69, 415–436. 28, 697–710.

For example, increase in intracellular calcium (Ca2+) levels through voltage- and ligand-dependent channels results in increased cAMP levels via activation of G-protein-coupled receptors.

One hypothesis regarding the influence of CREB on adult neurogenesis comes from a recent study that focused on polyunsaturated fatty acid (PUFA)-GPR40-CREB signaling (Yamashima, 2012). doi: 10.1111/nan.12107, Bruel-Jungerman, E., Rampon, C., and Laroche, S. (2007). (1994).

The translation of proteins from genes is crucial for memory consolidation (Flexner et al., 1965; Alberini and Kandel, 2015).

Compared to wild-type mice, these mice responded more quickly to depression treatment. Articles. New neurons and new memories: how does adult hippocampal neurogenesis affect learning and memory?

doi: 10.1038/334494a0, Yamashima, T. (2012). 6, 647–655. (2013) showed that phytoceramide administration enhanced memory via the upregulation of hippocampal pCREB and BDNF expression, which resulted in increased AHN. Autoradiographic and histological evidence of postnatal hippocampal neurogenesis in rats. Collectively, this evidence indicates that CREB has a central role in these processes and is necessary for both memory consolidation and LTP.

Z. Cortex 9, 249–256. Dysfunction of these neurotransmitters is also implicated in major depressive disorder.[15]. miRNAs are known to control both precursor cell survival and differentiation in adult neurogenesis. Science 194, 1178–1181. Sci. Adult neurogenesis is the process by which new neurons are generated in the brains of adults. Transcription factors of the CREB family exert their actions as homodimers or heterodimers, but the CREB-CREB homodimer is the most potent transcriptional activator (Dworkin and Mantamadiotis, 2010). Adult hippocampal neurogenesis, synaptic plasticity and memory: facts and hypotheses. New cells showed loss of expression of DCX and Pax6 transcription factor (both of which are related to cell maturity), impairments in rostral migratory stream (RMS) migration, decreased cell proliferation and survival, and increased morphological defects in newborn OB cells (Herold et al., 2011; Merz et al., 2011). found upstream of genes, within the promoter or enhancer regions. Copyright © 2015 Ortega-Martínez. Hippocampal CA field neurogenesis after pilocarpine insult: the hippocampal fissure as a neurogenic niche. Q2 connects with TAFII 130 (TBP [TATA-binding protein]-associated factorII 130) and recruits the transcription machinery to the promoter region. Proc. Neuronal competition and selection during memory formation. Front. The positive effects of CREB in AHN were inhibited when CREB expression was repressed. EMBO J. (1990). Sci. Ahn, S., Olive, M., Aggarwal, S., Krylov, D., Ginty, D. D., and Vinson, C. (1998). 10 Progress in understanding the cellular processes regulating gene expression networks in cognition is relevant to develop therapeutic interventions for age-related cognitive disorders. (2007).

That is, CREB modulates AHN, which affects memory consolidation. 7:a021741. doi: 10.1007/s11064-006-9213-9, Ghosh, A., Ginty, D. D., Bading, H., and Greenberg, M. E. (1994). Biophys. These NSCs give rise to new neurons, which are incorporated as new granule cells into hippocampal networks. Behav. 33, 1078–1086. Neurogenesis interferes with the retrieval of remote memories: forgetting in neurocomputational terms. These leucine residues tightly bind to leucine residues of another CREB protein forming a dimer. Epigenetic regulation of adult neural stem cells: implications for Alzheimer’s disease. Sci. doi: 10.1126/science.186870, Burton, C. Z., and Twamley, E. W. (2015). One or several copies of CRE are present within the regulatory regions of genes. The presence of phosphorylated CREB (pCREB) has been found in many new-born immature neurons in the most important neurogenic niches, including the DG in the SGZ (Nakagawa et al., 2002a,b; Jagasia et al., 2009), SVZ, and OB system (Giachino et al., 2005; Herold et al., 2011). doi: 10.1016/j.bbagen.2012.09.002, Fanselow, M. S., and Dong, H. W. (2010). Natl. p300/CBP proteins: HATs for transcriptional bridges and scaffolds.

Thus, many co-factors, including some that are directly affected by neuronal activity and growth factors, influence CREB-mediated regulation at the final stage (Merz et al., 2011). (2009). doi: 10.1002/hipo.20527, Sable, P., Kale, A., Joshi, A., and Joshi, S. (2014). AHN, which occurs for specific brain functions, involves not only new neuron formation but also integration of these new-born neurons into functional networks. (2015). (2010). Calcium regulation of gene expression in neuronal cells. Neurogenesis attributed to the SVZ, the largest neurogenic niche, is also responsible for generating astrocytes, oligodendrocytes, and OB interneurons (Lois and Alvarez-Buylla, 1994); which are involved in “olfactory memory” (enhanced odor differentiation; Sahay et al., 2011b). Long-term memory is facilitated by cAMP response element-binding protein overexpression in the amygdala. Science 323, 1074–1077. Dev. In this regard, several transgenic lines of CREB mice such as CREB-VP16, Y134F and DIEDML, which show enhanced STM, also exhibit upregulation of hippocampal BDNF expression, which is related to higher AHN. Natl.

114, 2363–2373.

(2014). 12, 1438–1443. Alzheimer Res. The author acknowledges Marie Curie fellowship and Åbo Akademi University for supporting SO-M. Perspect. Activation of protein kinase A induces neuronal differentiation of HiB5 hippocampal progenitor cells. doi: 10.5607/en.2012.21.4.136, Kida, S., Josselyn, S. A., Peña de Ortiz, S., Kogan, J. H., Chevere, I., Masushige, S., et al. Short-chain fatty acids inhibit growth hormone and prolactin gene transcription via cAMP/PKA/CREB signaling pathway in dairy cow anterior pituitary cells. Res. A lack of CREB protein is tied to memory loss, anxiety, and different forms of dementia. EMBO J. Dev. Neurosci.

In addition, microinfusions of BDNF or a BDNF inhibitor into the dorsal hippocampus were associated with improved or impaired STM, respectively.

CREB is a regulatory target for the protein kinase Akt/PKB. doi: 10.1016/j.jchemneu.2014.02.002, Zhang, Q., Liu, G., Wu, Y., Sha, H., Zhang, P., and Jia, J. In contrast to previous classical studies in adult mice, some studies have focused on the effect of these isoforms on neocortical plasticity in young mice to highlight the age-dependent role of CREB in neuroplasticity. A recent review discussed the functional roles of CREB as a positive regulator in the formation and enhancement of memory (Kida and Serita, 2014). Upregulation of CREB-mediated transcription enhances both short- and long-term memory. Localization of phosphorylated cAMP response element-binding protein in immature neurons of adult hippocampus. This phosphorylation establishes an effector role for CREB, initiating the translation of extracellular stimuli into gene expression (Yamashima, 2012). Regulation of the CREB signaling cascade in the visual cortex by visual experience and neuronal activity. 9:e1003310. A year after CREB was defined, Montminy and Bilezikjian (1987) described CREB as a cellular transcription factor that binds CRE and induces transcription of the somatostatin gene. In vivo, phase shift-inducing light pulses during the subjective night correlated with CREB phosphorylation in the SCN. In this regard, the role of CREB in AHN process has been widely investigated. Because hippocampus-dependent memory processes are altered in such diseases, understanding the underlying molecular mechanisms is important for restoring normal brain function. Nat. (2005) reported a significant decrease in number of newborn cells in the OB of transgenic CREM-null knockout mice. Inducible forebrain-specific ablation of the transcription factor creb during adulthood induces anxiety but no spatial/contextual learning deficits. The epigenetic mechanisms of DNA methylation has also been shown to regulate CREB signaling. These assumptions are also pertinent to in vivo experiments that have described how CREB signaling affects proliferation of NSC precursors enhancing this cellular mechanism (Kim et al., 2002; Dworkin et al., 2009; Grimm et al., 2009; Merz et al., 2011). Cognitive markers of psychotic unipolar depression: a meta-analytic study. doi: 10.1002/cne.20310, Suzuki, A., Fukushima, H., Mukawa, T., Toyoda, H., Wu, L. J., Zhao, M. G., et al. 4, 1313–1317. Neurosci. [5] CREB downregulation is implicated in the pathology of Alzheimer's disease and increasing the expression of CREB is being considered as a possible therapeutic target for Alzheimer's disease. Cell. doi: 10.1038/nature09817, Sahay, A., Wilson, D. A., and Hen, R. (2011b). 174, 580–588.

doi: 10.3390/molecules161210146, Zhang, X., Odom, D. T., Koo, S. H., Conkright, M. D., Canettieri, G., Best, J., et al. For example, clustering of CBP (CREB-binding protein) has recently been described as crucial, and the CBP paralog p300 enhances CREB functionality. 8:239. doi: 10.3389/fnbeh.2014.00239, Bourtchuladze, R., Frenguelli, B., Blendy, J., Cioffi, D., Schutz, G., and Silva, A. J.

Exp. 5, 448–453. Neurosci. In addition, CREB upregulation itself promotes AHN, leading to greater neuronal survival and postnatal hippocampal neurogenesis (Cameron and Glover, 2015).

CREB has been implicated in the regulation of embryonic and adult neurogenesis (Dworkin et al., 2009). CREB, memory enhancement and the treatment of memory disorders: promises, pitfalls and prospects. 25, 1058–1065. Behav. 100, 433–442. Front.

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