Central amygdala Fos expression during hypotensive or febrile, nonhypotensive endotoxemia in conscious rats

Nancy C. Tkacs, Jianhua Li, Alison M. Strack

Research output: Contribution to journalArticle

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Abstract

The distribution and time course of Fos expression in neurons in the central nucleus of the amygdala (CeA) were studied in endotoxemic rats in two separate experiments. In each case, the severity of the endotoxin (lipopolysaccharide; LPS) challenge was characterized by using physiological outcome variables, including blood pressure and heart rate. Throughout the rostrocaudal extent of the CeA, extensive Fos staining was found 3 hours after injection with a hypotensive close of Salmonella enteritidis LPS. Hypotension alone has been reported to induce Fos in the CeA; therefore, the remaining experiments were performed by using a lower dose of Escherichia coli LPS that did not cause hypotension. The nonhypotensive dose of E. coli LPS also induced Fos in large numbers of neurons of the CeA, with peak staining at 2 hours and Fos staining persisting for 6 hours after LPS injection. Tachycardia and fever after LPS also persisted for at least 6 hours. CoA Fos staining during nonhypotensive endotoxemia was predominantly located in the lateral subnucleus, although Fos-stained medial subnucleus neurons were also present. Additional forebrain regions that showed persistent Fos staining 6 hours after LPS included the parvocellular paraventricular nucleus of the hypothalamus, the bed nucleus of the stria terminalis, and the medial preoptic area. Forebrain regions that contained Fos-stained nuclei at earlier time points, but not at 6 hours, included the supraoptic nucleus, magnocellular regions of the paraventricular nucleus of the hypothalamus, the subfornical organ, and the organum vasculosum of the lamina terminalis. Few CeA neurons showed Fos staining in rats that were restrained in a ventilated plastic tube. Neurons in the lateral septal nucleus and the medial amygdaloid nucleus, which have numerous Fos-stained nuclei after stressors such as footshock or restraint, did not show Fos staining above control levels after LPS administration. Activation of CeA neurons after intravenous LPS may indicate persistent drive from vagal afferents and may implicate the CeA in the autonomic, neuroendocrine, and/or behavioral responses to this treatment.

Original languageEnglish (US)
Pages (from-to)592-602
Number of pages11
JournalJournal of Comparative Neurology
Volume379
Issue number4
DOIs
StatePublished - Mar 24 1997

Fingerprint

Endotoxemia
Fever
Staining and Labeling
Neurons
Septal Nuclei
Paraventricular Hypothalamic Nucleus
Prosencephalon
Hypotension
Hypothalamus
Subfornical Organ
Escherichia coli
Supraoptic Nucleus
Salmonella enteritidis
Injections
Preoptic Area
Coenzyme A
Central Amygdaloid Nucleus
Tachycardia
Endotoxins
Plastics

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

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title = "Central amygdala Fos expression during hypotensive or febrile, nonhypotensive endotoxemia in conscious rats",
abstract = "The distribution and time course of Fos expression in neurons in the central nucleus of the amygdala (CeA) were studied in endotoxemic rats in two separate experiments. In each case, the severity of the endotoxin (lipopolysaccharide; LPS) challenge was characterized by using physiological outcome variables, including blood pressure and heart rate. Throughout the rostrocaudal extent of the CeA, extensive Fos staining was found 3 hours after injection with a hypotensive close of Salmonella enteritidis LPS. Hypotension alone has been reported to induce Fos in the CeA; therefore, the remaining experiments were performed by using a lower dose of Escherichia coli LPS that did not cause hypotension. The nonhypotensive dose of E. coli LPS also induced Fos in large numbers of neurons of the CeA, with peak staining at 2 hours and Fos staining persisting for 6 hours after LPS injection. Tachycardia and fever after LPS also persisted for at least 6 hours. CoA Fos staining during nonhypotensive endotoxemia was predominantly located in the lateral subnucleus, although Fos-stained medial subnucleus neurons were also present. Additional forebrain regions that showed persistent Fos staining 6 hours after LPS included the parvocellular paraventricular nucleus of the hypothalamus, the bed nucleus of the stria terminalis, and the medial preoptic area. Forebrain regions that contained Fos-stained nuclei at earlier time points, but not at 6 hours, included the supraoptic nucleus, magnocellular regions of the paraventricular nucleus of the hypothalamus, the subfornical organ, and the organum vasculosum of the lamina terminalis. Few CeA neurons showed Fos staining in rats that were restrained in a ventilated plastic tube. Neurons in the lateral septal nucleus and the medial amygdaloid nucleus, which have numerous Fos-stained nuclei after stressors such as footshock or restraint, did not show Fos staining above control levels after LPS administration. Activation of CeA neurons after intravenous LPS may indicate persistent drive from vagal afferents and may implicate the CeA in the autonomic, neuroendocrine, and/or behavioral responses to this treatment.",
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Central amygdala Fos expression during hypotensive or febrile, nonhypotensive endotoxemia in conscious rats. / Tkacs, Nancy C.; Li, Jianhua; Strack, Alison M.

In: Journal of Comparative Neurology, Vol. 379, No. 4, 24.03.1997, p. 592-602.

Research output: Contribution to journalArticle

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N2 - The distribution and time course of Fos expression in neurons in the central nucleus of the amygdala (CeA) were studied in endotoxemic rats in two separate experiments. In each case, the severity of the endotoxin (lipopolysaccharide; LPS) challenge was characterized by using physiological outcome variables, including blood pressure and heart rate. Throughout the rostrocaudal extent of the CeA, extensive Fos staining was found 3 hours after injection with a hypotensive close of Salmonella enteritidis LPS. Hypotension alone has been reported to induce Fos in the CeA; therefore, the remaining experiments were performed by using a lower dose of Escherichia coli LPS that did not cause hypotension. The nonhypotensive dose of E. coli LPS also induced Fos in large numbers of neurons of the CeA, with peak staining at 2 hours and Fos staining persisting for 6 hours after LPS injection. Tachycardia and fever after LPS also persisted for at least 6 hours. CoA Fos staining during nonhypotensive endotoxemia was predominantly located in the lateral subnucleus, although Fos-stained medial subnucleus neurons were also present. Additional forebrain regions that showed persistent Fos staining 6 hours after LPS included the parvocellular paraventricular nucleus of the hypothalamus, the bed nucleus of the stria terminalis, and the medial preoptic area. Forebrain regions that contained Fos-stained nuclei at earlier time points, but not at 6 hours, included the supraoptic nucleus, magnocellular regions of the paraventricular nucleus of the hypothalamus, the subfornical organ, and the organum vasculosum of the lamina terminalis. Few CeA neurons showed Fos staining in rats that were restrained in a ventilated plastic tube. Neurons in the lateral septal nucleus and the medial amygdaloid nucleus, which have numerous Fos-stained nuclei after stressors such as footshock or restraint, did not show Fos staining above control levels after LPS administration. Activation of CeA neurons after intravenous LPS may indicate persistent drive from vagal afferents and may implicate the CeA in the autonomic, neuroendocrine, and/or behavioral responses to this treatment.

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