Frontiers in Neuroanatomy最新文献

Even though bats are the second most speciose group of mammals, neuroanatomical studies of their hippocampus are rare, particularly of small echolocating bats. Here, we provide a qualitative and quantitative neuroanatomical analysis of the hippocampus of small echolocating bats (Phyllostomidae and Vespertilionidae). Calcium-binding proteins revealed species- and family-specific patterns for calbindin and calretinin. Interneuron staining for both proteins was very rare in phyllostomids, while calretinin marked subpopulations of CA3 pyramidal neurons in both families. Parvalbumin expression was consistent across bats and similar to other species. A unique calretinin-positive calbindin-negative zone was observed at the superficial boundary of the CA3 pyramidal cell layer in phyllostomid bats. This zone defined a gap between pyramidal cells and the zinc-positive mossy fibers. We hypothesize that this gap might either stem from calretinin-positive afferents displacing the zinc-positive mossy fiber boutons, or from a complete segregation of neurochemically distinct mossy boutons. Furthermore, we observed a distinct dorsoventral shift in the length of the upper and lower blade of the granule cell layer in all species. In terms of hippocampal neuron numbers, bats were characterized by a rather small granule cell and subicular neuron population, but a well-developed CA3. In a correspondence analysis, preferred diet segregated phyllostomids into a hilus-dominant omnivorous and frugivorous species group, and a subiculum-dominant group containing vampire bats and nectivorous species. Although the two families overlapped considerably, the cellular composition of the phyllostomid hippocampus can be described as output dominant, while in vespertilionids neuron populations on the hippocampal input side are more dominant. Neuroanatomical and ecological variability and unique traits within echolocating bats as shown here can provide a rich source for investigating structure-function relationships.

Background: Pacinian corpuscles (PCs) are pressure- and vibration-sensitive mechanoreceptors found in hairless skin, external genitalia, joints, ligaments, lymph nodes, prostate, bladder, etc. While they are documented in the pancreas of cats, their presence in the normal pancreas remains speculative.

Purpose: The present study therefore investigated the distribution of PCs in the normal human pancreas and compared the findings with those in several other animal species.

Methods: The study subjects included 74 human cadaver specimens, 3 Cynictis penicillata, 2 Saguinus mystaxs, 1 Felis domesticus, and 10 Suncus murinus. Pancreatic tissues were prepared as paraffin sections for histological and immunohistochemical analyses of the main constituents of PCs (central axon, inner core, and outer core capsule).

Results: PCs were found in the pancreas of five human cadavers (7%), as well as in one C. penicillata, one S. mystax and one F. domesticus but not in S. murinus. The PCs varied in size, with the largest in the human pancreas measuring up to 1,106 μm-far exceeding those in animal pancreata, but less numerous than those in animals. Morphologically, animal PCs were mainly typical oval shapes, whereas PCs in the human pancreas were mostly irregular in shape. In addition, we found that PCs in animals and human pancreata had similar structures, with consistent expression of protein gene product 9.5, in axonic profiles, and diffuse vimentin immunoreactivity in the inner core, outer core, and capsule.

Conclusion: This study confirmed the presence of PCs in a small number of healthy humans and some animal pancreata. The number, distribution characteristics, and morphology of PCs in the pancreata of animals and humans are quite different; however, their structures and immunohistochemical profiles are similar. The presence of PCs in the normal human pancreas is also a mystery, and the physiological role of PCs in the human pancreas requires further clarification.

[This corrects the article DOI: 10.3389/fnana.2025.1649700.].

Huntingtin-associated protein 1 (HAP1) is a crucial component of the stigmoid body (STB) and is recognized as a neuroprotective interactor with causative proteins for several neurodegenerative disorders (NDs). Due to HAP1 protectivity, brain regions rich in STB/HAP1 are typically shielded from neurodegeneration, whereas areas with little or no STB/HAP1 are often affected in NDs. Mounting evidence suggests that serotonin (5-HT) neuron dysfunction contributes to various NDs. While the raphe nuclei denote the origin of 5-HT neurons, HAP1 protectivity has yet to be determined there. To accomplish this, the present study evaluated the expression and detailed neuroanatomical distribution of HAP1 throughout the rostral and caudal clusters of raphe nuclei in adult mice brains and their morphological relationships with 5-HT by employing Western blotting and immunohistochemistry. Our results indicated that in the rostral cluster, HAP1-ir cells were extensively distributed across the caudal linear raphe, median raphe, dorsal raphe, supralemniscal raphe, caudal part of the dorsal raphe, pre-pontine and pontine raphe nuclei. In the caudal cluster, HAP1-ir neurons were disseminated throughout the raphe magnus, raphe obscurus, raphe pallidus, parapyramidal, and raphe interpositus nuclei. Our double-immunofluorescence labeling results confirmed that most of the 5-HT neurons contained HAP1 immunoreactivity throughout the rostral and caudal clusters of the raphe nuclei. These suggest that HAP1 is crucial for modulating/protecting serotonergic functions, plausibly by upholding 5-HT neuronal plasticity/integrity by raising the threshold for neurodegeneration. Our current findings might provide a fundamental basis for further research aimed at elucidating the role of STB/HAP1 in the pathophysiology of serotonin neurons.

The glial fibrillary acidic protein (GFAP) is the principal intermediate filament protein and histochemical marker for astroglia. It appears contradictory that there are extended GFAP-poor or even GFAP-free areas in the brains of various vertebrate clades: cartilaginous and ray-finned fishes, and amniotes. The "Relevant Subsections: Extended GFAP-free areas in various vertebrates" section in this study reviews our GFAP mapping studies on the brains of 58 species within these clades, as well as mappings from other authors, and demonstrates that these areas appeared independently from one another in the more advanced groups of different clades; it raises the supposition that the lack of GFAP is an apomorphic phenomenon. The GFAP expression has withdrawn mainly relatively: the GFAP-immunonegative areas increased more than the immunopositive ones. Primarily, regions that expanded and increased in complexity during evolution lack GFAP immunopositivity (except for their perivascular glia). The absence of GFAP expression, however, does not indicate the lack of astroglia. In the areas immunonegative to GFAP, astrocytes were visualized using other markers, such as glutamine synthetase or S-100 protein. In birds and mammals, lesions induced GFAP expression in these areas. It shows that the ability to express GFAP is not lost but has become facultative. These data suggest that the lack of GFAP production may provide an evolutionary advantage. The "Discussion" section relates the GFAP "withdrawal" to other steps of evolution: the increasing complexity and thickening of the brain wall, as well as the appearance of the astrocytes, particularly protoplasmic astrocytes, and then examines the proposed evolutionary advantages and disadvantages of the absence of GFAP. The role of the relative "withdrawal" of GFAP expression in brain evolution remains to be definitively answered. The most probable candidates may include the absence of synthesizing an unnecessary protein, improved adaptation of astrocytes to the demands of neurons, and an increased capacity for synaptic plasticity. In contrast, one must consider that the withdrawal of GFAP may not be a primary phenomenon but rather a consequence of the evolution of neural networks.

The pituitary gland is central to endocrine regulation in vertebrates, coordinating key physiological processes such as growth, reproduction, and stress responses. In cetaceans, and particularly in large odontocetes like orcas (Orcinus orca), understanding pituitary structure is essential for advancing neuroendocrine research and informing welfare and health assessments. Despite their ecological, cognitive, and conservation significance, detailed morphological studies of the orca pituitary gland remain scarce. In this study, we conducted a comprehensive structural and ultrastructural analysis of the orca pituitary gland using postmortem samples from four captive individuals. We combined computed tomography, histology, immunohistochemistry, and transmission electron microscopy to examine the gland's anatomical organization and cellular composition. Our results reveal features consistent with other cetaceans as well as species-specific characteristics, including the distribution and morphology of endocrine cells within the adenohypophysis and neurohypophysis. These findings provide the first integrated anatomical and ultrastructural reference for the orca pituitary gland, offering valuable insights into cetacean neuroendocrinology and supporting improved species-specific welfare evaluation, health monitoring, and management practices for orcas under human care.

Introduction: The cerebellar cortex is now recognized as a functionally heterogeneous brain region involved not only in traditional motor functioning but also in higher-level emotional and cognitive processing. Similarly, cerebellar astrocytes also display a high degree of morphological and functional diversity based on their location. Yet, the morphological features and distribution of cerebellar astrocytes have yet to be quantified in the human brain.

Methods: To address this, we performed a comprehensive postmortem examination of cerebellar astrocytes in the healthy human brain using microscopy-based techniques. Purkinje cells (PCs) were also quantified due to their close relationship with Bergmann glia (BG). Using canonical astrocyte markers glial fibrillary acidic protein (GFAP) and aldehyde dehydrogenase-1 family member L1 (ALDH1L1), we first mapped astrocytes within a complete cerebellar hemisphere.

Results: Astrocytes were observed to be differentially distributed across cerebellar layers with their processes displaying known morphological features unique to humans. Stereological quantifications in three functionally distinct lobules demonstrated that the vermis lobule VIIA, folium displayed the lowest densities of ALDH1L1+ astrocytes compared with lobule III and crus I. Assessing cerebellar layers showed that the PC layer had the highest ALDH1L1+ densities while GFAP+ densities and astrocytes colocalizing (ALDH1L1+ GFAP+) were highest in the granule cell layer yet displayed the smallest GFAP-defined territories. PC parameters revealed subtle differences across lobules, with vermis folium VIIA having the lowest PC densities while a trend for the highest BG:PC ratio was observed in the cognitive lobule crus I. Lastly, to determine if these features differ from those of cerebellar astrocytes and PCs in species used to model human illnesses, we performed comparative analyses in mice and macaques showing both divergence and commonalities across species.

Discussion: The present study highlights the heterogeneity of astrocytes in the human cerebellum and serves as a valuable resource on cerebellar astrocyte and PC properties in the healthy human brain.

Introduction: Mutations in the methyl-CpG-binding protein-2 gene (MECP2), which cause Rett syndrome (RTT), disrupt neuronal activity; however, the impact of the MECP2 loss-of-function on the cytoarchitecture of medial entorhinal cortex layer II (MECII) neurons-crucial for spatial memory and learning-remains poorly understood.

Methods: In this study, we utilized Golgi staining and neuron tracing in the Mecp2^+/- mouse model of RTT to investigate the pyramidal and stellate cell alterations in MECII.

Results and discussion: Our findings revealed that pyramidal cells displayed a significant reduction in apical dendritic length, soma size, and spine density, while basal dendrites showed increased dendritic complexity and branching. On the other hand, stellate cells exhibited dendritic hypertrophy along with increased soma size, primary dendrites, and localized increase in dendritic intersections, despite an overall reduction in total dendritic length and spine density. These findings underscore the notion that MECP2 loss-of-function can disrupt MECII pyramidal and stellate cell cytoarchitecture in a cell-type-specific manner, emphasizing its critical role in maintaining proper dendritic morphology in circuits, which is crucial for learning and memory.