ronse at fr.u-strasbg.dpt-info wrote:
: I recently read on p. 6051 of
: A.K. Engel & al.: Proc. Natl. Acad. Sci. USA, Vol. 88, pp. 6048-6052, July
: that that neuronal responsiveness and receptive field properties in the
: visual area PMLS (posteromedial lateral suprasylivian sulcus), a visual
: area dealing with motion and global shape, are essentially unchanged after
: ablation of the primary visual area. They quoted as reference:
: P.D. Spear & T.P. Baumann: J. Neurophysiol., Vol. 42, pp. 31-56, 1979.
: R. Guedes & al.: Exp. Brain Res., Vol. 49, pp. 13-27, 1983.
: Now I always thought that visual information from the retina goes first to
: LGN, then to the primary visual area V1, from which axons make synapses
: with other visual areas. Thus destruction of the primary visual area leads
: to cortical blindness. There seems to be a contradiction.
Your confusion undoubtedly comes from not specifying the species. The
PMLS studies were in cat, whereas you are thinking about primates. In
the cat, thalamocortical projections are quite diverse, with direct
input to 17, 18, 19, and PMLS. This contrasts with the primate where
all of the geniculate input is to V1 (that is, area 17). Thus, in the
cat removal of area 17 does not eliminate visual input to cortex.
In fact, some people would claim that little is lost by area 17 ablations
in cats, although everybody agrees that the deficits are plain at
high spatial frequencies. On the other hand, lesions to V1 in monkeys
result in profound blindness in the part of the visual field corresponding
to the lesion. Blindsight may be the ability of humans with V1 damage
to orient to stimuli in the scotoma presumably based on subcortical
processing. It seems to me that the information in these subjects
about the visual stimuli to which they orient is consistent with almost
no cortical involvement. But I could be wrong.
saul+ at pitt.edu