Neurotrophins have been proposed to mediate several forms of activity-dependent competition in the central nervous system. A key element of such hypotheses is that neurotrophins act preferentially on active neurons; however, little direct evidence supports this postulate. We therefore examined, in ferret cortical brain slices, the interactions between activity and neurotrophins in regulating dendritic growth of layer 4 pyramidal neurons. Inhibition of spontaneous electrical activity, synaptic transmission, or L-type calcium channels each prevented the otherwise dramatic increase in dendritic arborizations elicited by brain-derived neurotrophic factor. In developing cortex, this requirement for conjoint neurotrophin signaling and activity provides a mechanism for selectively enhancing the growth and connectivity of active neurons.
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http://dx.doi.org/10.1016/s0896-6273(00)80239-1 | DOI Listing |
J Immunother Cancer
January 2025
Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu, China
Background: Siglec-E is an immune checkpoint inhibitory molecule. Expression of Siglec-E on the immune cells has been shown to promote tumor regression. This study aimed to develop an adenovirus (Ad) vaccine targeting Siglec-E and carbonic anhydrase IX (CAIX) (Ad-Siglec-E/CAIX) and to evaluate its potential antitumor effects in several preclinical renal cancer models.
View Article and Find Full Text PDFeNeuro
January 2025
University of Rochester Medical Center, Department of Neuroscience,
A unique pool of immature glutamatergic neurons in the primate amygdala, known as the paralaminar nucleus (PL), are maturing between infancy and adolescence. The PL is a potential substrate for the steep growth curve of amygdala volume during this developmental period. A microglial component is also embedded among the PL neurons, and likely supports local neuronal maturation and emerging synaptogenesis.
View Article and Find Full Text PDFCell Rep
January 2025
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address:
Tumor-draining lymph node dendritic cells (DCs) are poor stimulators of tumor antigen-specific CD4 T cells; however, the mechanism behind this defect is unclear. We now show that, in tumor-draining lymph node DCs, a large proportion of major histocompatibility complex class II (MHC-II) molecules retains the class II-associated invariant chain peptide (CLIP) fragment of the invariant chain bound to the MHC-II peptide binding groove due to reduced expression of the peptide editor H2-M and enhanced activity of the CLIP-generating proteinase cathepsin S. The net effect of this is that MHC-II molecules are unable to efficiently bind antigenic peptides.
View Article and Find Full Text PDFACS Appl Mater Interfaces
January 2025
Physical & Materials Chemistry Division, CSIR-National Chemical Laboratory, Pune, Maharashtra 411008, India.
This work aims to deal with the challenges associated with designing complementary bifunctional electrocatalysts and a separator/membrane that enables rechargeable zinc-air batteries (RZABs) with nearly solid-state operability. This solid-state RZAB was accomplished by integrating a bifunctional electrocatalyst based on Ru-RuO interface nanoparticles supported on nitrogen-doped (N-doped) graphene (Ru-RuO/NGr) and a dual-doped poly(acrylic acid) hydrogel (d-PAA) electrolyte soaked in KOH with sodium stannate additive. The catalyst shows enhanced activity and stability toward the two oxygen reactions, i.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
First Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang, China.
Background: Synaptic plasticity impairment plays a critical role in the pathogenesis of Alzheimer's disease (AD), Smad4, a central intracellular signal transmission mediator of transmission of transforming growth factor-β (TGF-β) signaling, plays a pivotal role in many biological processes, including cell differentiation, migration, apoptosis and tumorigenesis. Emerging evidence has demonstrated that Smad4 is also involved in the pathogenesis of AD. Once TGF-β signaling is stimulated, Smad4 interaction with Sp1 and Smad3 induces the transcriptional activation of APP.
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