Subdiaphragmatic vagotomy suppresses endotoxin-induced activation of hypothalamic corticotropin-releasing hormone neurons and ACTH secretion.

Gaykema, Ronald P.; Dijkstra, I.; Tilders, F. J. H.

doi:10.1210/endo.136.10.7664696

Cited by 150 publications

(85 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Vagal sensory input from the abdomen implicated in the central neural (Wan, et al, 1994), hyperthermic , and hormonal (Fleshner, et al, 1995;Gaykema, et al, 1995;Kapcala, et al, 1996) responses to inflammatory stimuli may have contributed to this response as may the action of circulating mediators on the area postrema (Cunningham et al, 1994). However, Fos appeared in this circumventricular organ only in the rats with the most intense dorsomedullary responses as reported previously during acute inflammation Ericsson, et al, 1994).…”

Section: Discussionsupporting

confidence: 55%

“…This surgical model mirrors the clinical course of sepsis and recreates a sequence of events that differs from that after a lethal dose of endotoxin in both time course and the release and distribution of inflammatory mediators (Mathiak, et al, 2000;Wichterman, et al, 1980). The presence of peritonitis and a surgically induced cecal abscess in the model may constitute a sustained stimulus to visceral sensory pathways that respond to tissue inflammation (Fleshner et al, 1995;Gaykema, et al, 1995;Kapcala et al, 1996;Wan, et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…The administration of bacterial endotoxin has gained wide use as a systemic inflammatory stimulus (Beishuizen and Thijs, 2003;Carlson et al, 1997;Gaykema et al, 1995;Wan et al, 1994;Watkins et al, 1994), but the utility of endotoxin administration as an experimental model of sepsis has been questioned (Mathiak et al, 2000;Wichterman et al, 1980). The central neural responses to acute doses of endotoxin Wan, et al, 1994) or inflammatory cytokines (Chan et al, 1993;Crane et al, 2003;Ericsson et al, 1994;Xu et al, 1999) have been well described and are likely to be present in sepsis but may comprise only a subset of the complete response to prolonged systemic infection.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Central neural distribution of immunoreactive Fos and CRH in relation to plasma ACTH and corticosterone during sepsis in the rat

Carlson

Chiu

Fiedler

et al. 2007

Experimental Neurology

View full text Add to dashboard Cite

Although brain pathways activated by sepsis may respond acutely to endotoxin administration, the long-term central response to sepsis is not known. We prepared male rats for hormonal sampling at the circadian nadir (AM) and peak (PM) after cecal ligation and puncture (CLP) or sham surgery. Diurnal variation of corticosterone was present on postoperative day (D) 3 and D4 after sham surgery but not after CLP. CLP increased Fos immunostaining in the nucleus of tractus solitarius (NTS), ventrolateral medulla, medullary raphe, parabrachial nucleus, hypothalamus, amygdala, bed nucleus of stria terminalis, and preoptic region. Fos responses were generally greatest on D1 but persisted to the AM of D4. The number of Fos-positive cell nuclei in the NTS on D3 and D4 did not differ but had greater variance on D3 than on D4 (P < 0.01) with a divergent response in the PM of D3 that was correlated with plasma ACTH (r = 0.927, P<0.01) but not with corticosterone. CLP increased CRH-staining intensity in the hypothalamic paraventricular neurons uniformly from D1 through D4 (P<0.01). Similar to Fos in NTS, this response was correlated with plasma ACTH (r = 0.738, P<0.05) and adrenal size (r = 0.730, P<0.05) in the PM of D3. Neuronal CRH became detectable after CLP in specific medullary areas on D1 and in the preoptic region on D3 and D4. Thus, the suppression of circadian variation by CLP was associated with central neural responses that increased in relation to plasma ACTH without apparent influence on the release of corticosterone.

show abstract

Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Central neural distribution of immunoreactive Fos and CRH in relation to plasma ACTH and corticosterone during sepsis in the rat

Carlson

Chiu

Fiedler

et al. 2007

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…These pieces of evidence suggest that the CeA response is independent of prostaglandin synthesis mechanisms and presumably reliant either on the production of other secondary signaling molecules or alternatively afferent pathways originating at the level of the NTS cells. With regard to the latter, systemic IL-1␤ signals might reach the NTS by means of visceral sensory afferents (Fleshner et al, 1995;Gaykema et al, 1995;Kapcala et al, 1996;Goehler et al, 1997;Ishizuka et al, 1997;Ek et al, 1998), although it remains to be investigated whether circulating IL-1␤-induced CeA cell recruitment depends on the activation of vagal afferent fibers.…”

Section: Putative Mechanisms For Cea Cell Recruitment By Systemic Il-1␤mentioning

confidence: 99%

Systemic administration of interleukin‐1β activates select populations of central amygdala afferents

Buller

Day

2002

J of Comparative Neurology

View full text Add to dashboard Cite

The central nucleus of the amygdala (CeA) is activated robustly by an immune challenge such as the systemic administration of the proinflammatory cytokine interleukin-1␤ (IL-1␤). Because IL-1␤ is not believed to cross the blood-brain barrier in any significant amount, it is likely that IL-1␤ elicits CeA cell recruitment by means of activation of afferents to the CeA. However, although many studies have investigated the origins of afferent inputs to the CeA, we do not know which of these also respond to IL-1␤. Therefore, to identify candidate neurons responsible for the recruitment of CeA cells by an immune challenge, we iontophoretically deposited a retrograde tracer, cholera toxin b-subunit (CTb), into the CeA of rats 7 days before systemic delivery of IL-1␤ (1 g/kg, i.a.). By using combined immunohistochemistry, we then quantified the number of Fos-positive CTb cells in six major regions known to innervate the CeA. These included the medial prefrontal cortex, paraventricular thalamus (PVT), ventral tegmental area, parabrachial nucleus (PB), nucleus tractus solitarius, and ventrolateral medulla. Our results show that after deposit of CTb into the CeA, the majority of double-labeled cells were located in the PB and the PVT, suggesting that CeA cell activation by systemic IL-1␤ is likely to arise predominantly from cell bodies located in these regions. These findings may have significant implications in determining the central pathways involved in generating acute central responses to a systemic immune challenge.

show abstract

“…For instance, endotoxin from E. coli can induce 1) a fever response in rabbits when administered intracerebroventricularly (16), and 2) activation of hypothalamic histaminergic neurons in rats leading to ACTH release (17). In addition, a recent study has demonstrated that subdiaphragmatic vagotomy can suppress the endotoxin-induced activation of hypothalamic corticotropin -releasing hormone and ACTH secretion (18).…”

Section: Introductionmentioning

confidence: 99%

Effect of bacterial lipopolysaccharide on gastric emptying of liquids in rats

Ef¹

1997

Braz J Med Biol Res

View full text Add to dashboard Cite

The objectives of the present investigation were 1) to study the effect of bacterial lipopolysaccharide (LPS) on rat gastric emptying (GE) and 2) to investigate a possible involvement of the vagus nerve in the gastric action of LPS. Endotoxin from E. coli (strain 055:B5) was administered sc, ip or iv to male Wistar rats (220-280 g body weight) at a maximum dose of 50 µg/kg animal weight. Control animals received an equivalent volume of sterile saline solution. At a given time period after LPS administration, GE was evaluated by measuring gastric retention 10 min after the orogastric infusion of a test meal (2 ml/100 g animal weight), which consisted of 0.9% NaCl plus the marker phenol red (6 mg/dl). One group of animals was subjected to bilateral subdiaphragmatic vagotomy or sham operation 15 days before the test. A significant delay in GE of the test meal was observed 5 h after iv administration of the endotoxin at the dose of 50 µg/kg animal weight. The LPS-induced delay of GE was detected as early as 30 min and up to 8 h after endotoxin administration. The use of different doses of LPS ranging from 5 to 50 µg/kg animal weight showed that the alteration of GE was dose dependent. In addition, vagotomized animals receiving LPS displayed a GE that was not significantly different from that of the sham control group. However, a participation of the vagus nerve in LPS-induced delay in GE could not be clearly demonstrated by these experiments since vagotomy itself induced changes in this gastric parameter. The present study provides a suitable model for identifying the mechanisms underlying the effects of LPS on gastric emptyin

show abstract

Subdiaphragmatic vagotomy suppresses endotoxin-induced activation of hypothalamic corticotropin-releasing hormone neurons and ACTH secretion.

Cited by 150 publications

References 9 publications

Central neural distribution of immunoreactive Fos and CRH in relation to plasma ACTH and corticosterone during sepsis in the rat

Central neural distribution of immunoreactive Fos and CRH in relation to plasma ACTH and corticosterone during sepsis in the rat

Systemic administration of interleukin‐1β activates select populations of central amygdala afferents

Effect of bacterial lipopolysaccharide on gastric emptying of liquids in rats

Contact Info

Product

Resources

About