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A growing body of evidence suggests that glial cells are involved in practically all aspects of neural function. Glial cells regulate the homeostasis of the brain, influence the development of the nervous system, modulate synaptic activity, and carry out the immune response inside the brain. In addition, they play an important role in the restoration of the nervous system after damage, and they also participate in various neurodegenerative disorders. In a similar way, the importance of stress and glucocorticoids (GCs) on brain function is being increasingly recognized. Within the brain, stress hormones target both neurons and glial cells. Through their actions on these cells, glucocorticoids exert organizational functions on various processes of the developing brain and contribute to neuronal plasticity in the adult brain. Moreover, stress and glucocorticoids have become especially attractive in the study of a number of neurodegenerative disorders. However, studies on the mechanisms behind glucocorticoid-induced regulation of brain function have been classically focused on their effects on neurons. In this review, we start by describing the main functions of glial cells and then proceed to present data highlighting the effects of stress and GCs on brain function. We conclude the review by presenting recent evidence linking stress and glucocorticoids to glial cell function.

Astrocytes are a target for steroid hormones and for steroids produced by the nervoussystem (neurosteroids). The effect of gonadal hormones and several neurosteroids in theformation of gliotic tissue has been assessed in adult male rats after a penetrating wound of thecerebral cortex and the hippocampal formation. The hormones testosterone, 17β‐estradiol and progesterone and the neurosteroids dehydroepiandrosterone, pregnenolone andpregnenolone sulfate resulted in a significant decrease in the accumulation of astrocytes in theproximity of the wound and in a decreased bromodeoxyuridine incorporation in reactiveastrocytes. Of all steroids tested, dehydroepiandrosterone was the most potent inhibitor of gliotictissue formation. These findings suggest that neurosteroids and sex steroids may affect brainrepair by down‐regulating gliotic tissue.

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Recent evidence indicates that astroglia may be involved in the synthesis of endogenous neurosteroids. The extension of glial fibrillary acidic protein (GFAP)-immunoreactive astroglial cell processes was assessed in hippocampal slice cultures from adult gonadectomized male rats under the influence of the neurosteroids dehydroepiandrosterone, dehydroepiandrosterone sulfate, dehydroepiandrosterone estereate, pregnenolone, pregnenolone sulfate, and pregnenolone oleate. The effects of neurosteroids were compared to those induced by the gonadal steroids testosterone, 17 beta-estradiol and progesterone. Astrocytes in hippocampal slice cultures had a morphology that was indistinguishable from that observed in the hippocampus fixed in situ. Castration of adult male rats resulted in a significant decrease in the extension of GFAP-immunoreactive processes, both in tissues fixed in situ and in slice cultures. In contrast, incubation of slice cultures from gonadectomized animals with pregnenolone, pregnenolone sulfate, 17 beta-estradiol, and testosterone enhanced the extension of GFAP-immunoreactive processes. While other steroids tested did not affect this parameter, dehydroepiandrosterone and its sulfate and estereate derivatives induced the transformation of astroglial cells into hypertrophic and highly GFAP immunoreactive cells with the morphological characteristics of reactive astroglia. We conclude that neurosteroids regulate the morphology and/or GFAP distribution of astrocytes in hippocampal slice cultures from adult rats.

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Recent studies confirm that astrocytes and neurons are associated with the synaptic transmission, particularly with the regulation of glutamate (Glu) levels. Therefore, they have the capacity to modulate the Glu released from neurons into the extracellular space. It has also been demonstrated an intense astrocytic and microglia response to physical or chemical lesions of the central nervous system. However, the persistence of the response of the glial cells in adult brain had not been previously reported, after the excitotoxic damage caused by neonatal dosage of monosodium glutamate (MSG) to newborn rats. In this study, 4 mg/g body weight of MSG were administered to newborn rats at 1, 3, 5, and 7 days after birth, at the age of 60 days the astrocytes and the microglia cells were analyzed with immunohistochemical methods in the fronto-parietal cortex. Double labeling to glial fibrillary acidic protein (GFAP) and BrdU, or isolectin-B(4) and BrdU identified astrocytes or microglia cells that proliferated; immunoblotting and immunoreactivity to vimentin served for assess immaturity of astrocytic intermediate filaments. The results show that the neonatal administration of MSG-induced reactivity of astrocytes and microglia cells in the fronto-parietal cortex, which was characterized by hyperplasia; an increased number of astrocytes and microglia cells that proliferated, hypertrophy; increased complexity of the cytoplasm extension of both glial cells and expression of RNAm to vimentin, with the presence of vimentin-positive astrocytes. This glial response to neuroexcitotoxic stimulus of Glu on the immature brain, which persisted to adulthood, suggests that the neurotransmitter Glu could trigger neuro-degenerative illnesses.

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