Glutamate receptor-driven activation of transcription factors in primary neuronal cultures

Condorelli, D. F.; Albani, P. Dell'; Amico, Carla; Łukasiuk, Katarzyna; Kaczmarek, Leszek; Giuffrida-Stella, Anna Maria

doi:10.1007/bf00967329

Cited by 50 publications

(21 citation statements)

References 43 publications

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“…Little is known about the mechanisms by which EGR-1 contributes to long-term synaptic plasticity, memory consolidation, and reconsolidation. In cultured neurons, both glutamatergic signaling (Condorelli et al 1994) and L-type voltage-gated calcium channels (Murphy et al 1991) have been shown to regulate EGR-1 expression. Further, EGR-1, along with the nuclear transcription factors Elk-1 and CREB, have been shown to be regulated by ERK/MAPK signaling during long-term potentiation (LTP) in the dentate gyrus (Davis et al 2000), suggesting that one or both of these transcription factors plays a critical role in ERK-driven EGR-1 transcription.…”

Section: Discussionmentioning

confidence: 99%

Early growth response gene 1 (Egr-1) is required for new and reactivated fear memories in the lateral amygdala

Maddox¹,

Monsey²,

Schafe³

2010

Learn. Mem.

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The immediate-early gene early growth response gene-1 (EGR-1, zif-268) has been extensively studied in synaptic plasticity and memory formation in a variety of memory systems. However, a convincing role for EGR-1 in amygdala-dependent memory consolidation processes has yet to emerge. In the present study, we have examined the role of EGR-1 in the consolidation and reconsolidation of amygdala-dependent auditory Pavlovian fear conditioning. In our first series of experiments, we show that EGR-1 is regulated following auditory fear conditioning in the lateral nucleus of the amygdala (LA). Next, we use antisense oligodeoxynucleotide (ODN) knockdown of EGR-1 in the LA to show that training-induced expression of EGR-1 is required for memory consolidation of auditory fear conditioning; that is, long-term memory (LTM) is significantly impaired while acquisition and short-term memory (STM) are intact. In a second set of experiments, we show that EGR-1 is regulated in the LA by retrieval of an auditory fear memory. We then show that retrieval-induced expression of EGR-1 in the LA is required for memory reconsolidation of auditory fear conditioning; that is, post-retrieval (PR)-LTM is significantly impaired while memory retrieval and PR-STM are intact. Additional experiments show these effects to be restricted to the LA, to be temporally graded, and unlikely to be due to nonspecific toxicity within the LA. Collectively, our findings strongly implicate a role for EGR-1 in both the initial consolidation and in the reconsolidation of auditory fear memories in the LA.

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Section: Discussionmentioning

confidence: 99%

Early growth response gene 1 (Egr-1) is required for new and reactivated fear memories in the lateral amygdala

Maddox¹,

Monsey²,

Schafe³

2010

Learn. Mem.

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“…In cultured cortical neurons (Condorelli et al, 1994;Murphy et al, 1991a,b) or primary cultures containing both cortical and striatal neurons (Vaccarino et al, 1993), NMDA receptor activation will induce c-fos expression. Likewise, in primary hippocampal cultures, NMDA receptor activation results in both CREB phosphorylation and c-fos expression (Bading et al, 1993(Bading et al, , 1995.…”

Section: Introductionmentioning

confidence: 97%

NMDA and D1 receptors regulate the phosphorylation of CREB and the induction ofc-fos in striatal neurons in primary culture

Das

Grunert

Williams

et al. 1997

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Numerous in vivo studies have demonstrated that psychostimulant drugs such as amphetamine and cocaine can induce the expression of the immediate early gene c-fos in striatal neurons via the activation of D1 dopamine receptors. NMDA receptor activation is also known to induce c-fos in the striatum. In the present study we have used a primary striatal neuronal culture preparation to examine the mechanisms whereby these stimuli lead to changes in gene expression. Direct application of NMDA to striatal cells in culture caused a rapid increase in the expression of c-fos as well as an increase in the phosphorylation of the transcription factor CRE binding protein (CREB). This was prevented by NMDA receptor antagonists, and required extracellular calcium, but did not involve L-type calcium channels. The induction of c-fos and CREB phosphorylation following NMDA were unaffected by inhibition of protein kinase C; tyrosine kinases or nitric oxide synthase. However, the response to NMDA was blocked by KN62, a selective inhibitor of calcium/calmodulin-dependent protein kinase. Application of the D1 agonist SKF 38393, or direct stimulation of adenylyl cyclase with forskolin, also resulted in the phosphorylation of CREB and the induction of c-fos in striatal neurons. These effects were blocked by the protein kinase A inhibitor H89. These observations are consistent with the hypothesis that calcium/calmodulin-dependent phosphorylation of CREB induced by NMDA, or cAMP-dependent phosphorylation of CREB induced by D1 agonists, underlie the induction of c-fos seen following activation of these receptors in striatal neurons.

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confidence: 99%

“…In primary cultures of cortical and striatal neurons, activation of NMDA receptors results in induction of c-fos, fosB, c-jun, and junB mRNA (Vaccarino et al, 1992;Condorelli et al, 1994). Glutamate stimulation also results in an NMDA receptordependent increase in AP-1-binding activity in cultured neurons (Condorelli et al, 1994). In vivo stimulation of NMDA receptors by intrastriatal injection of quinolinic acid results in the induction of Fos protein in the majority of striatal projection neurons (Berretta et al, 1992).…”

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confidence: 99%

Glutamate, But Not Dopamine, Stimulates Stress-Activated Protein Kinase and AP-1-Mediated Transcription in Striatal Neurons

1997

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Drugs that stimulate dopamine and glutamate receptors have been shown to induce the expression of AP-1 proteins (such as c-Fos and c-Jun) in the striatum and to induce binding of these proteins to AP-1 sites on DNA, leading to the hypothesis that AP-1-mediated transcription contributes to the long-term effects of these drugs. To examine this hypothesis, we compared the regulation of AP-1-mediated transcription to the inductions of AP-1-binding activity and genes encoding AP-1 proteins in primary cultures of striatal neurons. Although glutamate, dopamine, and forskolin (an activator of adenylate cyclase) all induce c-fos mRNA and AP-1 binding, we found, surprisingly, that only glutamate induces transcription of a transfected AP-1-driven fusion gene. To explore the basis for this discrepancy, we investigated the possibility that the phosphorylation of c-Jun may also be required for AP-1-mediated transcription in striatal neurons. Glutamate, but neither dopamine nor forskolin, raises the levels of phosphorylated c-Jun as well as the activity of a Jun kinase (SAPK /JNK) in striatal cultures. Both the glutamatergic induction of AP-1-mediated transcription and activation of SAPK/JNK appear to be mediated, at least in part, via NMDA receptors. In striatal neurons, the phosphorylation of AP-1 proteins produced by glutamate may be required to convert AP-1 protein expression and binding to transcriptional activation.

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Glutamate receptor-driven activation of transcription factors in primary neuronal cultures

Cited by 50 publications

References 43 publications

Early growth response gene 1 (Egr-1) is required for new and reactivated fear memories in the lateral amygdala

Early growth response gene 1 (Egr-1) is required for new and reactivated fear memories in the lateral amygdala

NMDA and D1 receptors regulate the phosphorylation of CREB and the induction ofc-fos in striatal neurons in primary culture

Glutamate, But Not Dopamine, Stimulates Stress-Activated Protein Kinase and AP-1-Mediated Transcription in Striatal Neurons

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