An Overview of the Epigenetic Modifications in the Brain under Normal and Pathological Conditions.

Epigenetic changes are changes in gene expression that do not involve alterations to the DNA sequence. These changes lead to establishing a so-called epigenetic code that dictates which and when genes are activated, thus orchestrating gene regulation and playing a central role in development, health, and disease. The brain, being mostly formed by cells that do not undergo a renewal process throughout life, is highly prone to the risk of alterations leading to neuronal death and neurodegenerative disorders, mainly at a late age.

The Mouse: A Translational Model of Human Neurological Conditions, or Simply a Good Tool for Better Understanding Neurodevelopment?

The first description of the mutation in mouse dates to more than fifty years ago, and later, its causative gene () was discovered in mouse, and its human orthologue () was demonstrated to be causative of lissencephaly 2 (LIS2) and about 20% of the cases of autosomal-dominant lateral temporal epilepsy (ADLTE). In both human and mice, the gene encodes for a glycoprotein referred to as reelin (Reln) that plays a primary function in neuronal migration during development and synaptic stabilization in adulthood. Besides LIS2 and ADLTE, and/or other genes coding for the proteins of the Reln intracellular cascade have been associated substantially to other conditions such as spinocerebellar ataxia type 7 and 37, -associated cerebellar hypoplasia, -associated lissencephaly, autism, and schizophrenia.

Decreased Expression of Synaptophysin 1 (SYP1 Major Synaptic Vesicle Protein p38) and Contactin 6 (CNTN6/NB3) in the Cerebellar Vermis of reln Haplodeficient Mice.

Reeler heterozygous mice (reln) are seemingly normal but haplodeficient in reln, a gene implicated in autism. Structural/neurochemical alterations in the reln brain are subtle and difficult to demonstrate. Therefore, the usefulness of these mice in translational research is still debated.

Caspase-3 Mediated Cell Death in the Normal Development of the Mammalian Cerebellum.

Caspase-3, onto which there is a convergence of the intrinsic and extrinsic apoptotic pathways, is the main executioner of apoptosis. We here review the current literature on the intervention of the protease in the execution of naturally occurring neuronal death (NOND) during cerebellar development. We will consider data on the most common altricial species (rat, mouse and rabbit), as well as humans.

Cell death and neurodegeneration in the postnatal development of cerebellar vermis in normal and Reeler mice.

Programmed cell death (PCD) was demonstrated in neurons and glia in normal brain development, plasticity, and aging, but also in neurodegeneration. (Macro)autophagy, characterized by cytoplasmic vacuolization and activation of lysosomal hydrolases, and apoptosis, typically entailing cell shrinkage, chromatin and nuclear condensation, are the two more common forms of PCD. Their underlying intracellular pathways are partly shared and neurons can die following both modalities, according to the type of death-triggering stimulus.

Improvement of a headspace solid phase microextraction-gas chromatography/mass spectrometry method for the analysis of wheat bread volatile compounds.

An improved method based on headspace solid phase microextraction combined with gas chromatography-mass spectrometry (HS-SPME/GC-MS) was proposed for the semi-quantitative determination of wheat bread volatile compounds isolated from both whole slice and crust samples. A DVB/CAR/PDMS fibre was used to extract volatiles from the headspace of a bread powdered sample dispersed in a sodium chloride (20%) aqueous solution and kept for 60min at 50°C under controlled stirring. Thirty-nine out of all the extracted volatiles were fully identified, whereas for 95 other volatiles a tentative identification was proposed, to give a complete as possible profile of wheat bread volatile compounds.

Neuronal cell death: an overview of its different forms in central and peripheral neurons.

The discovery of neuronal cell death dates back to the nineteenth century. Nowadays, after a very long period of conceptual difficulties, the notion that cell death is a phenomenon occurring during the entire life course of the nervous system, from neurogenesis to adulthood and senescence, is fully established. The dichotomy between apoptosis, as the prototype of programmed cell death (PCD ), and necrosis, as the prototype of death caused by an external insult, must be carefully reconsidered, as different types of PCD: apoptosis, autophagy, pyroptosis, and oncosis have all been demonstrated in neurons (and glia ).

Post-natal development of the Reeler mouse cerebellum: An ultrastructural study.

Reelin, an extracellular protein promoting neuronal migration in brain areas with a laminar architecture, is missing in the Reeler mouse (reelin(-/-)). Several studies indicate that the protein is also necessary for correct dendritic outgrowth and synapse formation in the adult forebrain. By transmission electron microscopy, we characterize the development and synaptic organization of the cerebellar cortex in Reeler mice and wild type control littermates at birth, postnatal day (P) 5, 7, 10 and 15.

Protein S100 immunoreactivity in glial cells and neurons of the Japanese quail brain.

In mammals, sparse data illustrated the neuronal expression of S100 protein in central and peripheral nervous system. Similar studies have not been performed in other vertebrate species, in particular in birds. We provide here a detailed description of the distribution of the calcium-binding protein S100 in neuronal and glial elements in the central nervous system of an avian species, the Japanese quail (Coturnix japonica) largely used for neuroanatomical and functional studies.