Reversible inactivation of the dorsal vagal complex blocks lipopolysaccharide-induced social withdrawal and c-Fos expression in central autonomic nuclei

Marvel, Francoise A; Chen, Chiao Chi; Badr, Nadia; Gaykema, Ronald P.; Goehler, Lisa E.

doi:10.1016/j.bbi.2003.09.004

Cited by 134 publications

(90 citation statements)

References 59 publications

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“…These findings were consistent with a study by Weiss and colleagues showing that local infusion of the 2-autoreceptor agonist, clonidine, to inhibit the hyperactive LC of chronically tailshocked rats immediately reversed their increased immobility in the forced swim test [36]. Similarly Marvel et al [37] and Gaykema and Goehler [27] have demonstrated that infusion of a local anesthetic near hyperactive A2 noradrenergic neurons in the dorsal vagal complex of endotoxin treated rats immediately reverses their behavioral inactivity as well as both the increased Fos responses of their stress regions (PVH, AMYG, BNST) and the reduced responses of their "active" network structures [HIPPO, ventral tegmental area (VTA), dorsal striatum and ventral tuberomammillary nucleus (VTN)]. Similar behavioral effects, though not completely identical neural ones, were obtained by immunotoxic lesion of the A2 neurons prior to endotoxin treatment supporting the hypothesis that the behavioral inactivity caused by the latter is mediated by the hyperactivity of these cells [38,39].…”

Section: Introductionsupporting

confidence: 81%

Toward the Rapid Treatment of Depression by Selective Inhibition of Central Stress Circuits

Stone¹

2012

TONEUROPPJ

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Abstract:A long standing problem with antidepressant drugs is their delayed onsets of action which has made them unsatisfactory in the rapid treatment of serious depressions involving agitated and suicidal behavior. Two new approaches to this problem involve the glutamatergic antagonist, ketamine, recently reviewed, and the acute inhibition of central stress circuits, which is the subject of the present review. The rationale behind stress-circuit inhibition comes from the findings that both clinical and experimental depressions are accompanied by increased neural activity in the stress network together with inhibited activity in regions underlying active motivated behaviors, and that both changes are reversed by effective antidepressant treatment. It has been shown further that direct pharmacological inhibition of central noradrenergic stress nuclei produces immediate reversal of depressive-like passive as well as sickness behaviors. Dipivalyl-6-fluoronorepinephrine (dp6FNE), a brain-permeable pro-drug of 6FNE, a full agonist at inhibitory brainadrenoceptors in brainstem noradrenergic stress nuclei, has been developed and found in preliminary studies to cause rapid reversal of both passivity and anhedonia as well as anxiolysis without significant hypoactivity in the open field. Low doses of agonists of glucocorticoid and 5HT1A autoreceptors, which respectively inhibit the hypothalamic-pituitaryadrenal axis and serotonergic stress systems, may also share these effects as well as potentiate the actions of dp6FNE. Anti-stress effects may also be involved in the rapid therapeutic effects found with intracerebral administration of first generation antidepressants and may prove helpful in potentiating the therapeutic actions of stimulants.

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Section: Introductionsupporting

confidence: 81%

Toward the Rapid Treatment of Depression by Selective Inhibition of Central Stress Circuits

Stone¹

2012

TONEUROPPJ

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“…As noted above, the PVH (Arborelius et al, 1999;Shumake et al, 2001), CeA (Siegle et al, 2007), BNST (Greenwood et al, 2005;Marvel et al, 2004;Stout et al, 2000), LC (Grant and Weiss, 2001), DR and periaqueductal gray (PAG) (Kollack-Walker et al, 1997;Miczek et al, 1999; In press), which are regions of the brain associated with stress, are known to be excessively activated in human and/or animal depression. Stress regions can be activated either by systemic ("bottom-up") or by processive ("top-down") stressors (Herman and Cullinan, 1997).…”

Section: Stress Area Activationmentioning

confidence: 99%

“…Systemic stresses that induce sickness behavior such as hemorrhage, ether and immune system activation produce a so-called "bottom-up" activation of stress regions in which there is little initial involvement of cortical structures. Marvel et al (2004) showed that the immune stimulant, lipopolysaccharide (LPS) produced intense neural activity of the dorsal vagal motor complex (DVMC), LC, PVH, BNS and CeA, which could be blocked (and sickness behavior alleviated) by local anesthesia of the DVMC. On the other hand "processive" stresses, such as restraint, footshock or social stress, which require cognitive processing and interpretation, activate limbic and thence lower stress centers by way of a "top-down" mechanism.…”

Section: Stress Area Activationmentioning

confidence: 99%

A final common pathway for depression? Progress toward a general conceptual framework

Stone

Yang

Quartermain

2008

Neuroscience & Biobehavioral Reviews

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Functional neuroimaging studies of depressed patients have converged with functional brain mapping studies of depressed animals in showing that depression is accompanied by a hypoactivity of brain regions involved in positively motivated behavior together with a hyperactivity in regions involved in stress responses. Both sets of changes are reversed by diverse antidepressant treatments. It has been proposed that this neural pattern underlies the symptoms common to most forms of the depression, which are the loss of positively motivated behavior and increased stress. The paper discusses how this framework can organize diverse findings ranging from effects of monoamine neurotransmitters, cytokines, corticosteroids and neurotrophins on depression. The hypothesis leads to new insights concerning the relationship between the prolonged inactivity of the positive motivational network during a depressive episode and the loss of neurotrophic support, the potential antidepressant action of corticosteroid treatment, and to the key question of whether antidepressants act by inhibiting the activity of the stress network or by enhancing the activity of the positive motivational system. Keywords depression; neuroimaging; fos; final common pathway; cytokines; corticosteroids; monoamines; neurotrophins; theory The quest for a final common pathway has long been goal of research in depression. Famous candidates in this search have included dysregulated brain monoamines (Schildkraut, 1965;

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“…The importance of the dorsal vagal complex (DVC) in social withdrawal that accompanies lipopolysaccharide (LPS) treatment was verified recently by Marvel et al (2004). The infusion of bupivacaine in the DVC decreased c-Fos expression in the NTS, SON, PVH, and CEA1 in response to i.p.…”

Section: Discussionmentioning

confidence: 93%

Inactivation of the Cerebral NFκB Pathway Inhibits Interleukin-1β-Induced Sickness Behavior and c-Fos Expression in Various Brain Nuclei

Nadjar

Bluthé

May

et al. 2005

Neuropsychopharmacol

107

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The behavioral effects of peripherally administered interleukin-1b (IL-1b) are mediated by the production of cytokines and other proinflammatory mediators at the level of the blood-brain interface and by activation of neural pathway. To assess whether this action is mediated by NFkB activation, rats were injected into the lateral ventricle of the brain with a specific inhibitor of NFkB activation, the NEMO Binding Domain (NBD) peptide that has been shown previously to abolish completely IL-1b-induced NFkB activation and Cox-2 synthesis in the brain microvasculature. NFkB pathway inactivation significantly blocked the behavioral effects of intraperitoneally administered IL-1b in the form of social withdrawal and decreased food intake, and dramatically reduced IL-1b-induced c-Fos expression in various brain regions as paraventricular nucleus, supraoptic nucleus, and lateral part of the central amygdala. These findings strongly support the hypothesis that IL-1b-induced NFkB activation at the blood-brain interface is a crucial step in the transmission of immune signals from the periphery to the brain that underlies further events responsible of sickness behavior.

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Reversible inactivation of the dorsal vagal complex blocks lipopolysaccharide-induced social withdrawal and c-Fos expression in central autonomic nuclei

Cited by 134 publications

References 59 publications

Toward the Rapid Treatment of Depression by Selective Inhibition of Central Stress Circuits

Toward the Rapid Treatment of Depression by Selective Inhibition of Central Stress Circuits

A final common pathway for depression? Progress toward a general conceptual framework

Inactivation of the Cerebral NFκB Pathway Inhibits Interleukin-1β-Induced Sickness Behavior and c-Fos Expression in Various Brain Nuclei

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