Astroglia from defined brain regions as studied with primary cultures

Hanssoń, Elisabeth

doi:10.1016/0301-0082(88)90008-1

Cited by 141 publications

(66 citation statements)

References 193 publications

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“…However, even though there was a signif icant reactivation of soman-inhibited acetylcholinesterase following (21,35,50,77). Dendritic swelling is suspected to represent an excitotoxic lesion similar to that previously documented for domoic acid (53,(71)(72)(73) (25,68). In addition, the findings that cardiomyopathy is a concomitant lesion, that soman induces vasoconstriction of cerebral vessels (61), and that during soman intoxication there is a lower proportion of increase of cerebral blood flow over glucose use in affected CNS regions imply the existence of a relative ischemia in these brain regions (65).…”

Section: Acetylcholinesterase Activitysupporting

confidence: 57%

Histomorphogenesis of Soman-Induced Encephalocardiomyopathy in Sprague-Dawley Rats

Tryphonas

Clement²

1995

Toxicol Pathol

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Section: Acetylcholinesterase Activitysupporting

confidence: 57%

Histomorphogenesis of Soman-Induced Encephalocardiomyopathy in Sprague-Dawley Rats

Tryphonas

Clement²

1995

Toxicol Pathol

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“…There is increasing evidence that astrocytes are not a homogeneous population (for review, see Hansson, 1988;Barres, 199 1). Several lines of evidence suggest that glia from different regions of the CNS differ in their ability to promote neurite outgrowth (Denis-Donini et al, 1984;Chamak et al, 1987;Autillo-Touati et al, 1988;Denis-Donini and Estenoz, 1988;Prochiantz et al, 1990;Qian et al, 1992).…”

Section: Glial Characterizationmentioning

confidence: 99%

“…Astrocytes from different anatomic regions have been found to express characteristic ion channel phenotypes, adhesive properties, and neurotransmitter receptors (for review, see Hansson, 1988;Barres, 199 1). Mesencephalic or striatal astrocytes in vitro synthesize and express distinct glycoproteins on their surface (Barbin et al, 1988).…”

Section: Androglia Influence the Number Of Primary Dendritesmentioning

confidence: 99%

Regional differences in glial-derived factors that promote dendritic outgrowth from mouse cortical neurons in vitro

Roux

Reh

1994

J. Neurosci.

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To determine whether glia from different CNS regions differ in their ability to support axons or dendrites, embryonic (E18) mouse cortical neurons were cocultured with early postnatal (P4) rat astroglial derived from cortex, retina, olfactory bulb, mesencephalon, striatum, and spinal cord. After 5 d in vitro, axon and dendrite outgrowth from isolated neurons was quantified with double-labeling immunohistochemical techniques. Whereas axonal growth was similar on the various monolayers, total primary dendritic outgrowth was nearly threefold greater on glia derived from the cortex, retina, and olfactory bulb than on glia derived from mesencephalon, striatum, or spinal cord. This effect was principally on the number of primary dendrites rather than the elongation of individual dendrites. Similar morphological differences were observed when cortical neurons were grown on polylysine in a noncontact coculture system with glia continuously conditioning the media. This selective promotion of dendrite growth was independent of neuron survival. These results indicate that there are regional differences in the ability of CNS glia to support dendritic growth and that this effect is due, in part, to release of a diffusable factor.

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“…Astroglial Cell Cultures-Primary astroglial cell cultures were prepared from P1 or P2 Sprague-Dawley rat pups (Charles River, Uppsala, Sweden) as previously described (4,36). In brief, the brains were removed and cerebral cortices were dissected and cleaned from meninges.…”

Section: Model Systemsmentioning

confidence: 99%

α1-Adrenergic Modulation of Metabotropic Glutamate Receptor-induced Calcium Oscillations and Glutamate Release in Astrocytes

Muyderman¹,

Ängehagen²,

Sandberg³

et al. 2001

Journal of Biological Chemistry

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Astrocytic responses to activation of metabotropic glutamate receptors group I (mGluRs I) and ␣ 1 -adrenoreceptors in cultured cells have been assessed using spectral analyzes and calcium imaging. Concentrationdependent changes were observed after stimulation with the mGluR I agonist (S)-3,5-dihydroxyphenylglycine (DHPG). These responses changed from a regular low frequency signal with sharp peaks at 1 M to a pronounced stage of irregularity at 10 M. After stimulation with 100 M the signal was again homogenous in shape and regularity but occurred at a higher frequency. In contrast, the spectral properties after stimulation with the ␣ 1 -adrenoreceptor agonist phenylephrine, exhibited considerable variation for all investigated concentrations. DHPG-induced increases in [Ca 2؉ ] i were also associated with astroglial glutamate release, whereas no release was observed after noradrenergic stimulation. Both DHPG-mediated calcium signaling and glutamate release were inhibited by preincubation with 10 or 100 M phenylephrine. Collectively, the present investigation provides new information about the spatialtemporal characteristics of astroglial intracellular calcium responses and demonstrates distinct differences between noradrenergic and glutamatergic receptors regarding intracellular calcium signaling and coupling to glutamate release. The noradrenergic modulation of DHPG-induced responses indicates that intracellular astroglial processes can be regulated in a bi-directional feedback loop between closely connected astrocytes and neurons in the central nervous system. Astrocytes, the main population of glial cells, form gap junction-coupled multicellular networks and communicate among themselves through variations in intracellular calcium concentration ([Ca 2ϩ ] i ) 1 (1). These cells express a calcium-based excitability in which receptor-mediated calcium elevations can propagate as intracellular waves over considerable distances (1, 2). A diverse range of [Ca 2ϩ ] i changes are induced in astrocytes after exposure to various neurotransmitters (2-6) and the cells display [Ca 2ϩ ] i oscillations and intracellular waves in response to neuronal activity (7-9). Previous results demonstrate the importance of glutamate for the mediation of these neuronal-glial interactions. However, the potential contribution of other important neurotransmitters such as those belonging to the noradrenergic system has not yet been fully investigated.Variations in astrocytic [Ca 2ϩ ] i mediate the uptake and release of different neuroactive substances (10) such as arachidonic acid, neurotrophins, and neurotransmitters, and via this mechanism possibly modulate synaptic transmission (11-13). Consistent with this, previous studies have shown that activation of glial metabotropic glutamate receptors in concert with ␤-adrenoreceptors (␤-AdRs) can result in depression of synaptic activity in which the release of cAMP from astrocytes is central (14). Furthermore, adrenergic and glutamatergic interactions can also greatly affect both cAMP-and ...

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Astroglia from defined brain regions as studied with primary cultures

Cited by 141 publications

References 193 publications

Histomorphogenesis of Soman-Induced Encephalocardiomyopathy in Sprague-Dawley Rats

Histomorphogenesis of Soman-Induced Encephalocardiomyopathy in Sprague-Dawley Rats

Regional differences in glial-derived factors that promote dendritic outgrowth from mouse cortical neurons in vitro

α1-Adrenergic Modulation of Metabotropic Glutamate Receptor-induced Calcium Oscillations and Glutamate Release in Astrocytes

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