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Connecting Synaptic Activity with Plasticity-Related Gene Expression: From Molecular Mechanisms to Neurological Disorders
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Journal Article
Connecting Synaptic Activity with Plasticity-Related Gene Expression: From Molecular Mechanisms to Neurological Disorders
2016
Overview
In this special issue, O. Khalaf and J. Gräff provided a comprehensive review on the mechanisms mediating the transformation from an unstable memory to a lasting one, including neural circuits and subpopulations of cells that can be recruited into a memory trace, as well as the structural changes occurring at synapses during memory formation. P. Espinosa et al. examined the effect of neonatal exposure to sex hormones in the programming of dopaminergic neurons resulting in increased expression of tyrosine hydroxylase in ventral tegmental area and substantia nigra. In particular, in the article by B. Seifert et al., they elegantly demonstrated that the amyloid-beta peptide causes a dysfunction in vesicular transport of brain derived neurotrophic factor in transgenic mouse models of Alzheimer’s disease. Understanding the precise interaction of synaptically relevant transcriptional regulation can have therapeutic potential for treatments and possibly improving these conditions, and the work by P. Lobos et al. fits within this premise: since it is known that oxidative stress contributes to the development of Alzheimer’s disease, they studied the effect of astaxanthin, an antioxidant having free access to the brain, on the aberrant calcium signaling and decreased expression of type-2 ryanodine receptors (RyR2) induced by amyloid-β peptide oligomers (AβOs).
Publisher
Hindawi Publishing Corporation,John Wiley & Sons, Inc,Wiley
