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The sequential development and growth of the subcortico-cortical fibres have been studied by means of acetylcholinesterase (AChE; acetylcholine acetylhydrolase; EC 3.1.1.7) histochemistry on the serial sections obtained from brains of human fetuses ranging from 10 to 28 weeks of gestation. It was found that thalamic and basal telencephalic fibres approaching the fetal auditory cortex have very strong AChE reactivity during a prolonged period of growth. In the youngest fetuses (10.5 weeks) a prominent fibre system was seen emerging from the ventroposterior thalamic territory while the auditory neopallium was free of AChE staining. In older fetuses (16–18 weeks) AChE-positive fibres originating in the ventroposterior thalamus and basal telencephalon penetrate the ‘subplate layer’ of the auditory cortex. On the basis of AChE reactivity of the ‘subplate layer’ the auditory cortex can be delineated from the surrounding neocortical areas. In the oldest fetuses (22–28 weeks) AChE-positive fibres of thalamic origin penetrate the developing cortical plate of the auditory cortex.

Little is known about the development of the human entorhinal cortex (EC), a major hub in a widespread network for learning and memory, spatial navigation, high‐order processing of object information, multimodal integration, attention and awareness, emotion, motivation, and perception of time. We analyzed a series of 20 fetal and two adult human brains using Nissl stain, acetylcholinesterase (AChE) histochemistry, and immunocytochemistry for myelin basic protein (MBP), neuronal nuclei antigen (NeuN), a pan‐axonal neurofilament marker, and synaptophysin, as well as postmortem 3T MRI. In comparison with other parts of the cerebral cortex, the cytoarchitectural differentiation of the EC begins remarkably early, in the 10th week of gestation (w.g.). The differentiation occurs in a superficial magnocellular layer in the deep part of the marginal zone, accompanied by cortical plate (CP) condensation and multilayering of the deep part of CP. These processes last until the 13–14th w.g. At 14 w.g., the superficial lamina dissecans (LD) is visible, which divides the CP into the lamina principalis externa (LPE) and interna (LPI). Simultaneously, the rostral LPE separates into vertical cell‐dense islands, whereas in the LPI, the deep LD emerges as a clear acellular layer. In the 16th w.g., the LPE remodels into vertical cell‐dense and cell‐sparse zones with a caudorostral gradient. At 20 w.g., NeuN immunoreactivity is most pronounced in the islands of layer II cells, whereas migration and differentiation inside‐out gradients are seen simultaneously in both the upper (LPE) and the lower (LPI) pyramidal layers. At this stage, the EC adopts for the first time an adult‐like cytoarchitectural organization, the superficial LD becomes discernible by 3T MRI, MBP‐expressing oligodendrocytes first appear in the fimbria and the perforant path (PP) penetrates the subiculum to reach its molecular layer and travels along through the Cornu Ammonis fields to reach the suprapyramidal blade of the dentate gyrus, whereas the entorhinal‐dentate branch perforates the hippocampal sulcus about 2–3 weeks later. The first AChE reactivity appears as longitudinal stripes at 23 w.g. in layers I and II of the rostrolateral EC and then also as AChE‐positive in‐growing fibers in islands of superficial layer III and layer II neurons. At 40 w.g., myelination of the PP starts as patchy MBP‐immunoreactive oligodendrocytes and their processes. Our results refute the possibility of an inside‐out pattern of the EC development and support the key role of layer II prospective stellate cells in the EC lamination. As the early cytoarchitectural differentiation of the EC is paralleled by the neurochemical development, these developmental milestones in EC structure and connectivity have implications for understanding its normal function, including its puzzling modular organization and potential contribution to consciousness content (awareness), as well as for its insufficiently explored deficits in developmental, psychiatric, and degenerative brain disorders.

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During the period from 9 to 35 years of age, the ethmoidal cells form completely or partly the bottom of the anterior cranial fossa on both sides of the cribriform plate. These cells, not covered by the frontal bone, form a thin bony wall covered by the dura mater. This roof may show different shapes. In our material, consisting of 32 specimens from human skulls, the following variations were found: (1) openings with a smooth margin; (2) rarefactions; (3) openings with an irregular margin, and (4) cells with a thin wall. The openings with a smooth margin (5 specimens) had dimensions of 2–10 mm. They occurred as single or multiple formations on one or both sides of the ethmoidal roof. Rarefactions and openings with an irregular margin were found in seven specimens. Openings with an irregular margin could be an artefact due to destruction or maceration. In the openings with a smooth margin, a close contact between nasal mucous membrane and dura has to be expected. This fact may play an important role in inflammation of the ethmoidal labyrinth as well as in surgical interventions. A thin wall of the roof of ethmoidal cells and rarefactions may also present a danger during surgery.

The administration of aluminium to uraemic rats leads to aluminium accumulation in different brain regions. Aluminium intoxication significantly alters brain gangliosides, the content of which is increased in uraemic animals. This phenomenon can be prevented by administration of 24R,25-dihydroxyvitamin D3 (24,25(OH)2D3). Our results could possibly find an application in the prevention of aluminium-induced encephalopathy in patients on haemodialysis.

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