Distributions of synaptic vesicle proteins and GAD65 in deprived and nondeprived ocular dominance columns in layer IV of kitten primary visual cortexare unaffected by monocular deprivation
Ma. Silver et Mp. Stryker, Distributions of synaptic vesicle proteins and GAD65 in deprived and nondeprived ocular dominance columns in layer IV of kitten primary visual cortexare unaffected by monocular deprivation, J COMP NEUR, 422(4), 2000, pp. 652-664
Two days of monocular deprivation (MD) of kittens during a critical period
of development is known to produce a loss of visual responses in the primar
y visual cortex to stimulation of the nondeprived eye, and 7 days of depriv
ation results in retraction of axon branches and loss of presynaptic sites
from deprived-eye geniculocortical arbors. The rapid loss of responsiveness
to deprived-eye visual stimulation could be due to a decrease in intracort
ical excitatory input to deprived-eye ocular dominance columns (ODCs) relat
ive to nondeprived-eye columns. Alternatively, deprived-eye visual response
s could be suppressed by an increase in intracortical inhibition in deprive
d columns relative to nondeprived columns. We tested these hypotheses in cr
itical period kittens by labeling ODCs in layer IV of primary visual cortex
with injections of the anterograde tracer Phaseolus vulgaris-leucoagglutin
in (PHA-L) into lamina A of the lateral geniculate nucleus (LGN). After eit
her 2 or 7 days of MD, densities of intracortical excitatory presynaptic si
tes within deprived relative to nondeprived ODCs were estimated by measurin
g synaptic vesicle protein (SVP) immunoreactivity (IR). Because most of the
synapses within layer IV of primary visual cortex are excitatory inputs fr
om other cortical neurons, levels of SVP-IR provide an estimate of the amou
nt of intracortical excitatory input. We also measured levels of immunoreac
tivity of the inhibitory presynaptic terminal marker glutamic acid decarbox
ylase (GAD)65 in deprived relative to nondeprived ODCs. Monocular deprivati
on (either 2 or 7 days) had no effect on the distributions of either SVP- o
r GAD65-IR in deprived and nondeprived columns. Therefore, the rapid loss o
f deprived-eye visual responsiveness following MD is due neither to a decre
ase in intracortical excitatory presynaptic sites nor to an increase in int
racortical inhibitory presynaptic sites in layer TV of deprived-eye ODCs re
lative to nondeprived columns. (C) 2000 Wiley-Liss, Inc.