Almost all of the information that reaches the cerebral cortex must come though a relay in the thalamus.For the visual pathways, the primary relay from the retina is in the lateral geniculate nucleus (LGN) of the thalamus, which sends the visual messages on to primary visual cortex (V1, or area 17).Other visual relays in the thalamus, the lateralis posterior (LP) nucleus and the pulvinar (PUL) send messages to higher cortical areas (areas 18, 19, and higher).Early in the development of the LGN, as the axons of the retinal input are settling into their final ordered position in the nucleus, the contacts established by the retinogeniculate axons show evidence for synaptic plasticity; that is, they can be modified by activity.Further, there is evidence that a protein associated with nerve fiber growth and synaptic plasticity (GAP43) is produced in the retina and sent along the retinogeniculate axons to the lateral geniculate nucleus.The plasticity and the protein are both reduced in the adult LGN, but in sharp contrast to this, in LP/PUL GAP43 protein is still present in the adult.There is evidence that this GAP43 comes from cells in higher cortical areas, which innervate LP/PUL and unlike retinal cells, continue to produce this protein.Further, we have preliminary evidence that synaptic plasticity can be induced in LP/PUL of the adult by stimulation of the axons that arise in the cortex and that this synaptic changes can be induced in LP/PUL of the adult by stimulation of the axons that arise in the cortex, and that this synaptic change occurs in parallel with phosphorylation (activation) of the GAP43 protein. We propose a study of LGN and LP/PUL to demonstrate that in an adult, when the LGN has lost most of its GAP43 and lost its synaptic plasticity, the GAP43 protein is still present in LP/PUL.We will try to show that synaptic plasticity is present in the adult LP/PUL, that the GAP43 protein is produced in the cerebral cortex and that it can be phosphorylated in LP/PUL by stimulation of the cortical input fibers. Such a result would demonstrate that visual thalamic relays dependent on cortical inputs continue to be plastic long after the relay that depends on retinal inputs has ceased to be modifiable.It would focus attention on a novel site, the thalamus rather than the cortex, for some important visual associative functions. The long-term implications could produce a significant shift in our understanding of the development of visual skills, and their developmental abnormalities.
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