The central nervous system is a highly complex network composed of various cell types, each one with different subpopulations. Each cell type has distinct roles for the functional operation of circuits, and ultimately, for brain physiology in general. Since the absolute number of each cell type is considered a proxy of its functional complexity, one approach to better understand how the brain works is to unravel its absolute cellularity and the quantitative relations between cell populations; in other words, how one population of cells is quantitatively structured, in relation to another. Oligodendrocytes are one of these cell types - mainly, they provide electric insulation to axons, optimizing action potential conduction. Their function has recently been revisited and their role extended, one example being their capability of providing trophic support to long axons. To determine the absolute cellularity of oligodendroglia, we have developed a protocol of oligodendrocyte quantification using the isotropic fractionator with a pan-marker for this cell type. We report a detailed assessment of specificity and universality of the oligodendrocyte transcription factor 2 (Olig2), through systematic confocal analyses of the C57BL/6 mouse brain. In addition, we have determined the absolute number (17.4 million) and proportion (about 20%) of this cell type in the brain (and in different brain regions), and tested if this population, at the intraspecific level, scales with the number of neurons in an allometric-based approach. Considering these numbers, oligodendrocytes proved to be the most numerous of glial cells in the mouse brain.

/pdf/the-absolute-number-of-oligodendrocytes-in-the-adult-mouse-30pbossgyh.pdf

The Absolute Number of Oligodendrocytes in the Adult Mouse Brain.

Zinc-finger genes Fez and Fez-like function in the establishment of diencephalon subdivisions

Celsr3 and Fzd3 regulate the development of reciprocal thalamocortical projections independently of their expression in cortical or thalamic neurons. To understand this cell non autonomous mechanism further, we tested whether Celsr3 and Fzd3 could act via Isl1-positive guidepost cells. Isl1-positive cells appear in the forebrain at embryonic day (E) 9.5-E10.5 and, from E12.5, they form 2 contingents in ventral telencephalon and prethalamus. In control mice, corticothalamic axons run in the ventral telencephalic corridor in close contact with Isl1-positive cells. When Celsr3 or Fzd3 is inactivated in Isl1-expressing cells, corticofugal fibers stall and loop in the ventral telencephalic corridor of high Isl1 expression, and thalamic axons fail to cross the diencephalon-telencephalon junction (DTJ). At E12.5, before thalamic and cortical axons emerge, pioneer projections from Isl1-positive cells cross the DTJ from both sides in control but not mutant embryos. These early projections appear to act like a bridge to guide later growing thalamic axons through the DTJ. Our data suggest that Celsr3 and Fzd3 orchestrate the formation of a scaffold of pioneer neurons and their axons. This scaffold extends from prethalamus to ventral telencephalon and subcortex, and steers reciprocal corticothalamic fibers.

Celsr3 and Fzd3 Organize a Pioneer Neuron Scaffold to Steer Growing Thalamocortical Axons

The thalamocortical tract carries sensory information to the neocortex. It has long been recognized that the neocortical pioneer axons of subplate neurons are essential for thalamocortical development. Herein we report that an axon guidance cue, draxin, is expressed in early-born neocortical neurons, including subplate neurons, and is necessary for thalamocortical development. In draxin(-/-) mice, thalamocortical axons do not enter the neocortex. This phenotype is sufficiently rescued by the transgenic expression of draxin in neocortical neurons. Genetic interaction data suggest that draxin acts through Deleted in colorectal cancer (DCC) and Neogenin (Neo1), to regulate thalamocortical projections in vivo. Draxin promotes the outgrowth of thalamic axons in vitro and this effect is abolished in thalamic neurons from Dcc and Neo1 double mutants. These results suggest that draxin from neocortical neurons controls thalamocortical projections into the neocortex, and that this effect is mediated through the DCC and Neo1 receptors.

/pdf/draxin-from-neocortical-neurons-controls-the-guidance-of-4o6u1lgi0i.pdf

Draxin from neocortical neurons controls the guidance of thalamocortical projections into the neocortex

In the treatment of localized prostate cancer, controlling the cancer and maintaining quality of life are important. Focal therapy of localized prostate cancer aims to treat the lesion/part of the prostate that includes the index lesion, which determines the prognosis. We performed a non‐systematic review of novel studies on focal therapy of localized prostate cancer as primary treatment published between 2016 and 2021. For mainly intermediate‐risk patients, therapeutic technology, such as cryoablation, brachytherapy, high‐intensity focused ultrasound, photodynamic therapy, microwave‐coagulation, electroporation, and laser ablation, etc., were performed. These procedures are minimally invasive and safe, and provide good functional outcome: a 94–100% pad‐free rate against urinary incontinence and 47–86% erectile function, which is sufficient for sexual intercourse. Accurate three‐dimensional mapping of the targeted lesion could be an essential navigation technique for therapeutic success. Intermediate‐ to short‐term oncological outcomes were good, resulting in downstaging of the patient's status to no clinically significant cancer; however, transition to conventional whole‐gland treatment was necessary in about 10–30% of patients. It is important to select appropriate patients by both multiparametric magnetic resonance imaging and targeted biopsy, and to follow‐up postoperatively with methods such as active surveillance. Clinically significant prostate‐specific antigen reduction, image response using preoperative and postoperative multiparametric magnetic resonance imaging, and histological analysis should be combined for follow‐up.

Focal therapy of localized prostate cancer

Thalamocortical axons (TCAs) pass through the prethalamus in the first step of their neural circuit formation. Although it has been supposed that the prethalamus is an intermediate target for thalamocortical projection formation, much less is known about the molecular mechanisms of this targeting. Here, we demonstrated the functional implications of the prethalamus in the formation of this neural circuit. We show that Olig2 transcription factor, which is expressed in the ventricular zone (VZ) of prosomere 3, regulates prethalamus formation, and loss of Olig2 results in reduced prethalamus size in early development, which is accompanied by expansion of the thalamic eminence (TE). Extension of TCAs is disorganized in the Olig2-KO dorsal thalamus, and initial elongation of TCAs is retarded in the Olig2-KO forebrain. Microarray analysis demonstrated upregulation of several axon guidance molecules, including Epha3 and Epha5, in the Olig2-KO basal forebrain. In situ hybridization showed that the prethalamus in the wild type excluded the expression of Epha3 and Epha5, whereas loss of Olig2 resulted in reduction of this Ephas-negative area and the corresponding expansion of the Ephas-positive TE. Dissociated cultures of thalamic progenitor cells demonstrated that substrate-bound EphA3 suppresses neurite extension from dorsal thalamic neurons. These results indicate that Olig2 is involved in correct formation of the prethalamus, which leads to exclusion of the EphA3-expressing region and is crucial for proper TCA formation. Our observation is the first report showing the molecular mechanisms underlying how the prethalamus acts on initial thalamocortical projection formation.

/pdf/development-of-the-prethalamus-is-crucial-for-2nms3dseqs.pdf

Development of the prethalamus is crucial for thalamocortical projection formation and is regulated by Olig2.

To examine the safety and efficacy of microwave tissue coagulation (MTC) for prostate cancer and assess its use in lesion‐targeted focal therapy in a non‐clinical study and a clinical phase II trial.

Microwave focal therapy of prostate cancer: a non‐clinical study and exploratory clinical trial

Expression of myelin genes in the developing chick retina

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Development of the prethalamus is crucial for thalamocortical projection formation and is regulated by Olig2.

Microwave focal therapy of prostate cancer: a non‐clinical study and exploratory clinical trial

Expression of myelin genes in the developing chick retina