Hemorrhage‐Induced Activations of Adrenocorticotropin Release and Catecholamine Metabolism in the Ventrolateral Medulla are Differently Affected by Glucocorticoid Feedback

Ponec, J; Lachuer, Joël; Suaud-Chagny, Marie-Françoise; Tappaz, Marcel

doi:10.1111/j.1365-2826.1992.tb00187.x

Cited by 6 publications

(4 citation statements)

References 38 publications

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“…The present demonstration of robust NGFI-B and c-fos expression appearing uniformly distributed across all major neuroendocrine and autonomic-related cell types in PVH is in keeping with the widespread involvement of CRF, AVP, and OT neurons in responses associated with metabolic mobilization and pressure and volume compensation following hemorrhage (for review, see Cowley, 1992). Furthermore, the induction of both cIEs in medullary catecholamine cell groups is consistent with previous findings that hemorrhage triggers activation of the catecholamine metabolism in the ventrolateral medulla (Quintin et al, 1987;Ponec et al, 1992) and that catecholaminergic projections from the medulla play pivotal roles in relaying pressure and volume-related information to the PVH and SO to mediate compensatory neuroendocrine responses (see Sawchenko and Swanson, 1982;Plotsky et al, 1989).…”

Section: Discussionsupporting

confidence: 87%

A comparison of two immediate-early genes, c-fos and NGFI-B, as markers for functional activation in stress-related neuroendocrine circuitry

et al. 1993

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The promoter regions of the rat corticotropin-releasing factor (CRF), oxytocin (OT), and vasopressin (AVP) genes contain sequences similar to the cis-acting response element identified for NGFI-B, an immediate-early gene structurally related to the steroid hormone receptor superfamily. Combined immuno- and hybridization histochemical approaches were used to determine whether challenges that influence the synthesis and secretion of CRF, OT, and/or AVP result in altered expression in neurosecretory neurons of NGFI-B and another immediate-early gene, c-fos, which is widely used as a marker for functionally activated neurons. NGFI-B mRNA was found to be expressed at constitutively high levels in the telencephalon, but not in the endocrine hypothalamus, of unperturbed controls; basal levels of c-fos expression were uniformly low throughout the CNS. NGFI-B and c-fos mRNAs, and Fos protein, were induced with a similar time course and in similar neuroendocrine cell types in response to acute hypotensive hemorrhage (15% reduction in blood volume), intravenous injection of interleukin-1 beta (IL-1 beta; 1.87 micrograms/kg), chronic salt loading (7 d maintenance on 2% saline), and acute bilateral adrenalectomy. c-fos mRNA and Fos protein were readily demonstrable in afferent pathways that have been implicated as mediating the neuroendocrine responses in the three stress paradigms; these include medullary catecholaminergic cell groups in response to IL-1 beta and hemorrhage, and cell groups lining the lamina terminalis in response to salt loading. Challenge-specific induction of NGFI-B expression was detectable in these extrahypothalamic cell groups, though with a lesser sensitivity than that required to reveal NGFI-B induction in the hypothalamus, or c-fos expression in these related afferents. These results establish NGFI-B as a useful adjunct to c-fos, for revealing synaptic and/or transcriptional activation in the magno- and parvocellular neurosecretory systems. Differences in the sensitivity of the two markers in revealing functionally related activation in extrahypothalamic regions speak to general issues concerning the use of immediate-early genes in mapping functional circuitry in the CNS.

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Section: Discussionsupporting

confidence: 87%

A comparison of two immediate-early genes, c-fos and NGFI-B, as markers for functional activation in stress-related neuroendocrine circuitry

et al. 1993

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“…With the maximal stimula tion used in this study an approximately 3-fold increase in ACTH was obtained. This amplitude was similar to that obtained by a stressful stimulus such as hemorrhage in comparable experimental conditions [38]. The delay of the response was quite short, the maximum response being observed between 2 and 3 min after the beginning of the stimulation.…”

Section: Discussionsupporting

confidence: 63%

“…Thus, blockade of central noradrenergic receptors through i.c.v. injection of appro priate antagonists greatly reduced or abolished the activa tion of the ACTH response to immobilisation stress [20], ether stress [28], hemorrhage [38], as well as the release of CRF in the portal blood following nitroprusside-induced hypotension or stimulation of the CA ascending bundle [27], These latter data clearly indicate that there exist cen tral adrenoceptors involved in the activation of the HPA axis following stimulation of some noradrenergic affer ents to the PVN. We speculate that the noradrenergic afferents from the A2 group of the dorsomedial medulla in contrast to those from the A1 group of the ventrolateral medulla do use NA as a transmitter.…”

Section: Discussionmentioning

confidence: 65%

Evidence that Activation of the Hypothalamo-Pituitary-Adrenal Axis by Electrical Stimulation of the Noradrenergic A1 Group Is Not Mediated by Noradrenaline

Gartside

Suaud-Chagny²,

Tappaz³

1995

Neuroendocrinology

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The paraventricular nucleus (PVN) of the hypothalamus, where the CRF-containing neurosecretory cells controlling the hypothalamo-pituitary-adrenal (HPA) axis are located, receives a dense noradrenergic innervation from the A1 group of the caudal ventrolateral medulla. In the present study we studied the relationship between release of noradrenaline (NA) in the PVN and activation of the HPA axis in response to electrical stimulation of the A1 region. In the urethane-anesthetized male rat, extracellular NA in the PVN was monitored on line by electrochemical recording while the activity of the HPA axis was estimated by measurement of ACTH in blood samples. A 1 min, 10 Hz stimulation evoked a significant increase of extracellular NA in the PVN as well as an ACTH surge in blood. The NA and ACTH response evoked by stimulation in the 3- to 14-Hz range were found to be frequency dependent. However, whilst the NA response increased in an exponential manner with respect to frequency, the ACTH response appeared to plateau between 10 and 14 Hz. Specific lesions of the noradrenergic terminals in the PVN, by bilateral local administration of 6-hydroxydopamine, markedly reduced the ACTH response to stimulation. Intracerebroventricular injection of desmethylimipramine, a NA uptake inhibitor, enhanced the increase in extracellular NA evoked by submaximal stimulation about 2.5-fold but did not modify the corresponding ACTH response. Combined intracerebroventricular injection of α-and β-adrenergic antagonists, phentolamine and propanolol respectively, did not prevent the ACTH response evoked by stimulation. Following stimulation of the caudal ventrolateral medulla, the ACTH response thus appears to result from the stimulation of the Al noradrenergic group projecting to the PVN. However, the inability of pharmacological manipulations which enhance or block central noradrenergic transmission to influence the ACTH response suggests that the noradrenergic endings in the PVN originating from the A1 group use a transmitter other than NA to activate the HPA axis at the PVN level.

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“…1992;Chan & Sawchenko 1994a;Li & Dampney 1994), augment catecholamine turnover (Quintin et al . 1987;Ponec et al . 1992) and increase TH levels (Schmitt et al .…”

Section: Discussionmentioning

confidence: 99%

Differential time‐ and dose‐related effects of haemorrhage on tyrosine hydroxylase and neuropeptide Y mRNA expression in medullary catecholamine neurons

Chan

Sawchenko

1998

Eur J of Neuroscience

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Hypotensive haemorrhage induces nuclear Fos expression and upregulates tyrosine hydroxylase (TH) mRNA in catecholamine-containing cell groups of the rat medulla oblongata. To shed light on the significance of the coexistence of neuropeptide Y (NPY) in aminergic neurons, the impact of graded levels of haemorrhage on temporal changes in the expression of TH and NPY mRNAs was compared; concurrent staining for Fos permitted comparisons between cells that ostensibly were and were not targeted by the stimulus. A 15% haemorrhage provoked increased NPY expression in all medullary catecholamine cell groups except the A2; these changes were detected predominantly in Fos-immunoreactive neurons (Fos-ir) at later (2-4 h) time points. Upregulation of TH and NPY mRNAs in Fos-ir neurons followed distinct time courses, with NPY responses peaking more rapidly, particularly in the C1 and C2 cell groups. Adrenergic cell groups displayed greater maximal increases in NPY expression than the A1 noradrenergic cell group while the converse was true of TH mRNA response. Increasing the severity of haemorrhage resulted in more pronounced increases in both mRNA responses in each aminergic region. These findings indicate that haemorrhage differentially affects TH and NPY expression in medullary catecholamine cell groups that participate in the maintenance of cardiovascular homeostasis. The differential nature of these responses suggests them not to be a simple consequence of metabolic alterations pursuant to increased synaptic activity. The prompt and robust NPY mRNA responses in adrenergic neurons suggests a mechanism by which peptide content of these cell groups' terminal projections is defended.

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Hemorrhage‐Induced Activations of Adrenocorticotropin Release and Catecholamine Metabolism in the Ventrolateral Medulla are Differently Affected by Glucocorticoid Feedback

Cited by 6 publications

References 38 publications

A comparison of two immediate-early genes, c-fos and NGFI-B, as markers for functional activation in stress-related neuroendocrine circuitry

A comparison of two immediate-early genes, c-fos and NGFI-B, as markers for functional activation in stress-related neuroendocrine circuitry

Evidence that Activation of the Hypothalamo-Pituitary-Adrenal Axis by Electrical Stimulation of the Noradrenergic A1 Group Is Not Mediated by Noradrenaline

Differential time‐ and dose‐related effects of haemorrhage on tyrosine hydroxylase and neuropeptide Y mRNA expression in medullary catecholamine neurons

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