culminating in suppression of LH secretion during fasting depends upon the steroidal status in both genders.c-Fos, the protein product of the c-fos protooncogene, is widely used as a sensitive and reliable marker of neuronal activation in specific circuits of the nervous system in response to a variety of stimuli [9]. In previous studies, however, using intact adult [10,11] and young [12] male rats, c-Fos expression was not found in the paraventricular nucleus (PVN) and the nucleus of the solitary tract (NTS) after 15-, 22-, 24-, 27-or 48-h fasting. Moreover, there are only a few reports concerning androgen-dependent potentiation of neuronal c-

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“…This acquired behavioral response is accompanied by a wide array of neural and endocrine changes. For example, administration of a powerful aversive substance, LiCl, enhances c-Fos-IR in a variety of brain sites, including the nucleus of the solitary tract, area postrema, CeA, PVN, and SON (31). In addition, an increase in the plasma OT and (to a lesser degree) VP levels and, thus, activation of OT and VP neurons in the PVN and SON, has been observed as a result of LiCl treatment (32,46).…”

Section: Discussionmentioning

confidence: 94%

Effect of peptide histidine isoleucine on consummatory behavior in rats

Olszewski

Wirth

Shaw

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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. Effect of peptide histidine isoleucine on consummatory behavior in rats. Am J Physiol Regul Integr Comp Physiol 284: R1445-R1453, 2003. First published February 20, 2003 10.1152/ajpregu.00554.2002-Peptide histidine isoleucine (PHI) and VIP are derived from the same precursor. While central VIP decreases food intake, potential effects of PHI on feeding have not been studied. In the current study, we found that PHI administered intracerebroventricularly (ICV) or into the hypothalamic paraventricular nucleus (PVN) or central nucleus of the amygdala (CeA) decreased food consumption in overnight-deprived rats. The magnitude of an anorexigenic response to PHI differed depending on the injection route: ICV-infused peptide evoked the most potent effect. We determined that that only PVN-and CeA-injected PHI did not have aversive consequences. In addition, we infused anorexigenic doses of PHI via the same routes and assessed Fos immunoreactivity of PVN oxytocin (OT) and vasopressin (VP) neurons using double immunohistochemistry. OT and VP are thought to promote feeding termination. PHI increased the percentage of Fos-positive OT neurons regardless of the injection route. PVN-and ICV-infused PHI induced activation of VP cells. We conclude that central PHI has an inhibitory influence on food intake in rats. The PVN, with OT and VP neurons, and CeA may be involved in the mediation of anorexigenic effects of PHI. conditioned taste aversion; oxytocin; vasopressin; paraventricular nucleus of the hypothalamus; amygdala PEPTIDE HISTIDINE ISOLEUCINE (PHI) belongs to the pituitary adenylate cyclase-activating polypeptide (PACAP)/ glucagon family derived from a common precursor protein, prepro-VIP. PHI, VIP, peptide histidine valine (PHV), and peptide histidine methionine, among others, are processed from this precursor molecule. Prepro-VIPrelated peptides, including PHI, share a structural homology, as well as a certain degree of functional similarities, e.g., by having a stimulatory effect on the release and/or synthesis of glucagon (8), prolactin (20,28,40), and melatonin (21, 37, 49), and by affecting circadian rhythmicity (2, 3), heart rate (38), vasomotor functions (15, 19), and activation of the hypothalamic-pituitaryadrenal (HPA) axis (4, 6).PHI is widespread throughout the central and peripheral nervous systems (12). The presence of this peptide has been demonstrated in numerous central regions, where PHI often colocalizes in neurons with other products of prepro-VIP (13). Interestingly, PHIcontaining neuronal elements are encompassed in several brain sites involved in the regulation of consummatory behavior, including the hypothalamic paraventricular (PVN), supraoptic (SON), and arcuate (ARC) nuclei, central nucleus of the amygdala (CeA), and bed nucleus of the stria terminalis (17, 30).The abundance of receptors for PHI in these feedingrelated areas has also been confirmed. There are two well-described subtypes of receptors for PHI, termed VIP1 and VIP2 (18,24,45). These receptors do not seem to be selective to PHI al...

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c-Fos Expression in Rat Brain and Brainstem Nuclei in Response to Treatments That Alter Food Intake and Gastric Motility

Cited by 153 publications

References 0 publications

PYY(3–36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats

PYY(3–36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats

Effect of Fasting on c-Fos Expression in the Hypothalamic Nuclei and Nucleus of the Solitary Tract in Male Rats: Time Course Study and the Role of Testosterone.

Effect of peptide histidine isoleucine on consummatory behavior in rats

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