RETRACTED: Evidence for involvement of the neural pathway containing the peripheral vagus nerve, medullary visceral zone and central amygdaloid nucleus in neuroimmunomodulation

Ge, Xu; Yang, Zhijun; Duan, Lingxun; Rao, Zhi-Ren

doi:10.1016/s0006-8993(01)02789-5

Cited by 22 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, direct and indirect pathways that originate in the caudal brainstem and propagate immune-related information from the periphery have been shown to play important role in the integration of brain responses to infection and injury (Gaykema et al, 2007). Additionally, it has been suggested that part of the peripheral immune information can be conveyed via vagal pathway to the catecholaminergic neurons in the medullary visceral zone from where it is transferred to the central amygdaloid nucleus (Ge et al, 2001). Such an approach suggests a complex interaction of the autonomous nervous system components with immune system elements in the response to injury-induced inflammation.…”

Section: Importance Of the Indirect Blast–brain Interacting Pathway Imentioning

confidence: 99%

The importance of systemic response in the pathobiology of blast-induced neurotrauma

Černak¹

2010

Front. Neur.

142

146

View full text Add to dashboard Cite

Due to complex injurious environment where multiple blast effects interact with the body parallel, blast-induced neurotrauma is a unique clinical entity induced by systemic, local, and cerebral responses. Activation of autonomous nervous system; sudden pressure increase in vital organs such as lungs and liver; and activation of neuroendocrine–immune system are among the most important mechanisms that contribute significantly to molecular changes and cascading injury mechanisms in the brain. It has been hypothesized that vagally mediated cerebral effects play a vital role in the early response to blast: this assumption has been supported by experiments where bilateral vagotomy mitigated bradycardia, hypotension, and apnea, and also prevented excessive metabolic alterations in the brain of animals exposed to blast. Clinical experience suggests specific blast–body–nervous system interactions such as (1) direct interaction with the head either through direct passage of the blast wave through the skull or by causing acceleration and/or rotation of the head; and (2) via hydraulic interaction, when the blast overpressure compresses the abdomen and chest, and transfers its kinetic energy to the body's fluid phase, initiating oscillating waves that traverse the body and reach the brain. Accumulating evidence suggests that inflammation plays important role in the pathogenesis of long-term neurological deficits due to blast. These include memory decline, motor function and balance impairments, and behavioral alterations, among others. Experiments using rigid body- or head protection in animals subjected to blast showed that head protection failed to prevent inflammation in the brain or reduce neurological deficits, whereas body protection was successful in alleviating the blast-induced functional and morphological impairments in the brain.

show abstract

Section: Importance Of the Indirect Blast–brain Interacting Pathway Imentioning

confidence: 99%

The importance of systemic response in the pathobiology of blast-induced neurotrauma

Černak¹

2010

Front. Neur.

142

146

View full text Add to dashboard Cite

show abstract

“…Candidate molecules triggering CNS inflammatory activities following systemic LPS include interleukins (IL-1β), tumor necrosis factor alpha (TNFα) and prostaglandins produced by perivascular macrophages and/or endothelial cells that line the blood-brain barrier (Maier et al, 1998, Goehler et al, 1999, Laflamme et al, 1999, Blatteis and Li, 2000, Schnydrig et al, 2007, Rivest, 2009). Another means of transmission is via peripheral nerves (including the vagus nerves), which transmit inflammation into the CNS via unknown mechanisms (Ge et al, 2001, Roth and De Souza, 2001, Wieczorek et al, 2005, Blatteis, 2007). …”

Section: Systemic and Cns Inflammationmentioning

confidence: 99%

Systemic inflammation impairs respiratory chemoreflexes and plasticity

Huxtable¹,

Vinit²,

Windelborn³

et al. 2011

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

Many lung and central nervous system disorders require robust and appropriate physiological responses to assure adequate breathing. Factors undermining the efficacy of ventilatory control will diminish the ability to compensate for pathology, threatening life itself. Although most of these same disorders are associated with systemic and/or neuroinflammation, and inflammation affects neural function, we are only beginning to understand interactions between inflammation and any aspect of ventilatory control (e.g. sensory receptors, rhythm generation, chemoreflexes, plasticity). Here we review available evidence, and present limited new data suggesting that systemic (or neural) inflammation impairs two key elements of ventilatory control: chemoreflexes and respiratory motor (vs. sensory) plasticity. Achieving an understanding of mechanisms whereby inflammation undermines ventilatory control is fundamental since inflammation may diminish the capacity for natural, compensatory responses during pathological states, and the ability to harness respiratory plasticity as a therapeutic strategy in the treatment of devastating breathing disorders, such as during cervical spinal injury or motor neuron disease.

show abstract

“…The implication of the NTS in immune sensing is also demonstrated by neuroanatomical studies using the expression of c-fos as a marker of neuronal activation. Multiple investigators have reported robust c-fos expression in the NTS subsequently to an intraperitoneal inflammation (Wan et al, 1993; Rivest and Laflamme, 1995; Sagar et al, 1995; Konsman et al, 2000; Ge et al, 2001). Similarly, tumor-bearing rats show c-fos expression in the NTS (Konsman and Blomqvist, 2005; Ruud and Blomqvist, 2007).…”

Section: How Do Pro-inflammatory Cytokines Alter Neural Activity?mentioning

confidence: 99%

Neurobiology of inflammation-associated anorexia

Gautron

Layé

2009

Front. Neurosci.

View full text Add to dashboard Cite

Compelling data demonstrate that inflammation-associated anorexia directly results from the action of pro-inflammatory factors, primarily cytokines and prostaglandins E2, on the nervous system. For instance, the aforementioned pro-inflammatory factors can stimulate the activity of peripheral sensory neurons, and induce their own de novo synthesis and release into the brain parenchyma and cerebrospinal fluid. Ultimately, it results in the mobilization of a specific neural circuit that shuts down appetite. The present article describes the different cell groups and neurotransmitters involved in inflammation-associated anorexia and examines how they interact with neural systems regulating feeding such as the melanocortin system. A better understanding of the neurobiological mechanisms underlying inflammation-associated anorexia will help to develop appetite stimulants for cancer and AIDS patients.

show abstract

RETRACTED: Evidence for involvement of the neural pathway containing the peripheral vagus nerve, medullary visceral zone and central amygdaloid nucleus in neuroimmunomodulation

Cited by 22 publications

References 0 publications

The importance of systemic response in the pathobiology of blast-induced neurotrauma

The importance of systemic response in the pathobiology of blast-induced neurotrauma

Systemic inflammation impairs respiratory chemoreflexes and plasticity

Neurobiology of inflammation-associated anorexia

Contact Info

Product

Resources

About