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        <title>Frontiers in Neuroanatomy | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/neuroanatomy</link>
        <description>RSS Feed for Frontiers in Neuroanatomy | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-14T19:07:55.817+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1822774</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1822774</link>
        <title><![CDATA[Stereological evaluation of the neuroprotective effects of curcumin on the spinal cord in a streptozotocin-induced diabetic rat model]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Burcu Delibaş</author><author>Ayşe İkinci Keleş</author><author>Arife Ahsen Kaplan</author><author>Berk Kocaman</author><author>Gamze Altun</author><author>Kıymet Kübra Tüfekci</author><author>Abit Aktaş</author><author>Süleyman Kaplan</author>
        <description><![CDATA[IntroductionThis study examined how curcumin influences spinal cord morphological parameters in rats with STZ-induced diabetes using unbiased stereological methods.MethodsFifty-six female Wistar albino rats were randomly divided into seven experimental groups (n = 8): Control, Sham, Curcumin, Diabetes Mellitus (DM), DM + Curcumin after 7 days (DC1), DM + Curcumin after 21 days (DC2), and DM + Curcumin simultaneously (DC3). Diabetes was induced via a single intraperitoneal dose of STZ (50 mg/kg). Curcumin was administered at a dose of 30 mg/kg via intragastric gavage for 14 consecutive days. C3–C5 spinal segments were collected at the end of the experiment, processed for histology, and stained with toluidine blue and cresyl violet for stereological analysis. Neuronal quantification in the anterior horn was performed using physical fractionator. The volume fractions of the spinal cord, including white matter (WM/total volume) and gray matter (GM/total volume), were estimated using the Cavalieri’s principle.ResultsThe diabetic (DM) group showed a significant reduction in motor neuron number compared with the Control group (p = 0.019), demonstrating diabetes-induced neuronal loss. In contrast, the DC2 treatment group showed a significant increase in motor neuron counts compared with DM (p = 0.04), suggesting a possible neuroprotective effect of curcumin. Total spinal cord volume did not differ significantly among groups. WM/Total ratio decreased in the Sham group but increased with curcumin (DC3). GM/Total ratio was lower in DC3 than Sham, and curcumin produced a non-significant improvement compared with diabetic rats. Increased caspase-3 immunoreactivity in the diabetic group indicates activation of apoptotic pathways, consistent with the observed reduction in motor neuron number and soma size. Furthermore, the marked increase in GFAP immunoreactivity, particularly in the DC2 group, reflects astrocyte activation and a reactive gliosis, which are commonly associated with metabolic stress and neuroinflammation in diabetic conditions.DiscussionCurcumin administration partially mitigated spinal motor neuron loss induced by experimental diabetes. The timing of curcumin treatment influenced its efficacy. These findings suggest that curcumin may have therapeutic potential for preventing diabetes-induced spinal cord neurodegeneration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1749335</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1749335</link>
        <title><![CDATA[Perisomatic innervation on the semilunar granule cells and outer molecular layer granule cells of the dentate gyrus of the mouse]]></title>
        <pubdate>2026-04-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Laura Rovira-Esteban</author><author>Isaac Vieco-Martí</author><author>Javier Herraiz-Cabanes</author><author>Emilio Varea</author><author>Juan Nacher</author><author>Carlos Crespo</author><author>José Miguel Blasco-Ibáñez</author>
        <description><![CDATA[Semilunar granule cells in the dentate gyrus represent a distinct type of granule cell, distinguished by their unique morphology and physiology. These cells are located within the inner molecular layer and the upper juxta-granule cell layer of the dentate gyrus. The presence of a smaller number of granule cells has also been observed in the outer molecular layer; however, the information regarding these cells is limited. In the present study, the perisomatic innervation that these two types of granule cells receive was characterized using confocal and electron microscopy. Our findings revealed that both semilunar granule cells and outer molecular layer granule cells receive substantial excitatory and inhibitory perisomatic contacts. The inhibitory contacts are derived from parvalbumin fast-spiking cells and cholecystokinin regular-spiking cells. The origin of excitatory contacts has been traced to hilar mossy cells and supramammillary afferents.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1794659</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1794659</link>
        <title><![CDATA[Pulvinar subdivisions and connectivity patterns across primate species: a comparative perspective]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Juliana G. M. Soares</author><author>Amaro R. A. Correia</author><author>Ricardo Gattass</author><author>Bruss Lima</author>
        <description><![CDATA[With the advances in our ability to perturb brain activity in recent years, new stimulation techniques have become essential tools in human neuroscience. Non-invasive stimulation methods, such as transcranial magnetic stimulation (TMS), as well as deep brain stimulation (DBS) delivered invasively to access deep brain structures, have been applied in both basic and clinical research and in the treatment of neurological conditions including Parkinson’s disease, essential tremor and epilepsy. In the context of epilepsy, neuromodulatory interventions have demonstrated encouraging results in reducing seizure frequency, bringing attention to the thalamic pulvinar nucleus as a potential target for stimulation in drug-resistant cases. To advance these and future therapies, it is necessary to have a more detailed understanding of the subdivisions and connectivity patterns of these nuclei. Although some human studies have employed diffusion imaging and fMRI, much of the current knowledge of pulvinar connectivity still comes from non-human primate (NHP) studies. The aim of this study is to review the cortico-pulvinar connectivity patterns of distinct pulvinar subregions across NHP species, alongside available human studies, to help optimize future basic and clinical research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1795807</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1795807</link>
        <title><![CDATA[Layer-specific cellular composition of mouse primary somatosensory and human temporal cortex: a direct 3D confocal counting approach]]></title>
        <pubdate>2026-04-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sergio Plaza-Alonso</author><author>Lidia Alonso-Nanclares</author><author>Silvia Tapia-González</author><author>Laura Fernández-García</author><author>Asta Kastanauskaite</author><author>Javier DeFelipe</author>
        <description><![CDATA[Accurate quantification of cellular composition is fundamental to understanding the structural and functional organization of the cerebral cortex. In the present study, we quantified the proportions of neurons, glia, and vascular cells (primarily endothelial cells) across the full cortical thickness (layers I–VI) of the mouse primary somatosensory cortex (S1HL) and the human temporal cortex (BA21) using immunocytochemical techniques and a direct 3D counting method. Over 25,000 cells in the mouse and 13,000 cells in the human cortex were individually identified and classified. For this purpose, we utilized EspINA software, which enables precise cell identification and volumetric analysis while preserving laminar and spatial context. Our results reveal marked species-specific differences in cellular proportions: neurons represent approximately 60% of all cells in the mouse S1HL but only 30% in the human BA21. These differences are reflected in the glia-to-neuron ratio (GNR) and non-neuron-to-neuron ratio (nNNR), which were consistently below 1.0 in the mouse (GNR: 0.4; nNNR: 0.6) but significantly higher in the human samples (GNR: 1.5; nNNR: 2.3). By overcoming the limitations of traditional stereological and tissue-homogenization techniques, this study provides a detailed laminar characterization of the cellular composition in these particular cortical regions (mouse S1HL and human BA21).]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1768036</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1768036</link>
        <title><![CDATA[A narrative review of motor control dual pathways: the corticospinal and reticulospinal tracts in synergy and differentiation]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yun Xing</author><author>Jiaxin Liu</author><author>Linrui Wu</author><author>Ke Zhang</author><author>Shengbo Yang</author>
        <description><![CDATA[The corticospinal tract (CST) and reticulospinal tract (RST) represent the core descending pathways within the central nervous system for motor control. This review elucidates the anatomical and functional interplay. Anatomically, the CST and RST fibers are spatially proximate within the spinal cord and are integrated into a continuous regulatory axis via the corticoreticular pathway. Functionally, they exhibit both synergy and specialization: the CST primarily governs contralateral distal limb fine motor control, whereas the RST, operating in a bilateral mode, regulates axial and proximal body movements, postural stability, and adaptation to strength training. Notably, following CST damage (e.g., stroke or spinal cord injury), the RST demonstrates remarkable plasticity and serves as a critical substrate for functional compensation and recovery. Furthermore, an imbalance in CST-RST function has been implicated in the pathophysiology of conditions such as post-stroke spasticity and multiple sclerosis. Therapeutic strategies targeting the CST-RST network, including neuromodulation and molecular interventions aimed at promoting axonal regeneration and modulating network excitability, present promising new directions for the treatment of neurological disorders. Future research should focus on deciphering the specific interactions at the spinal interneuron level to advance the development of precise rehabilitation strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1748518</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1748518</link>
        <title><![CDATA[Folic acid modulates the Notch1/NF-κB pathway in a rat model of lipopolysaccharide-activated hippocampal microglia]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Marwa Abd El-kader</author><author>Eman A. E. Farrag</author><author>Randa El-Gamal</author><author>Eman Mohamed El Nashar</author><author>Areej M. Alshehri</author><author>Rashid A. Aldahhan</author><author>Khulood M. Al-khater</author><author>Sara El-Desouky</author><author>M. W. El-Sherbeni</author><author>Neven A. Ebrahim</author>
        <description><![CDATA[IntroductionLipopolysaccharide (LPS) induces neuronal injury by stimulating microglia, which release pro-inflammatory markers and neurotoxic factors. Folate deficiency induces microglial activation and modulates nuclear factor-κB (NF-κB) p65 and neurogenic locus Notch homolog protein 1 (Notch1) expression in the hippocampus. This study investigated the neuroprotective effect of folic acid against LPS-induced neurotoxicity in rats, focusing on its modulation of microglial activation and the Notch1, NF-κB, and p65 signaling pathways.MethodsA total of 24 Sprague–Dawley male rats were assigned to four groups: control, folic acid, LPS, and folic acid + LPS. After sacrifice, the left cerebral hemisphere was subjected to histopathological assessment using hematoxylin and eosin (H&E) staining and immunohistochemical assessment using anti-GFAP, anti-Iba1, anti-cyclooxygenase-2 (COX-2), anti-tumor necrosis factor-α (TNF-α), and anti-NF-κB antibodies. The hippocampus was extracted from the right hemisphere and used to assess the gene expression of Notch1, TNF-α, interleukin-6 (IL-6), and COX-2 markers using real-time reverse transcription PCR.ResultsFolic acid ameliorated LPS-induced neuronal damage in the hippocampus, suppressed microglial activation (GFAP and Iba-1), downregulated Notch1 and NF-κB p65, and improved neuroinflammatory responses (TNF-α, IL-6, and COX-2), regardless of the region.ConclusionFolic acid exerted an equivalent neuroprotective effect in both the CA1 and CA3 regions by suppressing microglial activation and modulating the Notch1/NF-κB signaling pathway, thereby reducing neuroinflammation. These findings suggest that folic acid may serve as a potential adjuvant neuroprotective agent against inflammation-mediated neuronal injury.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1801873</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1801873</link>
        <title><![CDATA[Maternal gut dysbiosis is associated with altered enteric and cortical inhibitory circuit development]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mohammed M. Nakhal</author><author>Faheema Nafees</author><author>Ayishal B. Mydeen</author><author>Abdulaziz Al Ali</author><author>Sarah Baloch</author><author>Rawdha Alkhalaf</author><author>Hasan M. Albalas</author><author>Ghassan M. Albalas</author><author>Gadayer Alharbi</author><author>Yauhen Statsenko</author><author>Nour al-dain Marzouka</author><author>Mohammad I. K. Hamad</author>
        <description><![CDATA[IntroductionMaternal environmental factors critically influence neural circuit maturation during early development. The maternal gut microbiota has emerged as an important upstream regulator of offspring neurodevelopment, yet its role in shaping the structural organization of enteric and cortical inhibitory circuits remains poorly defined. Here, we examined whether gestational disruption of the maternal gut microbiota is associated with alterations in parallel enteric and cortical inhibitory circuit development.MethodsMaternal gut dysbiosis was induced in pregnant GAD67-GFP mice by oral vancomycin administration during gestation. Maternal and offspring microbiota were analyzed using full-length 16S rRNA gene sequencing to assess microbial diversity and vertical transmission. Offspring were examined at postnatal day 14 for intestinal morphology, altered barrier integrity, and enteric nervous system (ENS) organization. Cortical inhibitory circuits were analyzed by quantifying GAD67-positive interneuron density and performing three-dimensional morphological reconstruction in layers II/III of the somatosensory cortex, motor cortex, medial entorhinal cortex, and CA1 region of the hippocampus.ResultsMaternal dysbiosis significantly reduced microbial diversity and disrupted maternal–offspring microbial transmission. These changes were associated with impaired intestinal development, including reduced crypt height, thinning of the muscularis propria, fragmented Claudin-1 expression, and reduced Auerbach’s plexus area without changes in neuronal density, indicating altered enteric network organization. In the brain, maternal dysbiosis induced region-specific cortical vulnerability, with reduced dendritic length and branching of GAD67-positive interneurons in the somatosensory and motor cortices, while interneuron morphology in the medial entorhinal cortex and hippocampus was preserved. Interneuron density was selectively reduced in the motor cortex.DiscussionThese findings indicate that gestational maternal dysbiosis is associated with co-occurring structural alterations in intestinal and cortical inhibitory systems, selectively affecting inhibitory circuit architecture in sensorimotor regions. While the present model does not isolate microbiota-specific mechanisms from potential antibiotic-induced maternal physiological changes, the data support an association between disrupted maternal microbial ecology and offspring enteric and cortical neuroanatomical development during early postnatal life. These findings should be interpreted as descriptive associations and do not establish mechanistic gut–brain interactions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1749231</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1749231</link>
        <title><![CDATA[The effect of complex double-axis rotation model on GABAergic neurons in caudal ventrolateral medulla of rats along the vestibulo-sympathetic reflex pathway]]></title>
        <pubdate>2026-04-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jian Qi</author><author>Chen Chen</author><author>Qian Gao</author>
        <description><![CDATA[IntroductionMotion sickness is a common physiological disorder induced by with unusual movement exposure, characterized by conflicting motion signals that trigger vestibulo-sympathetic reflexes (VSR). These reflexes mediate autonomic responses to motion-induced stress. Previous studies have implicated the vestibular nucleus complex and the caudal ventrolateral medulla (CVLM) in VSR modulation. GABA (γ-aminobutyric acid), the primary inhibitory neurotransmitter in the central nervous system (CNS), plays a key role in both cardiovascular regulation and vestibular function. However, the specific contribution of GABAergic structures to motion sickness-related cardiovascular responses remains unclear.MethodsIn this study, we combined retrograde tracing and immunofluorescence labeling to investigate GABAergic pathways using complex double-axis rotation model. Fluoro-Gold (FG) was injected into the CVLM, while biotinylated dextran amine (BDA) was delivered to the medial vestibular nuclei (MVe).ResultsOur results revealed a bilateral distribution of GABAergic neurons, predominantly within the caudal raphe nuclei. Notably, a subset of these neurons was activated (as indicated by Fos immunoreactivity) and projected to the CVLM (as shown by retrograde labeling with FG) under complex double-axis rotation model. Furthermore, these same neurons also received direct inputs from the MVe, as evidenced by their labeling with BDA.DiscussionOur findings offer morphological evidence that GABAergic neurons in the caudal raphe nuclei participate in the cardiovascular responses evoked by motion sickness in a complex double-axis rotation model.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1779669</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1779669</link>
        <title><![CDATA[Neuroanatomical organization: the palato-pharyngeal complex as a sensory-motor hub]]></title>
        <pubdate>2026-03-30T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yong-Shin Hong</author><author>Young-Seok Park</author>
        <description><![CDATA[The pharynx has traditionally been described as a musculo-membranous conduit involved in respiration and deglutition. From a neuroanatomical perspective, however, this region also represents a multi-nerve interface where somatic afferents of the trigeminal nerve (V) and visceral afferents of the glossopharyngeal (IX) and vagus (X) nerves converge. In this review, we use the term Palato-Pharyngeal Complex (PPC) to describe this anatomically integrated region and discuss its potential role as a sensory–motor interface associated with brainstem circuits involving the nucleus tractus solitarius (NTS) and nucleus ambiguus (NA). We highlight the coordinated activity of the tensor veli palatini (innervated by V3) and the levator veli palatini (innervated by X) as an example of somatic–visceral motor integration within this region. Building on existing models of brainstem central pattern generators, we discuss a hierarchical control framework in which brainstem circuits may be modulated by supranuclear influences from cortical and limbic systems. Within this context, we introduce the concept of a Reflex–Volition Coupling (RVC) zone as a possible functional interface between reflexive brainstem rhythms and volitional or affective control. By integrating comparative and connectomic perspectives, this review outlines how branchial motor circuitry may support a range of behaviors including airway protection, vocalization, and speech. Together, these observations suggest that the PPC may represent an anatomically strategic interface linking peripheral cranial nerve afferents with brainstem integrative networks involved in arousal and behavioral coordination. This framework provides a basis for future studies exploring how oropharyngeal sensory pathways interact with central neural circuits.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1778296</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1778296</link>
        <title><![CDATA[A semi-automated pipeline integrating ImageJ/Fiji and StarDist for the reproducible quantification of cellular and optical density metrics in immunofluorescence images of brain tissue]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Technology and Code</category>
        <author>Sandra Isabel Marques</author><author>Helena Carmo</author><author>Félix Carvalho</author><author>João Pedro Silva</author><author>Susana Isabel Sá</author>
        <description><![CDATA[Quantitative immunofluorescence is widely used to assess molecular expression and cellular distribution across biological tissues, yet the analysis of large image datasets remains time-consuming and prone to user-dependent variability. To address these limitations, we herein developed a semi-automated workflow that integrates ImageJ/Fiji for image processing, StarDist for nuclear segmentation, and spreadsheet- or Python-based routines for data curation. The pipeline standardizes critical analytical steps, including scale calibration, region-of-interest (ROI) definition, channel selection, and z-stack handling, while preserving essential metadata through a structured file-naming system. Optical density and cell-number metrics are exported automatically in a consistent format, enabling efficient consolidation into a unified dataset. Subsequent curation can be performed either manually in a spreadsheet software or fully automatically through custom Python scripts, allowing extraction of sample identifiers, regions, and markers, as well as calculation of normalized intensity values. Comparison with existing protocols proved that this workflow adheres to widely accepted quantification principles while markedly improving reproducibility, consistency, and analytical throughput. This method offers a straightforward, transparent, and scalable solution for fluorescence-based quantification suitable for laboratories with varying levels of computational expertise.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1824372</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1824372</link>
        <title><![CDATA[Correction: Unveiling the mechanisms of neuropathic pain suppression: perineural resiniferatoxin targets Trpv1 and beyond]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Safa Shehab</author><author>Hayate Javed</author><author>Aishwarya Mary Johnson</author><author>Saeed Tariq</author><author>Challagandla Anil Kumar</author><author>Bright Starling Emerald</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1754934</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1754934</link>
        <title><![CDATA[Justo Gonzalo (1910–1986): a pioneer of brain dynamics]]></title>
        <pubdate>2026-03-18T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Isabel Gonzalo-Fonrodona</author>
        <description><![CDATA[The present work offers an overview of the pioneering contributions of the neuroscientist Justo Gonzalo to the study of the human cerebral cortex, within the historical context of his time and in relation to current research. Gonzalo initially trained under Gonzalo Rodríguez Lafora (a disciple of Santiago Ramón y Cajal) and always maintained a close relationship with him and his circle, connecting him to the Spanish Neurological School (Cajal’s school). He also trained in neurology in Austria and Germany (1933–1935). The research he called brain dynamics began during the Spanish Civil War (1936–1939) in a military hospital in Valencia, based on the study of patients with war-related brain injuries. Based on physiological criteria, Gonzalo described what he termed central syndrome of the cortex: a multisensory and bilaterally symmetrical disorder caused by a unilateral parieto-occipital cortical lesion in an associative area. He brought to light singular perceptual phenomena, and was the first to study inverted or tilted perception (visual, tactile, and auditory), the improvement of perception through increased stimulus intensity or the presence of additional stimuli, as well as other phenomena that remain little known today. These findings and the study of different cortical syndromes led Gonzalo to propose that the specificity of brain functions is gradually distributed throughout the cerebral cortex, giving rise to cortical gradients, whose overlap would result in fairly nonspecific or multisensory adaptive regions. This unitary approach went beyond the rigid cortical parcellation for the anatomical localization of brain functions, and is closely aligned with current studies. The interpretation of the central syndrome as analogous to the normal case, but with reduced excitability, led Gonzalo to apply scaling concepts that enabled him to develop formalizations and generalizations. He conducted this research in Spain, under very difficult conditions, with the support of the Cajal Institute. Despite the excellent international reception of his works in Spanish during the 1940s and 1950s, his contributions are scarcely known today due to the lack of timely publications in other languages. The publication of his works in English in 2023 has partially filled this gap.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1783101</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1783101</link>
        <title><![CDATA[Foxp2 mutations and abnormal brain and gastrointestinal development: insights from animal models of speech-language and autism spectrum disorders]]></title>
        <pubdate>2026-03-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Eriko Fujita-Jimbo</author><author>Genri Kawahara</author><author>Takashi Momoi</author>
        <description><![CDATA[Autism spectrum disorder (ASD) and speech and language disorder (SLD) are distinct neurodevelopmental conditions, yet both share overlapping communication impairments. Forkhead box P2 (FOXP2), a key transcription factor involved in speech and language development, harbors pathogenic mutations such as R553H, which cause SLD and have been suggested to contribute to aspects of ASD-related phenotypes. This review synthesizes insights from animal models to explore the molecular mechanisms by which Foxp2 mutations disrupt the development of the cerebral cortex, thalamus, and enteric nervous system. We highlight findings from heterozygous Foxp2 mutants and discuss severe phenotypes observed in homozygous Foxp2 mutants (Foxp2R552H/R552H and Foxp2R552H/R552H/mCherry-Tg mice), including profound ultrasonic vocalization deficits, brain malformations, and early lethality. Notably, these mice exhibit gastrointestinal abnormalities involving the epithelium, smooth muscle, and enteric nervous system, which are linked to impaired autoregulation and interference with Wnt signaling during development. Such observations underscore the relevance of the brain–gut–microbiome axis and Hirschsprung-like pathology in neurodevelopmental disorders. Finally, this review discusses future directions using gene-editing approaches in non-mammalian models—zebra finches, zebrafish, and Drosophila—to dissect neural networks underlying intellectual disability and communication deficits. Collectively, these studies provide a framework for understanding FOXP2-related molecular mechanisms in the pathogenesis of ASD and SLD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1768392</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1768392</link>
        <title><![CDATA[Age-related dopaminergic integrity in the SNpc and VTA: morphometric and volumetric findings in marmoset (Callithrix jacchus)]]></title>
        <pubdate>2026-03-10T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Maria M. O. Azambuja</author><author>Nelyane N. M. de Santana</author><author>Paulo L. A. G. Morais</author><author>Gabriel A. M. Vasiljevic</author><author>Jeferson S. Cavalcante</author><author>Adhil Bhagwandin</author><author>José R. L. P. Cavalcanti</author><author>Rovena Clara Engelberth</author>
        <description><![CDATA[Given a convergence of evidence indicating age-related vulnerability in nuclei associated with basal ganglia circuits, understanding the pattern of normal aging in non-human primates is essential for basic and applied research. To address this, we examined the age-dependent vulnerability of dopaminergic cells in the substantia nigra pars compacta (SNpc) and ventral tegmental area (VTA) of marmoset through morphoquantitative analysis of cytoarchitecture. Thus, we selected brain tissue from adult and aged marmosets processed for tyrosine hydroxylase (TH) immunohistochemistry. We estimated regional volume and counted TH-immunopositive (TH+) neurons in the SNpc and VTA. Statistical comparisons used permutation tests and Spearman’s tests to analyze differences between age groups. Although Spearman’s correlation test showed a negative correlation between regional volume and age and between TH+ cell number and age, no significant differences were found in either the permutation test or Spearman’s correlation for TH + neuronal number and for regional volume between the age groups for both nuclei. We concluded that aging in marmosets does not lead to significant loss of dopaminergic neurons or measurable volumetric reduction in the SNpc or VTA. Our results highlight the importance of understanding physiological aging in contrast to models characterized by structural degeneration, such as those found in pathological conditions. Understanding, in a promising experimental model as marmoset, the pattern of vulnerability and resilience of dopaminergic regions fills gaps in the literature and opens avenues for understanding molecular and functional changes related to aging.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1771439</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1771439</link>
        <title><![CDATA[Heterogeneity of astrocyte density, morphology and connexins in the mouse hippocampus]]></title>
        <pubdate>2026-03-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Annika Uelwer</author><author>Mamitha Sivakumar</author><author>Khojimurod Umirdinov</author><author>Fathima Faiba A. Purath</author><author>Lensa Oluma</author><author>Max Anstötz</author><author>Charlotte von Gall</author><author>Amira A. H. Ali</author>
        <description><![CDATA[The hippocampal formation is crucial for episodic learning and memory. In addition to neurons, astrocytes have also received increasing attention in recent years as essential components of brain networks by regulating the blood-brain barrier, eliminating waste products via the glymphatic system, supporting neuronal activity by providing energy supply and metabolic substrates, and regulating extracellular neurotransmitter levels. Astrocytes are heterogeneous and highly dynamic cells that respond to neuronal activity and dysfunction via morphological and functional changes. Astrocytic connexins (Cx) 30 and 43 form the molecular basis for gap junctions and hemichannels and are, thus, central to coupling, intercellular communication and network integration of astrocytes in the brain. However, little is known about the spatial heterogeneity of astrocyte density, morphology and Cx expression in the subregions and layers of the hippocampus. Therefore, in this study, we used immunohistochemistry to analyze the density and detailed morphological features of astrocytes and the spatial distribution of Cx30 and Cx43 in the layers of CA1, CA3 and dentate gyrus (DG). Astrocyte density correlated positively with the intensity of Cx30- and Cx43-immunoreaction (Ir). The stratum lacunosum moleculare (SLM) of CA1 and CA3 and the subgranular zone (SGZ) of DG showed the highest density of GFAP-positive (+) astrocytes and the strongest Cx30- and Cx43-Ir. The GFAP+ astrocytic processes had the largest radial extent in the pyramidal layer of CA1 and CA3 and in the granular layer of the DG. Our study provides a comprehensive anatomical and comparative mapping of astrocytic density, morphology and Cx distribution in the mouse hippocampus and provides an important basis for further studies on the dynamics of neuron-glial interaction under different physiological and pathological conditions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1783250</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1783250</link>
        <title><![CDATA[Prefrontal contributions to the executive control of visuospatial working memory across primate species]]></title>
        <pubdate>2026-03-09T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Louise Inger</author><author>Maureen A. Hagan</author>
        <description><![CDATA[The ability to gain volitional control over our thoughts and actions to perform goal directed behaviors is largely owed to working memory (WM). WM is a highly distributed process requiring multiple integrated brain regions. The brain regions employed in WM are in part dependent on the sensory input to be remembered. For instance, visual and posterior parietal areas are critical for spatial WM. However, the prefrontal cortex (PFC) appears to be the node at which all of these brain regions converge on in WM, regardless of the sensory input. Understanding how the PFC has evolved to mediate spatial WM across primate species creates a powerful gateway to providing translational insight into human WM processing. This mini-review will discuss three key neuroanatomical regions of the PFC thought to be involved in the executive control of spatial WM - the dorsolateral prefrontal cortex (DLPFC), the ventrolateral prefrontal cortex (VLPFC), and the frontal eye fields (FEF). In particular, the review will focus on comparison of these regions between humans, macaques, and marmosets to determine the reliability of studying these WM brain regions across species.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1780361</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1780361</link>
        <title><![CDATA[Postnatal expression of the transcription factor Ebf2 in motivation, reward, and pain-related circuits of the mouse brain]]></title>
        <pubdate>2026-03-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Moisés Martínez-Estrada</author><author>M. Blanca D. Cepeda-Varela</author><author>A. Damaris Salinas-Villarreal</author><author>Mara C. Obregón-Fuentes</author><author>Danna A. Real-Marín</author><author>Melani A. Balderas-Díaz</author><author>Viviana Zomosa-Signoret</author><author>Jesús Santana-Solano</author><author>Moisés Santillán-Zerón</author><author>Román Vidaltamayo</author>
        <description><![CDATA[IntroductionEarly B-cell factor 2 (Ebf2) is a transcription factor required for neuronal differentiation. However, its postnatal expression pattern and functional roles in the brain are not well characterized. This study examined the spatial distribution of Ebf2 in postnatal day 10 (P10) mouse brains and investigated its association with neural circuits mediating motivation, reward, and nociception.Materials and methodsEbf2-TGFP transgenic mice, which express green fluorescent protein (GFP) as a reporter for Ebf2, were utilized. Immunofluorescence labeling and high-resolution microscopy were employed to visualize Ebf2 expression. Image data were analyzed using a deep learning–based segmentation pipeline for soma and axon identification. Three-dimensional reconstructions were registered to the Allen Brain Atlas. Quantitative comparisons between hemizygous and Ebf2-null mutant genotypes were conducted using linear mixed-effects models with Bonferroni and false discovery rate (FDR) corrections.ResultsEbf2 expression was prominent in the dorsal diencephalic conduction system, including the septum, habenula, and interpeduncular nucleus. Ebf2 expression can also be detected in the lateral hypothalamic area, zona incerta, ventral tegmental area, and parabrachial nucleus. Expression was also detected in nociceptive and sensory-motor regions such as the periaqueductal gray, anterior pretectal nucleus, principal sensory nucleus of the trigeminal nerve, and superior colliculus. Ebf2-null mutant mice showed a significant reduction in Ebf2-TGFP cells across most of these regions.DiscussionThe results demonstrate that Ebf2 expression persists beyond embryonic development and is selectively enriched in neural circuits associated with motivation, reward processing, and nociceptive modulation. The marked reduction of Ebf2-TGFP expressing neurons in null mutants provides evidence for a postnatal requirement of Ebf2 in neuronal maintenance, rather than solely in early differentiation. Collectively, these findings broaden the functional scope of Ebf2 to include postnatal circuit stabilization and support its sustained regulatory role in brain systems that govern affective and pain-related behaviors.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1758626</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1758626</link>
        <title><![CDATA[Arterial supply of the interpeduncular part of the human oculomotor nerve]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Samra Hajrović</author><author>Ema Bexheti</author><author>Aleksandra Dožić</author><author>Sadi Bexheti</author><author>Dejan Ćetković</author><author>Helena Marić Kujundžić</author><author>Marko Simić</author><author>Sonja Milašinović</author><author>Uroš Mirčić</author><author>Zdravko Vitošević</author><author>Milan Milisavljević</author><author>Aleksandar Mirčić</author><author>Mila Ćetković</author>
        <description><![CDATA[The aim of this study was a detailed examination of the arterial vascularization of the interpeduncular cisternal part (ICP) of a proximal segment of the human oculomotor nerve (ON). The blood vessels of the ONs were carefully microdissected and studied in 30 brain hemispheres using 6.3× to 20× magnification of the stereoscopic microscope. The arteries were injected with the mixture of 10% India ink and gelatin. For better understanding, one brainstem specimen was prepared following a histological procedure, transversely serially cut into 5-μm thick slices, and stained with Luxol fast blue. Another injected midbrain specimen was cut in 1-mm-thick transverse sections, completely cleared with methylsalycilate, and analyzed under transmitted light. The common oculomotor arteries (COAs) and the small oculomotor branches, which participate in the vascularization of the dorsal and ventral surfaces of the ICPs of ONs, were analyzed and their diameters were measured. The dorsal COA was present in 83.33% of the ONs, one per nerve, with an average diameter of 213.57 μm. The ventral COAs were found in 76.67% of the ONs, one per nerve, with an average diameter of 137.64 μm. The mean diameter of the dorsal COAs was significantly higher than the mean diameter of the ventral COAs (p < 0.001). The oculomotor fine central vessels supplied the oculomotor root exit zone (OREZ) with the central type of myelin, and distally, fascicles of the rest of ICS with the peripheral type of myelin. The results describing the ON arteries may have diagnostic and microsurgical significance. The lack of detailed morphological analysis of the dorsal region related to the ventral arterial vessels of the ICP, along with measurements of the oculomotor arterial diameters, guided us to conduct this anatomical research to improve diagnostic procedures and the quality of microsurgical interventions in this region.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1717532</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1717532</link>
        <title><![CDATA[Search for marker proteins to assess blood–brain barrier development]]></title>
        <pubdate>2026-02-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yukari Shigemoto-Mogami</author><author>Kimiko Nakayama-Kitamura</author><author>Kaoru Sato</author>
        <description><![CDATA[The blood–brain barrier (BBB) separates the central nervous system from the peripheral blood circulation, and performs various functions such as dictating central nervous system (CNS)-specific pharmacokinetics, and maintaining brain homeostasis. While previous studies have clarified the mechanisms underlying cerebrovascular network development, details regarding in vivo BBB maturation remain unknown. In this regard, we previously reported that the development of physical tightness of the BBB and the formation of perivascular glial structures begins on postnatal day 4 and is almost complete by postnatal day 15. Moreover, the difficulty in predicting BBB permeability has hindered the development of CNS drugs, and microphysiological systems (MPSs) that mimic the BBB have been extensively developed to address this issue. Building on this information, in this study, we examined the temporal expression patterns of vascular proteins (CD31, Tie2, CD34, CD146, and agrin), tight junction proteins (ZO-1, claudin-5, and occludin), transporters (P-gp, BCRP, and Glut1), and transferrin receptors (TfRs) during the postnatal period, along with the development of BBB tightness. Based on their temporal expression patterns, these proteins were divided into five groups. We selected representative proteins from groups 1–5, respectively, and examined the temporal expression changes to determine the developmental stage of the BBB. The expression patterns of these proteins can be used to determine the maturation stage of BBB-MPSs.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnana.2026.1768558</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnana.2026.1768558</link>
        <title><![CDATA[A novel methodology for localizing pallidal deep brain stimulation leads]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Methods</category>
        <author>Benjamin Pobiel</author><author>Kevin J. O’Neill</author><author>Remi Patriat</author><author>Tara Palnitkar</author><author>Meghan E. Hill</author><author>Rachel C. Cole</author><author>Henry Braun</author><author>Stephanie L. Alberico</author><author>Biswaranjan Mohanty</author><author>Devyn Bauer</author><author>Michael C. Park</author><author>Scott E. Cooper</author><author>Jerrold L. Vitek</author><author>Noam Harel</author><author>Joshua E. Aman</author>
        <description><![CDATA[IntroductionPositioning of deep brain stimulation (DBS) leads is paramount for optimizing therapeutic efficacy in Parkinson’s disease (PD) and dystonia. Quantitative determination of lead position remains essential; however, current atlas-based targeting and stereotactic coordinate methods, while informative, limit patient specificity afforded by high-resolution reconstruction and introduce subjective variability.MethodsWe developed a novel pipeline in Unity™ to ingest 7T MRI-based reconstructions of DBS leads within the globus pallidus internus (GPi). Using anatomical landmarks and structure-specific algorithms, the GPi was parcellated into 12 anatomically-based subregions in a semi-automated, reproducible manner. Active contact positions were localized relative to a novel coordinate system developed from a GPi-based bounding box. A novel distance-to-border metric remapped contacts onto a common atlas (PD25) for population comparison against the same contacts mapped onto a common left GPi space using mid-commissural point (MCP) coordinates (Schaltenbrand-Wahren atlas).ResultsFifteen leads from 10 PD subjects were used for ellipsoid fitting of active contact locations, resulting in an elliptical volume of 38.94 mm3 when using MCP coordinates, compared to a volume of 5.08 mm3 with our GPi-specific coordinates. The mean distance-to-ellipse centroid was 3.45 ± 1.57 mm for MCP coordinates and 2.03 ± 0.82 for our GPi-specific coordinates. Our distance-to-border remapping metric yielded mean adjustments of 0.81 mm (y-axis) and 1.61 mm (z-axis). A subset of six GPi active contacts were plotted with post-DBS motor improvement scores, demonstrating the ability to link lead location with clinical outcomes.ConclusionOur novel software provides a quantifiable lead location with respect to the anatomical target, enhancing patient-specific lead localization by avoiding some of the pitfalls of either structure-to-atlas normalization or traditional stereotactic coordinates.]]></description>
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