Induction of CRE-Mediated Gene Expression by Stimuli That Generate Long-Lasting LTP in Area CA1 of the Hippocampus

Impey, Soren; Mark, Melanie D.; Villacres, Enrique C.; Poser, Steven; Chavkin, Charles; Storm, Daniel R.

doi:10.1016/s0896-6273(00)80120-8

Cited by 556 publications

(409 citation statements)

References 83 publications

(27 reference statements)

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“…These findings raise the possibility that SE drives CREB-dependent transcription, which in turn stimulates IGF-1 expression in microglia. To explore this idea, we examined the pattern of CRE-mediated gene expression in the dentate gyrus at 2-days post-SE using mice transgenic for a CRE-regulated β-galactosidase reporter construct (Impey et al, 1996). Consistent with our recent work showing that SE triggers microgliosis and induction of CRE-mediated gene expression , we present representative data in Fig.…”

Section: Signaling and Se-induced Progenitor Cell Proliferationsupporting

confidence: 59%

IGF‐1 receptor‐mediated ERK/MAPK signaling couples status epilepticus to progenitor cell proliferation in the subgranular layer of the dentate gyrus

Choi

Cho

Hoyt

et al. 2008

Glia

132

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Adult progenitor cell proliferation in the subgranular zone (SGZ) of the dentate gyrus is a dynamic process that is modulated by an array of physiological process, including locomotor activity and novel environmental stimuli. In addition, pathophysiological events, such as ischemia and status epilepticus (SE), have been shown to stimulate neurogenesis. Currently, limited information is available regarding the extracellular stimuli, receptors, and downstream intracellular effectors that couple excitotoxic stimulation to progenitor cell proliferation. Here we show that pilocarpineinduced SE triggers a set of signaling events that impinge upon the p42/44 mitogen-activated protein kinase (MAPK) pathway to drive progenitor cell proliferation in the SGZ at 2-days post-SE. Increased proliferation was dependent on insulin-like growth factor-1 (IGF-1), which was localized to activated microglia near the SGZ. Using a combination of techniques, we show that IGF-1 is a CREB-regulated gene and that SE triggered CRE-dependent transcription in microglia at 2-days post-SE. Together, these data identify a potential signaling program that couples SE to progenitor cell proliferation. SE triggers CREB-dependent transcription in reactive microglia. As a CREB-target gene, IGF-1 expression is upregulated, and by 2-days post-SE, IGF-1 triggers MAPK pathway activation in progenitor cells and, in turn, an increase in progenitor cell proliferation.

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Section: Signaling and Se-induced Progenitor Cell Proliferationsupporting

confidence: 59%

IGF‐1 receptor‐mediated ERK/MAPK signaling couples status epilepticus to progenitor cell proliferation in the subgranular layer of the dentate gyrus

Choi

Cho

Hoyt

et al. 2008

Glia

132

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“…Only stimuli that give rise to increases in nuclear calcium will cause CRE-mediated transcriptional responses. This provides a possible explanation for the finding that CRE-mediated gene expression can be induced by multiple trains of highfrequency electrical stimulation of neurons, but not by a single high-frequency stimulus (Impey et al, 1996). The former, but not the latter, stimulus may be associated with a sustained calcium influx into the cell, giving rise to larger increases in nuclear calcium.…”

Section: Cre-mediated Calcium-activated Transcriptionmentioning

confidence: 91%

Calcium Controls Gene Expression via Three Distinct Pathways That Can Function Independently of the Ras/Mitogen-Activated Protein Kinases (ERKs) Signaling Cascade

et al. 1997

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Calcium ions are the principal second messenger in the control of gene expression by electrical activation of neurons. However, the full complexity of calcium-signaling pathways leading to transcriptional activation and the cellular machinery involved are not known. Using the c-fos gene as a model system, we show here that the activity of its complex promoter is controlled by three independently operating signaling mechanisms and that their functional significance is cell type-dependent. The serum response element (SRE), which is composed of a ternary complex factor (TCF) and a serum response factor (SRF) binding site, integrates two calcium-signaling pathways. In PC12 cells, calcium-regulated transcription mediated by the SRE requires the TCF site and is not inhibited by expression of the dominant-negative Ras mutant, RasN17, nor by the MAP kinase kinase 1 inhibitor PD 98059. In contrast, TCF-dependent transcriptional regulation by nerve growth factor or epidermal growth factor is mediated by a Ras/MAP kinases (ERKs) pathway targeting the TCF Elk-1. In AtT20 cells and hippocampal neurons, calcium signals can stimulate transcription via a TCFindependent mechanism that requires the SRF binding site. The cyclic AMP response element (CRE), which cooperates with the TCF site in growth factor-regulated transcription, is a target of a third calcium-regulated pathway that is little affected by the expression of RasN17 or by PD 98059. Thus, calcium can stimulate gene expression via a TCF-, SRF-, and CRE-linked pathway that can operate independently of the Ras/MAP kinases (ERKs) signaling cascade in a cell type-dependent manner.

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“…Transgenic mice carrying LacZ reporters driven by the fos promoter [1] or a virally derived CREB-sensitive promoter [2] laid the groundwork for fluorescencebased approaches. A number of early attempts to create fluorescence-based reporters of neuronal activity (many of which were never reported), were unsuccessful.…”

Section: Fluorescent Reporters Of Inducible Gene Expressionmentioning

confidence: 99%

Visualizing circuits and systems using transgenic reporters of neural activity

Barth

2007

Current Opinion in Neurobiology

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Genetically encoded sensors of neural activity enable visualization of circuit-level function in the central nervous system. Although our understanding of the molecular events that regulate neuronal firing, synaptic function, and plasticity has expanded rapidly over the past fifteen years, an appreciation for how cellular changes are functionally integrated at the circuit level has lagged. A new generation of tools that employ fluorescent sensors of neural activity promises unique opportunities to bridge the gap between cellular and system-levels analysis.This review will focus on genetically-encoded sensors. A primary advantage of these indicators is that they can be non-selectively introduced to large populations of cells using either transgenic or viral-mediated approaches. This ability removes the non-trivial obstacles of how to get chemical indicators into cells of interest, a problem that has dogged investigators who have been interested in mapping neural function in the intact CNS. Five different types of approaches and their relative utility will be reviewed here: 1) reporters of immediate-early gene (IEG) activation using promoters such as c-fos and arc, 2) voltage-based sensors, such as GFPcoupled Na + and K + channels, 3) Cl − based sensors, 4) Ca ++ -based sensors, such as Camgaroo and the troponin-based TN-L15, and 5) pH-based sensors, which have been particularly useful for examining synaptic activity of highly convergent afferents in sensory systems in vivo. Particular attention will be paid to reporters of IEG expression, since these tools employ the built-in threshold function that occurs with activation of gene expression, provoking new experimental questions by expanding the timescale of analysis for circuit and system-level functional mapping. Fluorescent reporters of inducible gene expressionImmediate-early gene expression (IEG) can be a reliable marker of elevated neuronal firing, reporting activity over time scales that range from minutes to hours compared to ms and seconds for voltage-or ion-based sensors. In ion-based approaches, indicators are constitutively present in the cell, and the fluorescent protein must be engineered to be a sensor with rapid onset and offset kinetics to achieve temporal fidelity with the process being measured. In contrast, monitoring IEG expression can be directly coupled to transcription of the reporter gene. However, because maturation of the fluorophore is required for detection, a temporal delay may be introduced into reporter detection. This delay in reporting activity is advantageous in that it expands the types of experimental questions that can be addressed. For example, do IEGexpressing cells remain more excitable after stimulus cessation? Are cells activated by two temporally distinct stimuli (i.e. training and recall in a memory task) overlapping or distinct?

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Induction of CRE-Mediated Gene Expression by Stimuli That Generate Long-Lasting LTP in Area CA1 of the Hippocampus

Cited by 556 publications

References 83 publications

IGF‐1 receptor‐mediated ERK/MAPK signaling couples status epilepticus to progenitor cell proliferation in the subgranular layer of the dentate gyrus

IGF‐1 receptor‐mediated ERK/MAPK signaling couples status epilepticus to progenitor cell proliferation in the subgranular layer of the dentate gyrus

Calcium Controls Gene Expression via Three Distinct Pathways That Can Function Independently of the Ras/Mitogen-Activated Protein Kinases (ERKs) Signaling Cascade

Visualizing circuits and systems using transgenic reporters of neural activity

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