Astrocyte-to-microglia communication via Sema4B-Plexin-B2 modulates injury-induced reactivity of microglia.

After central nervous system injury, a rapid cellular and molecular response is induced. This response can be both beneficial and detrimental to neuronal survival in the first few days and increases the risk for neurodegeneration if persistent. Semaphorin4B (Sema4B), a transmembrane protein primarily expressed by cortical astrocytes, has been shown to play a role in neuronal cell death following injury.

An affinity for brainstem microglia in pediatric high-grade gliomas of brainstem origin.

Background: High-grade gliomas (HGG) in children have a devastating prognosis and occur in a remarkable spatiotemporal pattern. Diffuse midline gliomas (DMG), including diffuse intrinsic pontine gliomas (DIPG), typically occur in mid-childhood, while cortical HGGs are more frequent in older children and adults. The mechanisms behind this pattern are not clear.

Human iPSC-derived astrocytes from ALS patients with mutated C9ORF72 show increased oxidative stress and neurotoxicity.

Background: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects motor neurons (MNs). It was shown that human astrocytes with mutations in genes associated with ALS, like C9orf72 (C9) or SOD1, reduce survival of MNs. Astrocyte toxicity may be related to their dysfunction or the release of neurotoxic factors.

Nitric oxide as a messenger between neurons and satellite glial cells in dorsal root ganglia.

Abnormal neuronal activity in sensory ganglia contributes to chronic pain. There is evidence that signals can spread between cells in these ganglia, which may contribute to this activity. Satellite glial cells (SGCs) in sensory ganglia undergo activation following peripheral injury and participate in cellular communication via gap junctions and chemical signaling.

Vasoactivity of the rat endovascular trophoblast.

Introduction: Rat endovascular trophoblasts (EVasT) express smooth muscle (SM) proteins and contract ex vivo upon exposure to endothelin-1 (ET1) via receptors A and B (ETA, ETB). Presently, we investigated the EVasT response to NOS inhibition (N-Nitro-l-arginine methyl ester hydrochloride, l-NAME), and potentiation by NO donor [S-Nitroso-N-Acetyl-D,l-Penicillamine (SNAP)] following KCl precontraction. M&M: Luminal surface area (LSA) of remodeled spiral artery rings (SAR) devoid of SM was measured ex vivo upon exposure to l-NAME alone; l-NAME and ET1 representing the combined contractile effect of both ET1 receptors; l-NAME with ET1 and ETA antagonist, representing the isolated contractile effect via ETB.

Systemic inflammation activates satellite glial cells in the mouse nodose ganglion and alters their functions.

Satellite glial cell (SGCs) in trigeminal and dorsal root ganglia are altered structurally and functionally under pathological conditions associated with chronic pain. These changes include reactive gliosis, augmented coupling by gap junctions, and increased responses to ATP via purinergic P2 receptors. Similar information for nodose ganglia (NG), which receive sensory inputs from internal organs via the vagus nerves, is missing.

Phenotypic changes in satellite glial cells in cultured trigeminal ganglia.

Satellite glial cells (SGCs) are specialized cells that form a tight sheath around neurons in sensory ganglia. In recent years, there is increasing interest in SGCs and they have been studied in both intact ganglia and in tissue culture. Here we studied phenotypic changes in SGCs in cultured trigeminal ganglia from adult mice, containing both neurons and SGCs, using phase optics, immunohistochemistry and time-lapse photography.

Peripheral inflammation augments gap junction-mediated coupling among satellite glial cells in mouse sympathetic ganglia.

Intercellular coupling by gap junctions is one of the main features of glial cells, but very little is known about this aspect of satellite glial cells (SGCs) in sympathetic ganglia. We used the dye coupling method to address this question in both a prevertebral ganglion (superior mesenteric) and a paravertebral ganglion (superior cervical) of mice. We found that in control ganglia, the incidence of dye coupling among SGCs that form the envelope around a given neuron was 10-20%, and coupling between SGCs around different envelopes was rare (1.

Gap junctions in dorsal root ganglia: possible contribution to visceral pain.

Peripheral injuries can lead to sensitization of neurons in dorsal root ganglia (DRGs), which can contribute to chronic pain. The neurons are sensitized by a combination of physiological and biochemical changes, whose full details are still obscure. Another cellular element in DRGs are satellite glial cells (SGCs), which surround the neurons, but little is known about their role in nociception.