Glial Cells in Neurotoxicity Development

Abstract

Neuroglial cells of the central nervous system include the astrocytes, oligodendrocytes, and microglia. Their counterparts in the peripheral nervous system are the Schwann cells. The term neuroglia comes from an erroneous concept originally coined by Virchow (1850), in which he envisioned the neurons to be embedded in a layer of connective tissue. The term, or its shortened form--glia, has persisted as the preferred generic term for these cells. A reciprocal relationship exists between neurons and glia, and this association is vital for mutual differentiation, development, and functioning of these cell types. Therefore, perturbations in glial cell function, as well as glial metabolism of chemicals to active intermediates, can lead to neuronal dysfunction. The purpose of this review is to explore neuroglial sites of neurotoxicant actions, discuss potential mechanisms of glial-induced or glial-mediated central nervous system and peripheral nervous system damage, and review the role of glial cells in neurotoxicity development.

Can Children with Autism Recover? If So, How?

“…By contributing to excitotoxicity and suboptimal cellular energetics they could exacerbate the neurochemistry underlying the stress response and contribute to excessive arousal, as well as to a more general phenomenon of cortical noise with decreased signal-to-noise ratio that could contribute to abnormal thresholding and diminished specificity in response to sensory stimulation The astroglial activation component of immune activation may well lead to the hypoperfusion often seen in children with ASD (e.g. Degirmenci et al 2008), since activated astroglia are enlarged and can reduce brain capillary lumen by as much as 50%, reducing oxygen support of brain tissue, increasing the difficulty of eliminating waste products to the blood system, and hence and impairing the cellular activities associated with neural activity and synchronization (Aschner et al 1999). Over time, this could result in various areas of the brain developing in poor relation to one another, with each area of the brain perhaps developing hypersensitivities or special properties, but making it difficult for multiple neural systems to work in concert (see Muller 2007 for a review on lack of synchronicity in autism).…”

Secondary Lymphoid Tissue Chemokine (CCL21) Activates CXCR3 to Trigger a Cl− Current and Chemotaxis in Murine Microglia

“…Microglial activation is thus a general response to pathological processes in the CNS in which the ramified microglia transform into an ameboid macrophage like phenotype (3,4). Because microglia are the first cells in the CNS to respond to neuronal damage, a neuron-microglia communication system has been proposed (4,5). One candidate for such a signaling molecule is an ␣ chemokine ligand (CCL21) 3 ; damaged neurons in vitro and in vivo rapidly induce CCL21 expression (6).…”

Sodium para-aminosalicylate protected cultured basal ganglia astrocytes from manganese-induced DNA damages and alteration of amino acid neurotransmitter levels

“…High levels of Mn exposure can trigger a series of intracellular events which may lead to injury in different cells (Aschner et al, 1999;Chen et al, 2002;Wang et al, 2014), however the mechanism of Mn-induced astrocytes injury is unclear. Herein, we used primary cultures of rat basal ganglia astrocytes in order to examine the molecular action involved in Mn-induced Fig.…”