A Systematic, Open-Science Framework for Quantification of Cell-Types in Mouse Brain Sections Using Fluorescence Microscopy.

The ever-expanding availability and evolution of microscopy tools has enabled ground-breaking discoveries in neurobiology, particularly with respect to the analysis of cell-type density and distribution. Widespread implementation of many of the elegant image processing tools available continues to be impeded by the lack of complete workflows that span from experimental design, labeling techniques, and analysis workflows, to statistical methods and data presentation. Additionally, it is important to consider open science principles (e.

Resorbable Mg-Containing Phosphates for Bone Tissue Repair.

Materials based on Mg-containing phosphates are gaining great relevance in the field of bone tissue repair via regenerative medicine methods. Magnesium ions, together with condensed phosphate ions, play substantial roles in the process of bone remodeling, affecting the early stage of bone regeneration through active participation in the process of osteosynthesis. In this paper we provide a comprehensive overview of the usage of biomaterials based on magnesium phosphate and magnesium calcium phosphate in bone reconstruction.

Purinergic signaling in nervous system health and disease: Focus on pannexin 1.

Purinergic signaling encompasses the cycle of adenosine 5' triphosphate (ATP) release and its metabolism into nucleotide and nucleoside derivatives, the direct release of nucleosides, and subsequent receptor-triggered downstream intracellular pathways. Since the discovery of nerve terminal and glial ATP release into the neuropil, purinergic signaling has been implicated in the modulation of nervous system development, function, and disease. In this review, we detail our current understanding of the roles of the pannexin 1 (PANX1) ATP-release channel in neuronal development and plasticity, glial signaling, and neuron-glial-immune interactions.

Early-Age Running Enhances Activity of Adult-Born Dentate Granule Neurons Following Learning in Rats.

Cognitive reserve, the brain's capacity to draw on enriching experiences during youth, is believed to protect against memory loss associated with a decline in hippocampal function, as seen in normal aging and neurodegenerative disease. Adult neurogenesis has been suggested as a specific mechanism involved in cognitive (or neurogenic) reserve. The first objective of this study was to compare learning-related neuronal activity in adult-born versus developmentally born hippocampal neurons in juvenile male rats that had engaged in extensive running activity during early development or reared in a standard laboratory environment.

Selective loss of AMPA receptor subunits at inhibitory neuron synapses in the cerebellum of the ataxic stargazer mouse.

AMPA receptor subunits (GluA1-4) are trafficked to membrane synaptic sites by transmembrane AMPA receptor regulatory proteins (TARPs). In the stargazer mutant mouse, expression of TARP-γ2 (stargazin) is severely reduced, resulting in cerebellar ataxia. Stargazer granule cells (GCs) have a complete loss of functional AMPARs, as γ2 is their main TARP; hence mossy fiber (MF)-GC synapses are silent.

Spatial learning-induced increase in agmatine levels at hippocampal CA1 synapses.

Agmatine, a metabolite of L-arginine, is considered as a novel putative neurotransmitter. It has been detected in axon terminals that synapse with pyramidal cells in the hippocampus, a brain region that is critically involved in spatial learning and memory. However, the role of agmatine in learning and memory is poorly understood.

Loss of calcium channels in the cerebellum of the ataxic and epileptic stargazer mutant mouse.

The stargazer mouse displays cerebellar ataxia and absence epilepsy as a result of a single, recessive mutation on chromosome 15 which silences the expression of the voltage-dependent calcium channel (VDCC) subunit gamma2, termed stargazin. Stargazin is the predominant gamma-subunit expressed in the cerebellum and is essential for correct assembly and trafficking of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-subtype of glutamate receptors (AMPARs) to postsynaptic membranes. As a functional association between AMPARs and VDCCs has been reported, and loss of stargazin results in a loss of AMPA receptors at cerebellar synapses, we investigated whether the loss of stargazin might also change the expression levels of calcium channels at cerebellar synapses.

Selective reduction in synaptic proteins involved in vesicle docking and signalling at synapses in the ataxic mutant mouse stargazer.

The spontaneous recessive mutant mouse stargazer has a specific and pronounced deficit in brain-derived neurotrophic factor (BDNF) mRNA expression in the cerebellum. Cerebellar granule cells, in particular, show a selective and near-total loss of BDNF. The mutation involves a defect in the calcium channel subunit Cacng2.