Spatial asymmetries in neural connectivity have an important role in creating basic building blocks of neuronal processing. A key circuit module of directionally selective (DS) retinal ganglion cells is a spatially asymmetric inhibitory input from starburst amacrine cells. It is not known how and when this circuit asymmetry is established during development. Here we photostimulate mouse starburst cells targeted with channelrhodopsin-2 (refs 6-8) while recording from a single genetically labelled type of DS cell. We follow the spatial distribution of synaptic strengths between starburst and DS cells during early postnatal development before these neurons can respond to a physiological light stimulus, and confirm connectivity by monosynaptically restricted trans-synaptic rabies viral tracing. We show that asymmetry develops rapidly over a 2-day period through an intermediate state in which random or symmetric synaptic connections have been established. The development of asymmetry involves the spatially selective reorganization of inhibitory synaptic inputs. Intriguingly, the spatial distribution of excitatory synaptic inputs from starburst cells is significantly more symmetric than that of the inhibitory inputs at the end of this developmental period. Our work demonstrates a rapid developmental switch from a symmetric to asymmetric input distribution for inhibition in the neural circuit of a principal cell.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1038/nature09711 | DOI Listing |
Cancer Prev Res (Phila)
December 2024
Rutgers, The State University of New Jersey, Piscataway, NJ, United States.
This study aimed to assess how ursolic acid (UA) can protect human skin keratinocytes from damage caused by ultraviolet B (UVB) radiation. Utilizing an omics-based approach, we characterized the features of photodamage and investigated the potential of UA to reverse HaCaT cell subpopulation injury caused by UVB radiation. The most significant changes in metabolite levels after UA treatment were in pathways associated with phosphatidylcholine biosynthesis, arginine and proline metabolism.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
A.M. Butlerov Chemistry Institute, Kazan Federal University, 18 Kremlyovskaya Str., 420008 Kazan, Russia.
Cancer is one of the most common diseases in developed countries. Recently, gene therapy has emerged as a promising approach to cancer treatment and has already entered clinical practice worldwide. RNA interference-based therapy is a promising method for cancer treatment.
View Article and Find Full Text PDFBioconjug Chem
December 2024
Department of Chemistry and Center of Excellence for Innovation in Chemistry, Faculty of Science, Kasetsart University, Bangkok 10900, Thailand.
Front Immunol
November 2024
Department of Radiology, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Resveratrol (Res), a Chinese herbal extract, has demonstrated a remarkable and distinct antitumor effect, characterized by prolonged efficacy and minimal adverse reactions. However, the bioavailability of Res in animals is hindered by limited absorption rates. Therefore, it is crucial to enhance the tumor-targeting ability of resveratrol to optimize cancer treatment outcomes by improving its bioavailability.
View Article and Find Full Text PDFInt J Nanomedicine
November 2024
Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, 510632, People's Republic of China.
Introduction: T-cell acute lymphoblastic leukemia (T-ALL) is a malignant hematological disease with limited targeted therapy options. Overexpression of B-cell lymphoma/leukemia 11B is frequently observed in T-ALL and contributes to leukemogenesis. Knockdown of BCL11B inhibits T-ALL cell proliferation and induces apoptosis, making it a potential therapeutic target.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!