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Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Using diverse experimental methods, studies in the early 1990s showed that Pb2+ is a potent noncompetitive antagonist of the NMDAR.364–367 Pb2+ exposure during brain development was also shown to alter NMDAR composition368–370 and modifies downstream signaling in the rat hippocampus.352,371 Specifically, Pb2+ exposure reduces cAMP response-element binding (CREB) phosphorylation and binding activity in the nucleus.371,372 CREB is a transcription factor whose activity is controlled by phosphorylation at multiple sites by several kinases, including the Ca2+/calmodulin-dependent protein kinase II (CaMKII),373 an enzyme whose activity and protein levels are reduced as a result of developmental Pb2+ exposure.352 CREB activation regulates transcription of BDNF,374–376 suggesting that Pb2+-induced impairments in CREB activation alter BDNF transcription and thus negatively modulate a number of neuronal pathways, including presynaptic and postsynaptic targets.
Naturally Occurring Polymers—Animals
Published in Charles E. Carraher, Carraher's Polymer Chemistry, 2017
One of the active agents is cyclic AMP. A protein called CREB (for CRE-binding protein; CRE is simply a specific DNA unit, part of a gene, that is called the cyclic AMP response element or site) is activated altering the shape and functioning of the synapse in our brains when exposed to cyclic AMP (10.12) or some related compound in our brains. Genes that are activated are called CRE genes with the name being the initials of cyclic AMP response elements. CREB, when phosphorylated, binds to the CREs near certain genes acting as a transcription factor and turning on or activating the genes. Animals without the CREB-producing gene are able to learn but do not possess long-term memory. It is believed by some that the CREB-related genes are in fact essential to our learning and memory and act as master switches in activating other genes necessary in our learning/memory process. The CREB gene is on chromosome 2. A related and essential gene that helps CREB perform is found on chromosome 16 and is given the name CREBBP.
Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Structural changes in dendrites and synapses require synthesis of new proteins, which implies that second messengers and some of their targets are involved in activating transcription factors, that is, proteins that control the transcription of genetic information from DNA to messenger RNA. One such ubiquitous transcription factor is the cAMP response element-binding protein (CREB) that is activated through phosphorylation by PKA, CaMKIV, a relative of CaMKII (Section 6.3.1), and other kinases that translocate to the nucleus. Dendrites have the metabolic machinery for local protein synthesis, as required for fast changes in structure and function.
Effects of 5.8 GHz microwave on hippocampal synaptic plasticity of rats
Published in International Journal of Environmental Health Research, 2022
Gang Rui, Li-Yuan Liu, Ling Guo, Yi-Zhe Xue, Pan-Pan Lai, Peng Gao, Jun-Ling Xing, Jing Li, Gui-Rong Ding
Synaptophysin and PSD95 are located in the presynaptic membrane and postsynaptic membrane, and are closely related to synaptic plasticity(Becher et al. 1999; El-Husseini et al. 2000). p-CREB and CREB are important nuclear transcription factors, not only play an important role in regulating the processes of neuronal differentiation, maturation and death, but also participate in the regulation of memory formation and synaptic plasticity(Silva et al. 1998; Kandel 2001; Dawson and Ginty 2002; Pittenger and Duman 2008; Mamiya et al. 2009; Luo et al. 2017). The results of WB showed that (Figure 5), after exposure for 15 days, the protein level of PSD95, Synaptophysin, p-CREB and CREB in hippocampus did not significantly change in Microwave 2 h group or Microwave 4 h group, compared with Sham group (P > 0.05).
Neurophysiological and molecular approaches to understanding the mechanisms of learning and memory
Published in Journal of the Royal Society of New Zealand, 2021
Shruthi Sateesh, Wickliffe C. Abraham
AD is a progressive age related neurodegenerative disease that has traditionally been diagnosed by functional deficits beginning with self-reporting of impaired episodic memory (Dubois et al. 2007). AD is characterised by the widespread accumulation of extracellular plaques containing amyloid-β (Aβ) that are generated by amyloidogenic processing of amyloid precursor protein, and intraneuronal hyperphosphorylated tau leading to neurofibrillary tangles, neuroinflammation and cell loss. Additionally, build-up of intraneuronal Aβ is observed as an early event in transgenic animal models (Kumar et al. 2013). Transgenic mouse models of AD have revealed cytoarchitectural changes, such as significant reductions in dendritic spine density in both cortical and subcortical regions early in the disease that are highly correlated with cognitive deficits (Spires-Jones and Knafo 2012). The mouse models also exhibit age-dependent spatial memory impairments and attenuated NMDAR-mediated LTP in both the CA1 and dentate gyrus regions (Chapman et al. 1999; Yamin 2009). Additionally, the expression of various transcription factors is downregulated in AD brain, including cyclic AMP (cAMP)-responsive element-binding protein (CREB). CREB is known to be vital for L-LTP, learning, and memory (Pugazhenthi et al. 2011). These and many other similar findings have driven the hypothesis that the impairment in LTP mechanisms underpins the impaired learning and memory (Shankar et al. 2008), especially early in the disease. Thus one therapeutic strategy for AD may centre on finding treatments that can rescue LTP.
Lead alters intracellular protein signaling and suppresses pro-inflammatory activation in TLR4 and IFNR-stimulated murine RAW 264.7 cells, in vitro
Published in Journal of Toxicology and Environmental Health, Part A, 2019
R.J. Williams, E. Karpuzoglu, H. Connell, D.J. Hurley, S.D Holladay, R.M. Gogal
CREB is a transcription factor downstream from the CaM kinases and activated through phosphorylation. Cytoplasmic expression and phosphorylation were observed in RAW 264.7 cells cultured with Pb and stimulated with LPS, rIFNγ or LPS + rIFNγ however, these parameters did not differ from the activation and phosphorylation in cells cultured with any comparable treatment in the absence of Pb. In the present study, the addition of Pb did not significantly alter cytoplasmic or nuclear expression of activated CREB (pCREB) in any cell treatment at any time point (Figure 4(c,d)).