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      Dorsal and Ventral Medullary Catecholamine Cell Groups Contribute Differentially to Systemic Interleukin-1β-Induced Hypothalamic Pituitary Adrenal Axis Responses

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          Medial parvocellular paraventricular corticotropin-releasing hormone (mPVN CRH) cells are critical in generating hypothalamic-pituitary-adrenal (HPA) axis responses to systemic interleukin-1β (IL-1β). However, although it is understood that catecholamine inputs are important in initiating mPVN CRH cell responses to IL-1β, the contributions of distinct brainstem catecholamine cell groups are not known. We examined the role of nucleus tractus solitarius (NTS) and ventrolateral medulla (VLM) catecholamine cells in the activation of mPVN CRH, hypothalamic oxytocin (OT) and central amygdala cells in response to IL-1β (1 µg/kg, i.a.). Immunolabelling for the expression of c- fos was used as a marker of neuronal activation in combination with appropriate cytoplasmic phenotypic markers. First we confirmed that PVN 6-hydroxydopamine lesions, which selectively depleted catecholaminergic terminals, significantly reduced IL-1β-induced mPVN CRH cell activation. The contribution of VLM (A1/C1 cells) versus NTS (A2 cells) catecholamine cells to mPVN CRH cell responses was then examined by placing ibotenic acid lesions in either the VLM or NTS. The precise positioning of these lesions was guided by prior retrograde tracing studies in which we mapped the location of IL-1β-activated VLM and NTS cells that project to the mPVN. Both VLM and NTS lesions reduced the mPVN CRH and OT cell responses to IL-1β. Unlike VLM lesions, NTS lesions also suppressed the recruitment of central amygdala neurons. These studies provide novel evidence that both the NTS and VLM catecholamine cells have important, but differential, contributions to the generation of IL-1β-induced HPA axis responses.

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          Most cited references 11

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          Dissociation of oxytocin, vasopressin and corticotropin secretion during different types of stress.

           Patrick Gibbs (1984)
          Oxytocin (OT), vasopressin (AVP), and corticotropin (ACTH) levels were measured in peripheral plasma of male rats subjected to one of three models of stress: restraint, cold, or ether. ACTH secretion was increased in all three groups compared to unstressed controls. OT secretion was increased in rats subjected to restraint or ether but not cold. AVP secretion was increased only by ether stress. The data suggest that the hypothalamic and neurohypophysial contribution to the control of ACTH secretion may vary in response to different types of stress.
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            Evidence for the involvement of the central adrenergic system in interleukin 1-induced adrenocortical response.

            The role of central catecholamines in the mediation of adrenocortical activation, induced by interleukin 1 (IL-1), was investigated by measuring ACTH and corticosterone in serum. Adult male rats were injected with either vehicle or the neurotoxin 6-hydroxydopamine (6-OHDA) into the lateral ventricle or the ventral noradrenergic ascending bundle. In vehicle-injected rats, 2 U of IL-1, injected intraventricularly, produced a 5- and 15-fold increase in ACTH and CS, respectively, in serum, 120 min after the injection of IL-1. In contrast, 6-OHDA, injected either intraventricularly or into the ventral noradrenergic ascending bundle, abolished the response to an intracerebral injection of IL-1. In addition, in rats pretreated with the alpha 1-adrenergic antagonist, prazosin, IL-1 failed to activate the adrenocortical axis. In other rats pretreated with the beta-adrenergic antagonist, propranolol, the adrenocortical response did not significantly differ from that of vehicle-pretreated rats. These results suggest that central adrenergic transmission, originating at the ventral noradrenergic ascending bundle and acting through alpha 1-adrenergic receptors, is involved in the adrenocortical response to IL-1.
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              Comparison of ibotenate and kainate neurotoxicity in rat brain: a histological study.

              The neurotoxic properties of ibotenate and kainate after intracerebral application were compared in several regions of the rat brain. Ibotenate, being 5-10 times less toxic than kainate, caused lesions which were generally found to extend spherically from the tip of the injection cannula. In contrast, kainate injections often resulted in neuronal degeneration distant from the site of infusion, thus severely limiting its use as a tool for causing lesions in neurobiological studies. In some of the brain regions examined (hippocampus, septum), neurons appeared differentially susceptible to kainate but uniformly vulnerable to ibotenate. Some cell groups, such as those in the medial septum and the locus coeruleus, proved highly resistant to kainate but could be selectively ablated by ibotenate. These findings, together with differences between the two toxins in the evolution of neuronal degeneration (exemplified here in the hippocampal formation), appear to support previous suggestions that ibotenate and kainate exert their excitotoxic actions via different mechanisms. On the other hand, neuropathological changes caused in the cerebellum did not differ, since both ibotenate and kainate preferentially destroyed granule cells. Two nuclei, the arcuate nucleus of the hypothalamus and the nucleus of the fifth nerve, were found to be extremely resistant to either neurotoxin.

                Author and article information

                S. Karger AG
                February 2001
                23 February 2001
                : 73
                : 2
                : 129-138
                Department of Physiology and Pharmacology, University of Queensland, Brisbane, Australia
                54629 Neuroendocrinology 2001;73:129–138
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 2, References: 44, Pages: 10
                Neuroimmune Interactions


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