|  Help  |  About  |  Contact Us

Publication : Aberrant development of excitatory circuits to inhibitory neurons in the primary visual cortex after neonatal binocular enucleation.

First Author  Deng R Year  2021
Journal  Sci Rep Volume  11
Issue  1 Pages  3163
PubMed ID  33542365 Mgi Jnum  J:313759
Mgi Id  MGI:6512809 Doi  10.1038/s41598-021-82679-2
Citation  Deng R, et al. (2021) Aberrant development of excitatory circuits to inhibitory neurons in the primary visual cortex after neonatal binocular enucleation. Sci Rep 11(1):3163
abstractText  The development of GABAergic interneurons is important for the functional maturation of cortical circuits. After migrating into the cortex, GABAergic interneurons start to receive glutamatergic connections from cortical excitatory neurons and thus gradually become integrated into cortical circuits. These glutamatergic connections are mediated by glutamate receptors including AMPA and NMDA receptors and the ratio of AMPA to NMDA receptors decreases during development. Since previous studies have shown that retinal input can regulate the early development of connections along the visual pathway, we investigated if the maturation of glutamatergic inputs to GABAergic interneurons in the visual cortex requires retinal input. We mapped the spatial pattern of glutamatergic connections to layer 4 (L4) GABAergic interneurons in mouse visual cortex at around postnatal day (P) 16 by laser-scanning photostimulation and investigated the effect of binocular enucleations at P1/P2 on these patterns. Gad2-positive interneurons in enucleated animals showed an increased fraction of AMPAR-mediated input from L2/3 and a decreased fraction of input from L5/6. Parvalbumin-expressing (PV) interneurons showed similar changes in relative connectivity. NMDAR-only input was largely unchanged by enucleation. Our results show that retinal input sculpts the integration of interneurons into V1 circuits and suggest that the development of AMPAR- and NMDAR-only connections might be regulated differently.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

3 Authors

12 Bio Entities

Trail: Publication

0 Expression