Tumor necrosis factor-α, interleukin-1β and nitric oxide induce calcium transients in distinct populations of cells cultured from the rat area postrema

Wuchert, Florian; Ott, Daniela; Rafalzik, Sandra; Roth, Joachim; Gerstberger, R.

doi:10.1016/j.jneuroim.2008.10.010

Cited by 32 publications

(19 citation statements)

References 59 publications

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“…The antibody recognizes a glycosylated protein of 90–110 kD; the level of CD68 expression in a cell is correlated with phagocytic activity. The antibody has been used specifically to immunostain microglia in rat or mouse brain sections and in primary glial cultures (Bauer et al, 1994, Hughes et al, 2002, Wuchert et al, 2009). …”

Section: Methodsmentioning

confidence: 99%

Effects of acoustic trauma on the auditory system of the rat: The role of microglia

Baizer

Wong

Manohar³

et al. 2015

Neuroscience

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Exposure to loud, prolonged sounds (acoustic trauma, AT) leads to the death of both inner and outer hair cells (IHCs and OHCs), death of neurons of the spiral ganglion and degeneration of the auditory nerve. The auditory nerve (8cn) projects to the three subdivisions of the cochlear nuclei (CN), the dorsal cochlear nucleus (DC) and the anterior (VCA) and posterior (VCP) subdivisions of the ventral cochlear nucleus. There is both anatomical and physiological evidence for plastic reorganization in the denervated CN after AT. Anatomical findings show axonal sprouting and synaptogenesis; physiologically there is an increase in spontaneous activity suggesting reorganization of circuitry. The mechanisms underlying this plasticity are not understood. Recent data suggest that activated microglia may have a role in facilitating plastic reorganization in addition to removing trauma-induced debris. In order to investigate the roles of activated microglia in the CN subsequent to acoustic trauma we exposed animals to bilateral noise sufficient to cause massive hair cell death. We studied four groups of animals at different survival times: 30 days, 60 days, 6 months and 9 months. We used silver staining to examine the time course and pattern of auditory nerve degeneration, and immunohistochemistry to label activated microglia in the denervated CN. We found both degenerating auditory nerve fibers and activated microglia in the CN at 30 and 60 days and 6 months after AT. There was close geographic overlap between the degenerating fibers and activated microglia, consistent with a scavenger role for activated microglia. At the longest survival time, there were still silver-stained fibers but very little staining of activated microglia in overlapping regions. There were, however, activated microglia in the surrounding brainstem and cerebellar white matter.

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Section: Methodsmentioning

confidence: 99%

Effects of acoustic trauma on the auditory system of the rat: The role of microglia

Baizer

Wong

Manohar³

et al. 2015

Neuroscience

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“…Circumventricular organs also play a role in CNS responses to inflammation by allowing either LPS or cytokines to interact directly with neurons and glia. For example, the area postrema contains cells that are activated by LPS, TNFα, and IL-1β (Wuchert et al, 2008; Wuchert et al, 2009). Since the capacity for LPS penetration across the BBB is low (Banks and Robinson, 2010), recent research has highlighted multiple alternative transmission mechanisms.…”

Section: Models Of Inflammationmentioning

confidence: 99%

The impact of inflammation on respiratory plasticity

Hocker

Stokes

Powell

et al. 2017

Experimental Neurology

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Breathing is a vital homeostatic behavior and must be precisely regulated throughout life. Clinical conditions commonly associated with inflammation, undermine respiratory function may involve plasticity in respiratory control circuits to compensate and maintain adequate ventilation. Alternatively, other clinical conditions may evoke maladaptive plasticity. Yet, we have only recently begun to understand the effects of inflammation on respiratory plasticity. Here we review some of common models used to investigate the effects of inflammation and discuss the impact of inflammation on nociception, chemosensory plasticity, medullary respiratory centers, motor plasticity in motor neurons and respiratory frequency, and adaptation to high altitude. We provide new data suggesting glial cells contribute to CNS inflammatory gene expression after 24 hours of sustained hypoxia and inflammation induced by 8 hours of intermittent hypoxia inhibits long-term facilitation of respiratory frequency. We also discuss how inflammation can have opposite effects on the capacity for plasticity, whereby it is necessary for increases in the hypoxic ventilatory response with sustained hypoxia but inhibits phrenic long term facilitation after intermittent hypoxia. This review highlights gaps in our knowledge about the effects of inflammation on respiratory control (development, age, and sex differences). In summary, data to date suggest plasticity can be either adaptive or maladaptive and understanding how inflammation alters the respiratory system is crucial for development of better therapeutic interventions to promote breathing and for utilization of plasticity as a clinical treatment.

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“…As such, activated microglial cells show de novo synthesis of the respective antigen (Bauer et al, 1994;Damoiseaux et al, 1994). The antibody recognizes a single-chain glycoprotein of 110 kDa (manufacturer's data sheet) and has been used specifically to stain microglia in rat or mouse brain sections as well as primary glial cultures (Bauer et al, 1994;Hughes et al, 2002;Wuchert et al, 2009). Moreover, the anti-CD68 antibody (synonym: ED1) recognizes perivascular cells other than activated microglia (Graeber et al, 1989; see also CD163/ ED2).…”

Section: Cluster Of Differentiation 68 (Cd68/ed1)mentioning

confidence: 99%

Spatiotemporal nuclear factor interleukin‐6 expression in the rat brain during lipopolysaccharide‐induced fever is linked to sustained hypothalamic inflammatory target gene induction

Damm

Luheshi

Gerstberger

et al. 2010

J of Comparative Neurology

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Rats injected with lipopolysaccharide (LPS) show brain-controlled sickness symptoms, including fever. In these animals, early genomic activation of brain cells was previously monitored by immunohistochemical detection of transcription factors such as nuclear factor (NF)-κB or signal transducer and activator of transcription (STAT)3 and was linked to the initiation or maintenance of the febrile response. To investigate whether NF-IL6 might be another important transcription factor implicated in this kind of immune-to-brain signaling, rats were injected with LPS (100 μg/kg, intraperitoneally) or phosphate-buffered saline, and brains were analyzed by immunohistochemistry, real-time PCR, or Western blot 4, 6, 8, and 10 hours later. Moderate to strong LPS-induced nuclear NF-IL6 immunoreactivity (IR) occurred in a time-dependent manner within circumventricular organs, namely, the vascular organ of the lamina terminalis, the subfornical organ, the area postrema, and the median eminence, brain structures with a leaky blood-brain barrier. Furthermore, nuclear NF-IL6-IR was observed in the pituitary gland, the choroid plexus, and the meninges as well as blood vessels throughout the entire brain. Endothelial, microglial, and ependymal cells, astrocytes, perivascular macrophages, and neurons exhibited LPS-induced nuclear NF-IL6-IR; mRNA levels of NF-IL6, responsive inflammatory genes, and NF-IL6 protein levels were significantly elevated. As opposed to observations on STAT3 or NFκB, the percentage of NF-IL6-reactive cells increased in parallel to late phases of the febrile response. In conclusion, these results suggest a potential role for NF-IL6 in the maintenance or possibly the termination of LPS-induced fever. Moreover, we propose NF-IL6 to be a delayed brain cell activation marker.

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Tumor necrosis factor-α, interleukin-1β and nitric oxide induce calcium transients in distinct populations of cells cultured from the rat area postrema

Cited by 32 publications

References 59 publications

Effects of acoustic trauma on the auditory system of the rat: The role of microglia

Effects of acoustic trauma on the auditory system of the rat: The role of microglia

The impact of inflammation on respiratory plasticity

Spatiotemporal nuclear factor interleukin‐6 expression in the rat brain during lipopolysaccharide‐induced fever is linked to sustained hypothalamic inflammatory target gene induction

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