Anatomy of visual afferents in salamander brain

1980 ◽  
Vol 67 (4) ◽  
pp. 203-204 ◽  
Author(s):  
B. Fritzsch ◽  
W. Himstedt
Keyword(s):  
1975 ◽  
Vol 90 (1) ◽  
pp. 153-158 ◽  
Author(s):  
T. Ohno ◽  
U. Misgeld ◽  
S.T. Kitai ◽  
A. Wagner
Keyword(s):  

1987 ◽  
Vol 404 (1-2) ◽  
pp. 332-334 ◽  
Author(s):  
Michael Sperl ◽  
Gerhard Manteuffel

2021 ◽  
Vol 9 (5) ◽  
Author(s):  
Luis Millan ◽  
Juan Charaven

Terminal fields of a certain pathway result denervated if the regeneration after the lesion of the pathway fails. If the lesion happened in a young animal, terminal fields of other nervous pathways that are spatially coincident or are close to the denervated field, growth of axon collaterals or reactive synaptogenesis could take place and reinervate deafferented neurons. In that way these denervated neurons can be recruited for functional compensatory responses and can convey information to areas that result enriched with additional inputs to be processed. The present paper reviews the plastic reactions that take place in the superior colliculus, a mesencephalic layered structure, after the neonatal suppression of its visual afferents that terminate in its superficial layers. The postlesional reactive ascending growth of somatosensory afferents that in control animals innervate intermediate and deep collicular layers invade the superficial layers and connect with visually deafferented cells that result recruited for descendent collicular responses and to send sensory information to the visual cortex via the colliculo-geniculate payhway. In that way in neonatally deafferented animals, somatosensory information gains additional territory to be processed. Two somatosensory connections to the superior collicuus will be discussed in this review. One ascending from the cuneitorm nucleus and the other descending that originates in the barrel cortex.


1975 ◽  
Vol 15 (5) ◽  
pp. 603-609 ◽  
Author(s):  
James H. O'Brien ◽  
Stuart M. Rosenblum
Keyword(s):  

1979 ◽  
Vol 49 (2) ◽  
pp. 499-528 ◽  
Author(s):  
John Michael Williams

D-lysergic acid diethylamide (LSD) produces distortions of visual perception and analgesia. Evidence is advanced from a functional standpoint that the observed visual effects result from an attenuation of light-evoked input to the dorsal lateral geniculate nucleus (LGN) from the purely centripetal pathways of the retina. More slowly responding visual afferents or those with more complex receptive fields seem to be affected most. LSD analgesia, accompanied by severe psychotic symptoms, appears to result from drug actions on a centrifugally controlled pain system involving neurons of the midbrain raphe.


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