The developmental mechanism that contributes to the highly organized axonal connections within the cerebral cortex is not well understood. This is partly due to the lack of molecular markers specifically expressed in corticocortical associative neurons during the period of circuit formation. We have shown previously that latexin, a carboxypeptidase A inhibitor, is expressed in intrahemispheric corticocortical neurons from the second postnatal week in the rat (Arimatsu et al. [1999] Cereb. Cortex 9:569-576). In the present study, we first demonstrate in the adult rat that the orphan nuclear receptor Nurr1 is coexpressed in latexin-expressing neurons located in layer V, sublayer VIa, and the white matter of the lateral sector of the neocortex, and also in latexin-negative early born neurons in sublayer VIb of the entire neocortex. Virtually all Nurr1-expressing neurons exhibit immunoreactivity for phosphate-activated glutaminase but not for gamma-aminobutyric acid, suggesting that they are glutamatergic-excitatory neurons. By combining Nurr1 immunohistochemistry and 5-bromo-2'-deoxyuridine-birthdating, we then show that Nurr1 is expressed in (early born) subplate neurons and (later born) presumptive latexin-expressing neurons from embryonic day 18 onward. Finally, by combination of Nurr1 immunohistochemistry and retrograde tracing, we show that Nurr1-expressing neurons, including those in sublayer VIb, contribute predominantly to long-range intrahemispheric corticocortical projections. These results raise the possibility that Nurr1 plays a role in the establishment and maintenance of normal corticocortical circuitry and function.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1002/cne.10875 | DOI Listing |
Neurol Res Pract
January 2025
Institute of Clinical Epidemiology and Biometry, Julius-Maximilians-Universität Würzburg (JMU), Haus D7, Josef-Schneider-Straße 2, 97080, Würzburg, Germany.
Background: Comprehensive clinical data regarding factors influencing the individual disease course of patients with movement disorders treated with deep brain stimulation might help to better understand disease progression and to develop individualized treatment approaches.
Methods: The clinical core data set was developed by a multidisciplinary working group within the German transregional collaborative research network ReTune. The development followed standardized methodology comprising review of available evidence, a consensus process and performance of the first phase of the study.
Stem Cell Res Ther
January 2025
Department of Neurosurgery, The First Medical Centre, Chinese PLA General Hospital, Beijing, 100853, China.
Background: Closed head injury (CHI) provokes a prominent neuroinflammation that may lead to long-term health consequences. Microglia plays pivotal and complex roles in neuroinflammation-mediated neuronal insult and repair following CHI. We previously reported that induced neural stem cells (iNSCs) can block the effects of CXCL12/CXCR4 signaling on NF-κB activation in activated microglia by CXCR4 overexpression.
View Article and Find Full Text PDFActa Neuropathol Commun
January 2025
Department of Physiology and Pharmacology, Sapienza University of Rome, 00185, Rome, Italy.
The generation of retinal models from human induced pluripotent stem cells holds significant potential for advancing our understanding of retinal development, neurodegeneration, and the in vitro modeling of neurodegenerative disorders. The retina, as an accessible part of the central nervous system, offers a unique window into these processes, making it invaluable for both study and early diagnosis. This study investigates the impact of the Frontotemporal Dementia-linked IVS 10 + 16 MAPT mutation on retinal development and function using 2D and 3D retinal models derived from human induced pluripotent stem cells.
View Article and Find Full Text PDFBMC Pharmacol Toxicol
January 2025
Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin, 240003, Nigeria.
Background: Glia mediated neuroinflammation and degeneration of inhibitory GABAergic interneurons are some of the hall marks of pyrethroid neurotoxicity. Here we investigated the sex specific responses of inflammatory cytokines, microglia, astrocyte and parvalbumin positive inhibitory GABAergic interneurons to λ-cyhalothrin (LCT) exposures in rats.
Methods: Equal numbers of male and female rats were given oral corn oil, 2 mg/kg.
Mol Neurodegener
January 2025
The Picower Institute for Learning and Memory, Cambridge, MA, USA.
Many diseases and disorders of the nervous system suffer from a lack of adequate therapeutics to halt or slow disease progression, and to this day, no cure exists for any of the fatal neurodegenerative diseases. In part this is due to the incredible diversity of cell types that comprise the brain, knowledge gaps in understanding basic mechanisms of disease, as well as a lack of reliable strategies for delivering new therapeutic modalities to affected areas. With the advent of single cell genomics, it is now possible to interrogate the molecular characteristics of diverse cell populations and their alterations in diseased states.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!