Excitatory amino acid-, except 1S,3R-ACPD, induced transient high stimulation of phosphoinositide metabolism during hippocampal neuron development

Blanc, Emmanuel; Vignes, Michel; Récasens, Max

doi:10.1016/0736-5748(95)00058-5

Cited by 10 publications

(12 citation statements)

References 64 publications

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“…15 min prior to agonist stimulation. IPs were extracted with perchloric acid and separated on Dowex 1X8 formate‐form columns (Biorad, France) as previously described (Blanc et al . 1995b).…”

Section: Methodsmentioning

confidence: 99%

“…Previously, Blanc et al . (1995b) have shown that both iGluR and mGluR agonists stimulate PLC during in vitro development of hippocampal neurons in primary culture, which thus could be a suitable experimental model to study the role of PLC‐activating GluR in developmental plasticity.…”

Section: Introductionmentioning

confidence: 94%

“…IP measurements were performed as previously described (Blanc et al, 1995b). Brie¯y, phosphoinositides were labeled for 24 h by incorporation of 3 mCi per dish [ 3 H]-inositol.…”

Section: Inositol Phosphate (Ip) Measurementsmentioning

confidence: 99%

“…15 min prior to agonist stimulation. IPs were extracted with perchloric acid and separated on Dowex 1X8 formateform columns (Biorad, France) as previously described (Blanc et al, 1995b). Inositol mono-and bis-phosphate (IP 1 and IP 2 ) formation was measured, while no accumulation of inositol tris-phosphate could be detected in our experimental conditions.…”

Section: Inositol Phosphate (Ip) Measurementsmentioning

confidence: 99%

“…Previously, Blanc et al (1995b) have shown that both iGluR and mGluR agonists stimulate PLC during in vitro development of hippocampal neurons in primary culture, which thus could be a suitable experimental model to study the role of PLC-activating GluR in developmental plasticity. To further establish this putative role, we have modi®ed in vitro development of hippocampal neurons by treating them with a neurotrophic factor, basic ®broblast growth factor (bFGF), known to support both neuronal survival and neuritic extension (Walicke et al, 1986;Mattson et al, 1989;Miyagawa et al, 1993;Aoyagi et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

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Potentiation of glutamatergic agonist‐induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation

Blanc

Jallageas

Récasens

et al. 1999

Eur J of Neuroscience

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We investigated the modulation by growth factors of phospholipase C (PLC)-linked glutamate receptors during in vitro development of hippocampal cultures. In defined medium, glial cells represent between 3 and 14% of total cell number. When we added basic fibroblast growth factor (bFGF) 2 h after plating, we found: (i) a neuroprotection from naturally occurring death for up to 5 days; (ii) a proliferation of glial cells from day 3; and (iii) a potentiation of quisqualate (QA)-induced inositol phosphate (IP) formation from 1 to 10 days in vitro (DIV) and 1S, 3R-amino-cyclopentane-1,3-dicarboxylate (ACPD) response from 3 to 10 DIV. The antimitotic cytosine-beta,D-arabinofuranoside (AraC) blocked glial cell proliferation induced by bFGF, but not neuroprotection. Under these conditions, the early potentiation of the QA response (1-3 DIV) was not changed, while the ACPD and late QA response potentiations were prevented (5-10 DIV). Epidermal growth factor was not neuroprotective but it induced both glial cell proliferation and late QA or ACPD potentiation. Surprisingly, the early bFGF-potentiated QA-induced IP response was blocked by 6, 7-dinitro-quinoxaline-2,3-dione (DNQX), suggesting the participation of ionotropic (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate (KA) receptors. The delayed bFGF-potentiated ACPD-induced IP response is inhibited by (S)-alpha-methyl-4-carboxyphenylglycine (MCPG), indicating possible activation of glial metabotropic receptors. These results suggest that, in hippocampal cultures, bFGF modulates AMPA and metabotropic glutamate receptors linked to the IP cascade, possibly in relation to the regulation of neuronal survival and glial cell proliferation, respectively.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

“…IP measurements were performed as previously described (Blanc et al, 1995b). Brie¯y, phosphoinositides were labeled for 24 h by incorporation of 3 mCi per dish [ 3 H]-inositol.…”

Section: Inositol Phosphate (Ip) Measurementsmentioning

confidence: 99%

Section: Inositol Phosphate (Ip) Measurementsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Potentiation of glutamatergic agonist‐induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation

Blanc

Jallageas

Récasens

et al. 1999

Eur J of Neuroscience

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Transient expression of the glial glutamate transporters GLAST and GLT in hippocampal neurons in primary culture

2000

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The extracellular glutamate concentration is kept low by glutamate transporters in the plasma membranes. Here we have studied the expression of the glutamate transporters GLAST, GLT and EAAC during the in vitro development of embryonic hippocampal neurons grown in a defined (serum free) medium. Immunochemistry studies showed that both the GLAST and GLT proteins are expressed in a subpopulation of neurons at the early, but not at the later stages of the cultures. Glial cells expressing the GLAST and GLT proteins were found at all stages. EAAC was only detected in neurons. This is one of the first evidence of a neuronal ability to express GLAST.

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Opposite effects of α₁‐ and β‐adrenoceptor stimulation on both glutamate‐ and γ‐aminobutyric acid‐mediated spontaneous transmission in cultured rat hippocampal neurons

Croce

Astier

Récasens

et al. 2002

J of Neuroscience Research

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The effects of adrenergic receptor stimulation on spontaneous synaptic transmission were investigated in cultured rat hippocampal neurons by recording spontaneous excitatory and inhibitory postsynaptic currents (sEPSC and sIPSC). Noradrenaline (NA) inhibited sEPSC in a concentration-dependent manner, with maximal effect at 10 microM. The alpha(1)- and alpha(2)-adrenoceptor-selective agonists cirazoline and clonidine induced an inhibition of sEPSC appearance, whereas the beta-adrenoceptor agonist isoproterenol elicited an increase. The inhibitory effect of NA was reversed by alpha(1)-adrenoceptor blockade. The participation of gamma-aminobutyric acid (GABA)(B)-receptor stimulation in the inhibitory effect of NA was further examined. GABA(B)-receptor stimulation with baclofen induced a strong inhibition of bursting activity, which was fully reversed by the GABA(B) antagonist CGP 55845. By itself, CGP 55845 exerted a stimulatory effect on sEPSC frequency. In the presence of CGP 55845, the inhibitory effects of cirazoline and clonidine were maintained. NA (1, 10, and 100 microM) and alpha-adrenoceptor agonists decreased miniature EPSC and IPSC occurrence, whereas beta-adrenergic stimulation increased it. In 50% of the cells examined, NA (1, 10 microM) had a stimulatory effect on sIPSC, whereas, in the remaining 50% of cells, NA (1, 10 microM) had an inhibitory effect. In all the cells, 100 microM NA induced an inhibition of sIPSC. The inhibitory effect of NA was due to alpha(1)-receptor stimulation, whereas the excitatory effect was due to beta-receptor stimulation. In cultured hippocampal neurons, spontaneous excitatory and inhibitory synaptic transmissions are both similarly altered by adrenoceptor stimulation. However, in a subset of cells, low concentrations of NA mediate an increase of sIPSC via beta-adrenoceptor activation.

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Excitatory amino acid-, except 1S,3R-ACPD, induced transient high stimulation of phosphoinositide metabolism during hippocampal neuron development

Cited by 10 publications

References 64 publications

Potentiation of glutamatergic agonist‐induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation

Potentiation of glutamatergic agonist‐induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation

Transient expression of the glial glutamate transporters GLAST and GLT in hippocampal neurons in primary culture

Opposite effects of α₁‐ and β‐adrenoceptor stimulation on both glutamate‐ and γ‐aminobutyric acid‐mediated spontaneous transmission in cultured rat hippocampal neurons

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Excitatory amino acid-, except 1S,3R-ACPD, induced transient high stimulation of phosphoinositide metabolism during hippocampal neuron development

Cited by 10 publications

References 64 publications

Potentiation of glutamatergic agonist‐induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation

Potentiation of glutamatergic agonist‐induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation

Transient expression of the glial glutamate transporters GLAST and GLT in hippocampal neurons in primary culture

Opposite effects of α1‐ and β‐adrenoceptor stimulation on both glutamate‐ and γ‐aminobutyric acid‐mediated spontaneous transmission in cultured rat hippocampal neurons

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Opposite effects of α₁‐ and β‐adrenoceptor stimulation on both glutamate‐ and γ‐aminobutyric acid‐mediated spontaneous transmission in cultured rat hippocampal neurons