Colocalization of receptors for vasoactive peptides on astrocytes of cultured rat spinal cord and brain stem: electrophysiological effects of atrial and brain natriuretic peptide, neuropeptide Y and bradykinin

Hösli, L.; Hösli, Elisabeth; Kaeser, H E; Lefkovits, Michael

doi:10.1016/0304-3940(92)90817-q

Cited by 32 publications

(9 citation statements)

References 15 publications

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“…Y receptors in cells of the astrocytic lineage in vitro have been widely demonstrated in vitro (Hosli et al, 1992;Abounader et al, 1999;St-Pierre et al, 2000). By contrast, there is a single report of Y receptors in glial cells in situ (Pickel et al, 1998).…”

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confidence: 88%

“…It has been shown that NPY can depolarize astrocytic membrane potentials (Hosli et al, 1992) and depolarization seems to play an important role in promoting astrocyte proliferation (MacFarlane and Sontheimer, 2000). Normal Mü ller cells highly express inwardly rectifying K ϩ (KIR) channels and also various depolarization-activated K ϩ channels (Bringmann et al, 1999).…”

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confidence: 99%

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Y1 receptor of neuropeptide Y as a glial marker in proliferative vitreoretinopathy and diseased human retina

Soler

Gallo

Dodds

et al. 2002

Glia

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The Y1 receptor of neuropeptide Y (NPY) has been demonstrated in glial cells of astrocytic lineage in vitro. We have studied the immunohistochemical expression of Y1 receptors in the glia of the diseased human retina, in tissue samples obtained after surgery for proliferative vitreoretinopathy. In this condition, glia and other cell types migrate and form epi- or subretinal membranes. Both diseased retinas (n = 8) and PVR membranes (n = 43) contained numerous Y1-immunoreactive cells. In the diseased retina, the Y1 antiserum labeled cells with the morphological radial pattern characteristic of Müller cells, whereas in the membranes, label appeared in a large population of elongate cells, measuring up to 250 microm. In both retina and membranes, double labeling demonstrated that the vast majority of Y1-immunoreactive cells were also labeled by a glial fibrillary acidic protein (GFAP) antibody, indicating their glial origin. Retinal regions devoid of GFAP immunoreactivity also lacked the Y1 label. None of these markers was detected in Müller cells of normal retina. Y1 immunoreactivity did not co-localize with smooth muscle actin immunoreactivity, a marker of myofibroblasts. Expression of Y1 receptors would characterize reactive and proliferating glial cells of the diseased retina and could perhaps be involved in the proliferation of injured glial cells causing regrowth of PVR membranes and the consequent secondary retinal detachments.

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confidence: 88%

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confidence: 99%

Y1 receptor of neuropeptide Y as a glial marker in proliferative vitreoretinopathy and diseased human retina

Soler

Gallo

Dodds

et al. 2002

Glia

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“…Bradykinin induced microglial migration by stimulating B 1 receptors In the brain, BK receptors are expressed in all major cell types, neurons (Delmas et al, 2002), astrocytes, oligodendrocytes (Ritchie et al, 1987;Gimpl et al, 1992;Hosli et al, 1992;Lin and Chuang, 1992;Stephens et al, 1993), and microglial cells (Noda et al, 2003). Two subtypes of BK receptors have been distinguished, termed B 1 and B 2 receptors.…”

Section: Discussionmentioning

confidence: 99%

Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

et al. 2007

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Bradykinin (BK) is produced and acts at the site of injury and inflammation. In the CNS, migration of microglia toward the lesion site plays an important role pathologically. In the present study, we investigated the effect of BK on microglial migration. Increased motility of cultured microglia was mimicked by B 1 receptor agonists and markedly inhibited by a B 1 antagonist , but not by a B 2 receptor antagonist. BK induced chemotaxis in microglia isolated from wild-type and B 2 -knock-out mice but not from B 1 -knock-out mice. BK-induced motility was not blocked by pertussis toxin but was blocked by chelating intracellular Ca 2ϩ or by low extracellular Ca 2ϩ , implying that Ca 2ϩ influx is prerequisite. Blocking the reverse mode of Na ϩ /Ca 2ϩ exchanger (NCX) completely inhibited BK-induced migration. The involvement of NCX was further confirmed by using NCX ϩ/Ϫ mice; B 1 -agonist-induced motility and chemotaxis was decreased compared with that in NCX ϩ/ϩ mice. Activation of NCX seemed to be dependent on protein kinase C and phosphoinositide 3-kinase, and resultant activation of intermediate-conductance (IK-type) Ca 2ϩ -dependent K ϩ currents (I K(Ca) ) was activated. Despite these effects, BK did not activate microglia, as judged from OX6 staining. Using in vivo lesion models and pharmacological injection to the brain, it was shown that microglial accumulation around the lesion was also dependent on B 1 receptors and I K(Ca) . These observations support the view that BK functions as a chemoattractant by using the distinct signal pathways in the brain and, thus, attracts microglia to the lesion site in vivo.

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“…Both BK receptors belong to the family of seven transmembrane receptors and are coupled to G-proteins (G q/11 and G i/o ). BK receptors are not only present on neurons (Delmas et al 2002), but also on all types of glial cells, astrocytes, and oligodendrocytes (Gimpl et al 1992;Hosli et al 1992;Lin and Chuang 1992;Stephens et al 1993a,b) and, as recently demonstrated, also on microglial cells (Noda et al 2003(Noda et al , 2004. In astrocytes, BK stimulates the release of arachidonic acid (Burch and Kniss 1988;Kaeser et al 1988) and induces the calcium-dependent release of glutamate and IL-6 expression (Parpura et al 1994;Schwaninger et al 1999).…”

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confidence: 93%

“…2002), but also on all types of glial cells, astrocytes, and oligodendrocytes (Gimpl et al. 1992; Hosli et al. 1992; Lin and Chuang 1992; Stephens et al.…”

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confidence: 99%

Neuroprotective role of bradykinin because of the attenuation of pro‐inflammatory cytokine release from activated microglia

Нода

Kariura

Pannasch

et al. 2006

Journal of Neurochemistry

121

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Bradykinin (BK) has been reported to be a mediator of brain damage in acute insults. Receptors for BK have been identified on microglia, the pathologic sensors of the brain. Here, we report that BK attenuated lipopolysaccharide (LPS)-induced release of tumor necrosis factor-alpha (TNF-a) and interleukin-1b from microglial cells, thus acting as an anti-inflammatory mediator in the brain. This effect was mimicked by raising intracellular cAMP or stimulating the prostanoid receptors EP2 and EP4, while it was abolished by a cAMP antagonist, a prostanoid receptor antagonist, or by an inhibitor of the inducible cyclooxygenase (cyclooxygenase-2). BK also enhanced formation of prostaglandin E 2 and expression of microsomal prostaglandin E synthase. Expression of BK receptors and EP2/EP4 receptors were also enhanced. Using physiological techniques, we identified functional BK receptors not only in culture, but also in microglia from acute brain slices. BK reduced LPS-induced neuronal death in neuron-microglia cocultures. This was probably mediated via microglia as it did not affect TNF-a-induced neuronal death in pure neuronal cultures. Our data imply that BK has anti-inflammatory and neuroprotective effects in the central nervous system by modulating microglial function.

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Colocalization of receptors for vasoactive peptides on astrocytes of cultured rat spinal cord and brain stem: electrophysiological effects of atrial and brain natriuretic peptide, neuropeptide Y and bradykinin

Cited by 32 publications

References 15 publications

Y1 receptor of neuropeptide Y as a glial marker in proliferative vitreoretinopathy and diseased human retina

Y1 receptor of neuropeptide Y as a glial marker in proliferative vitreoretinopathy and diseased human retina

Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

Neuroprotective role of bradykinin because of the attenuation of pro‐inflammatory cytokine release from activated microglia

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Colocalization of receptors for vasoactive peptides on astrocytes of cultured rat spinal cord and brain stem: electrophysiological effects of atrial and brain natriuretic peptide, neuropeptide Y and bradykinin

Cited by 32 publications

References 15 publications

Y1 receptor of neuropeptide Y as a glial marker in proliferative vitreoretinopathy and diseased human retina

Y1 receptor of neuropeptide Y as a glial marker in proliferative vitreoretinopathy and diseased human retina

Bradykinin-Induced Microglial Migration Mediated by B1-Bradykinin Receptors Depends on Ca2+Influx via Reverse-Mode Activity of the Na+/Ca2+Exchanger

Neuroprotective role of bradykinin because of the attenuation of pro‐inflammatory cytokine release from activated microglia

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Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger