Ma. Silver et Mp. Stryker, Synaptic density in geniculocortical afferents remains constant after monocular deprivation in the cat, J NEUROSC, 19(24), 1999, pp. 10829-10842
Monocular eyelid closure in cats during a critical period in development pr
oduces both physiological plasticity, as indicated by a loss of responsiven
ess of primary visual cortical neurons to deprived eye stimulation, and mor
phological plasticity, as demonstrated by a decrease in the total length of
individual geniculocortical arbors representing the deprived eye. Although
the physiological plasticity appears maximal after 2 d of monocular depriv
ation (MD), the shrinkage of deprived-eye geniculocortical arbors is less t
han half-maximal at 4 d and is not maximal until 7 d of deprivation, at whi
ch time the deprived arbors are approximately half their previous size. To
study this form of plasticity at the level of individual thalamocortical sy
napses rather than arbors, we developed a new double-label colocalization t
echnique. First, geniculocortical afferent arbors serving either the depriv
ed or nondeprived eye were labeled by injection of the anterograde tracer P
haseolus vulgaris leucoagglutinin into lamina A of the lateral geniculate n
ucleus. Then, using antibodies to synaptic vesicle proteins, we identified
presynaptic terminals within the labeled arbors in layer IV of the primary
visual cortex. Analysis of serial optical sections obtained using confocal
microscopy allowed measurement of the numerical density of presynaptic site
s and the relative amounts of synaptic vesicle protein in geniculocortical
afferents after both 2 and 7 d of MD. We found that the density of synapses
in geniculocortical axons was similar for deprived and nondeprived afferen
ts, suggesting that this feature of the afferents is conserved even during
periods in which synapse number is reduced by half in deprived-eye arbors.
These results are not consistent with the hypothesis that a rapid loss of d
eprived-eye geniculocortical presynaptic sites is responsible for the promp
t physiological effects of MD.