Quantitative electron microscopic analysis of synaptic input from cortical areas 17 and 18 to the dorsal lateral geniculate nucleus in cats

1994 ◽  
Vol 349 (2) ◽  
pp. 259-268 ◽  
Author(s):  
Zoltán Vidnyánszky ◽  
József Hámori
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Synaptic Input ◽  
Microscopic Analysis ◽  
Electron Microscopic Analysis ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Electron Microscopic ◽  
Cortical Areas ◽  
Lateral Geniculate ◽  
Areas 17 And 18 ◽  
Dorsal Lateral Geniculate

Age dependent modification of cytochrome oxidase activity in the cat dorsal lateral geniculate nucleus following removal of primary visual cortex

1996 ◽  
Vol 13 (5) ◽  
pp. 805-816 ◽  
Author(s):  
Bertram R. Payne ◽  
Stephen G. Lomber
Keyword(s):  
Visual Cortex ◽  
Cytochrome Oxidase ◽  
Lateral Geniculate Nucleus ◽  
Oxidase Activity ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Cytochrome Oxidase Activity ◽  
Lateral Geniculate ◽  
Areas 17 And 18 ◽  
C Complex ◽  
Dorsal Lateral Geniculate

AbstractThe purpose of the present study was to assess changes in the levels of cytochrome oxidase (CO) activity in the dorsal lateral geniculate nucleus (dLGN) of the adult cat following removal of primary visual cortical areas 17 and 18 on the day of birth (P1), P28, or in adulthood (≫6 months). Cytochrome oxidase activity was measured in histological sections 9 or more months after the cortical ablation. Control measures obtained from intact cats show that CO activity is normally highest in the A-laminae of dLGN, and slightly lower in the C-complex. Following visual cortex ablations incurred at any age, CO activity levels are reduced in the A-laminae. This reduction is most profound following ablations incurred on P28 or in adulthood. In contrast, CO activity in the C-complex of dLGN is at nearly normal levels following ablations on P1 or P28, but not in adulthood. These findings contribute to our understanding of the role played by the dLGN in the transfer of visual signals along retino-geniculo-extrastriate pathways that expand following early removal of areas 17 and 18. Moreover, they have implications for our understanding of spared behavioral functions attributed to the extrastriate cortex in cats which incurred early damage of areas 17 and 18.

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