Norepinephrine in the paraventricular nucleus stimulates corticosterone release

Leibowitz, Sarah F.; Díaz, Sonia Pértega; Tempel, Donna L.

doi:10.1016/0006-8993(89)91069-x

Cited by 74 publications

(27 citation statements)

References 54 publications

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“…Unilateral norepinephrine microinjection produced a significant increase in plasma corticosterone levels, in accord with many previous studies documenting elevations in plasma ACTH and corticosterone titers after central NE administration (Szafarczyk et al, 1987;Leibowitz et al, 1989). These effects are likely mediated principally by ␣1 adrenergic receptors located on CRFexpressing PVH neurons .…”

Section: Norepinephrine Microinjection Produces Robust Pvh Activationsupporting

confidence: 88%

Neurotransmitter Regulation of Cellular Activation and Neuropeptide Gene Expression in the Paraventricular Nucleus of the Hypothalamus

2002

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Norepinephrine (NE), glutamate (Glu), and GABA have been identified as important neurotransmitters governing neuroendocrine mechanisms represented in the paraventricular nucleus of the hypothalamus (PVH). Microinjection studies were used to compare the efficacy of these transmitter mechanisms in stimulating PVH output neurons. Local administration of NE provoked an increase in plasma corticosterone levels and Fos induction in the both the parvocellular and magnocellular divisions of the nucleus. This treatment also stimulated a robust increase in corticotropin-releasing factor (CRF) heteronuclear (hn) RNA in the parvocellular PVH and a more subtle, although reliable, increase in arginine vasopressin (AVP) hnRNA in this same compartment. Local administration of the GABA A receptor antagonist bicuculline methiodide (BMI) resulted in increased plasma corticosterone and, in contrast to NE treatment, Fos induction limited primarily to the parvocellular PVH.BMI elicited marked increases in both CRH and AVP hnRNAs within the parvocellular division of the nucleus. Over a wide range of concentrations, Glu failed to produce reliable increases in corticosterone secretion and induced only weak activational responses limited primarily to non-neurosecretory regions of the PVH. Local Glu administration did, however, provoke Fos induction in identified GABAergic neurons immediately adjoining the PVH, suggesting that the muted response to Glu may be a consequence of concurrent activation of local inhibitory interneurons. These results support a differential involvement of adrenergic, glutamatergic and GABAergic mechanisms in regulating neurosecretory populations of the PVH and suggest that involvement of local circuit neurons must be carefully considered in the interpretation of microinjection studies.

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Section: Norepinephrine Microinjection Produces Robust Pvh Activationsupporting

confidence: 88%

Neurotransmitter Regulation of Cellular Activation and Neuropeptide Gene Expression in the Paraventricular Nucleus of the Hypothalamus

2002

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“…First, our NE injections elevated circulating ACTH/corticosterone, confirming many reports (Szafarczyk et al, 1987;Leibowitz et al, 1988Leibowitz et al, , 1989Saphier and Feldman, 1989;Itoi et al, 1994Itoi et al, , 1999Helmreich et al, 2001;Cole and Sawchenko, 2002). Second, corticosterone elevations reportedly occur only from PVH-injected NE [with a small effect in dorsomedial hypothalamus (DMH)] and not from NE injected into surrounding areas (Leibowitz et al, 1989). Our corticosterone-producing injections were restricted to PVH (i.e., not DMH), suggesting a direct action of NE.…”

Section: Interpreting the Effects Of Central Ne Microinjection Evidensupporting

confidence: 87%

Catecholaminergic Control of Mitogen-Activated Protein Kinase Signaling in Paraventricular Neuroendocrine NeuronsIn VivoandIn Vitro: A Proposed Role during Glycemic Challenges

Khan¹,

Ponzio²,

Sanchez‐Watts³

et al. 2007

J. Neurosci.

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We show that systemic insulin and 2-DG, and PVH-targeted NE microinjections, rapidly elevated PVH phospho-ERK1/2 levels. NE increased Crh and c-fos expression, together with circulating ACTH/corticosterone. However, because injections also increased c-Fos mRNA in other brain regions, we used hypothalamic slices maintained in vitro to clarify whether NE activates PVH neurons without contribution of inputs from distal regions. In slices, bath-applied NE triggered robust phospho-ERK1/2 immunoreactivity in PVH (including CRH) neurons, which attenuated markedly in the presence of the ␣ 1 adrenoceptor antagonist, prazosin, or the MAP kinase kinase (MEK) inhibitor, U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene). Therefore, at a systems level, local PVH delivery of NE is sufficient to account for hindbrain activation of CRH neuroendocrine neurons during glycemic challenge. At a cellular level, these data provide the first demonstration that MAP kinase signaling cascades (MEK3 ERK) are intracellular transducers of noradrenergic signals in CRH neurons, and implicate this transduction mechanism as an important component of central neuroendocrine responses during glycemic challenge.

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“…Neuroimmunomodulation 1998;5: [22][23][24][25][26][27][28][29][30][31][32][33][34][35] Leo/Callahan/Bonneau lymphocytes were cultured in 2.5 ml of supplemented IMDM in 35-mm tissue culture dishes for 3 days at 37°C/5% CO 2 . Cells derived from these cultures were examined for HSV-specific lytic activity by 51 Cr release assay.…”

mentioning

confidence: 99%

Peripheral Sympathetic Denervation Alters Both the Primary and Memory Cellular Immune Responses to Herpes simplex Virus Infection

Leo

Callahan

Bonneau

1998

Neuroimmunomodulation

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Numerous studies have sought to delineate the impact of neuroendocrine function on overall immune responsiveness. Using various murine models, we and others have previously shown that both adrenal-dependent and adrenal-independent mechanisms associated with psychological stress modulate components of both the primary and memory cellular immune responses to herpes simplex virus type 1 (HSV-1) infection. We have extended these studies by determining the impact of 6-hydroxydopamine (6-OHDA)-mediated peripheral sympathetic denervation on both responses. C57BL/6 mice treated with 6-OHDA (200 mg/kg) exhibited reduced generation of both primary lymph node- and splenic-derived cytotoxic T lymphocytes (CTL) following a local (footpad) and systemic HSV infection, respectively. 6-OHDA also suppressed activation of HSV-specific memory CTL (CTLm). In both models, alterations in cytokine production and lymphocyte subset distribution were also observed. Administration of 6-OHDA also resulted in substantial but transient activation of the hypothalamic-pituitary-adrenal (HPA) axis as was indicated by a dramatic elevation of serum corticosterone and hypothalamic Fos expression. Moreover, the corticosterone levels were directly correlated with the extent of CTLm activation. Together, these findings suggest that peripheral sympathetic denervation alters immune function through activation of the HPA axis.

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Norepinephrine in the paraventricular nucleus stimulates corticosterone release

Cited by 74 publications

References 54 publications

Neurotransmitter Regulation of Cellular Activation and Neuropeptide Gene Expression in the Paraventricular Nucleus of the Hypothalamus

Neurotransmitter Regulation of Cellular Activation and Neuropeptide Gene Expression in the Paraventricular Nucleus of the Hypothalamus

Catecholaminergic Control of Mitogen-Activated Protein Kinase Signaling in Paraventricular Neuroendocrine NeuronsIn VivoandIn Vitro: A Proposed Role during Glycemic Challenges

Peripheral Sympathetic Denervation Alters Both the Primary and Memory Cellular Immune Responses to Herpes simplex Virus Infection

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