Morphological changes in cultured astrocytes following exposure to calcium ionophores

Fawthrop, D.J.; Evans, Richard J.

doi:10.1016/0304-3940(87)90391-0

Cited by 15 publications

(9 citation statements)

References 23 publications

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“…Based on our results, this regulation by astrocytic processes involves feeding-associated functions such as blood glucose and blood pressure and perhaps appetite as well. Yet, the underlying mediators for changing astrocyte processes are still unclear, which, however, could be related to intracellular calcium since it determines cell morphology (Fawthrop and Evans, 1987; Molotkov et al, 2013; Otsu et al, 2015) and/or autophagy since it is more activated in the brain during fasting (Alirezaei et al, 2010). Despite these questions, IKKβ/NF-κB appears important, given that IKKβ/NF-κB activation or inhibition can both rapidly alter astrocytic process plasticity along with or prior to the accordant induction of physiological effects.…”

Section: Discussionmentioning

confidence: 99%

Astrocytic Process Plasticity and IKKβ/NF-κB in Central Control of Blood Glucose, Blood Pressure, and Body Weight

et al. 2017

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Summary Central regulation of metabolic physiology is mediated critically through neuronal functions; however, if astrocytes are also essential remains unclear. Here we show that the high-order processes of astrocytes in the mediobasal hypothalamus displayed shortening in fasting while elongation in fed status. Chronic overnutrition and astrocytic IKKβ/NF-κB upregulation similarly impaired astrocytic plasticity leading to sustained shortening of high-order processes. In physiology, astrocytic IKKβ/NF-κB upregulation resulted in early-onset effects including glucose intolerance and blood pressure rise and late-onset effects including body weight and fat gain. Appropriate inhibition in astrocytic IKKβ/NF-κB protected against chronic overnutrition from impairing astrocytic plasticity and these physiological functions. Mechanistically, astrocytic regulation of hypothalamic extracellular GABA level and therefore BDNF expression were found partly accountable. Hence, astrocytic process plasticity and IKKβ/NF-κB play significant roles in central control of blood glucose, blood pressure and body weight as well as the central induction of these physiological disorders leading to disease.

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Section: Discussionmentioning

confidence: 99%

Astrocytic Process Plasticity and IKKβ/NF-κB in Central Control of Blood Glucose, Blood Pressure, and Body Weight

et al. 2017

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“…Ca"-free saline blocked the effect; however, ionomycin did not reproduce it. A23187 or ionomycin caused rat cortical astrocytes to reversibly change from flat, protoplasmic, epithelioid cells t o spinous, process-bearing cells (Fawthrop and Evans, 1987). However, Ca2+-free saline alone or Ca2+ ionophores in Ca2+-free saline induced similar morphological changes.…”

Section: Cytoskeletal Plasticity and Glial Calciummentioning

confidence: 93%

Glial calcium

Finkbeiner

1993

Glia

194

140

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This review summarizes current knowledge relating intracellular calcium and glial function. During steady state, glia maintain a low cytosolic calcium level by pumping calcium into intracellular stores and by extruding calcium across the plasma membrane. Glial Ca2+ increases in response to a variety of physiological stimuli. Some stimuli open membrane calcium channels, others release calcium from intracellular stores, and some do both. The temporal and spatial complexity of glial cytosolic calcium changes suggest that these responses may form the basis of an intracellular or intercellular signaling system. Cytosolic calcium rises effect changes in glial structure and function through protein kinases, phospholipases, and direct interaction with lipid and protein constituents. Ultimately, calcium signaling influence glial gene expression, development, metabolism, and regulation of the extracellular milieu. Disturbances in glial calcium homeostasis may have a role in certain pathological conditions. The discovery of complex calcium-based glial signaling systems, capable of sensing and influencing neural activity, suggest a more integrated neuro-glial model of information processing in the central nervous system.

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“…The present study therefore confirms and extends our previous observations on the independence of β‐adrenoreceptor mediated stellation of cultured pituicytes ( 7) and supports and extends the results and the conclusions of the studies on glioma‐derived cells ( 10–12). The observations on Ca 2+ ‐dependence of the morphological changes exhibited by other types of astrocyte in primary culture ( 13, 14) may reflect slight differences of the culture environment or experimental protocols used in these two studies and our own. Alternatively, the different Ca 2+ ‐sensitivities of the processes of stellation and destellation found in different studies using primary cultured astrocytes may reflect a real difference between astrocytes derived from different sources (i.e.…”

Section: Discussionmentioning

confidence: 81%

“…There are two explanations for the apparently conflicting evidence concerning the role of Ca 2+ in controlling astrocyte morphology. First, the studies were performed using different types of astrocytes: glioma‐derived cells ( 10–12) and primary cultured cells ( 7, 13, 14). Second, in previous studies, either stellation ( 7, 12–14) or destellation ( 10, 11), but not both processes, was examined in any single study.…”

Section: Discussionmentioning

confidence: 99%

“…Further evidence against a role for Ca 2+ in mediating changes of astrocyte morphology was obtained by Shain and colleagues ( 12) who demonstrated that stellation of LMR55 astroglial cells is independent of [Ca] i . In contrast, studies on cultured astrocytes derived from embryonic brain have shown that extracellular Cd 2+ and Co 2+ can block stellation ( 13) and that elevation of [Ca] i alone is sufficient to induce stellation ( 14).…”

mentioning

confidence: 96%

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Calcium‐Independent, Tyrosine Phosphorylation‐Dependent Effects of Serum on the Morphology of Cultured Neurohypophysial Astrocytes

Ramsell

Cobbett

2000

J Neuroendocrinology

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Activation of adenylate cyclase induces cultured neurohypophysial astrocytes (pituicytes) to change from a protoplasmic, nonstellate form to a stellate form. Stellation is inhibited and reversed (destellation) by serum. The objective of the present studies was to examine the roles of Ca2+ and tyrosine phosphorylation in mediating these morphological changes. The effects of forskolin (to induce stellation) and serum (to inhibit and reverse stellation) were not affected by replacement of Ca2+ with Co2+ in the medium or by treatment of cultures with thapsigargin. However, genistein, a specific inhibitor of tyrosine kinase(s), significantly reduced the effect of serum on forskolin-induced stellation. Also, dephostatin, a specific inhibitor of tyrosine phosphatase, inhibited forskolin-induced stellation. In contrast, genistein did not have a dramatic effect on serum-induced destellation. The data demonstrate that morphological changes exhibited by cultured pituicytes are independent of Ca2+ but may be modulated by the activity of tyrosine kinase(s) and phosphatase(s).

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Morphological changes in cultured astrocytes following exposure to calcium ionophores

Cited by 15 publications

References 23 publications

Astrocytic Process Plasticity and IKKβ/NF-κB in Central Control of Blood Glucose, Blood Pressure, and Body Weight

Astrocytic Process Plasticity and IKKβ/NF-κB in Central Control of Blood Glucose, Blood Pressure, and Body Weight

Glial calcium

Calcium‐Independent, Tyrosine Phosphorylation‐Dependent Effects of Serum on the Morphology of Cultured Neurohypophysial Astrocytes

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