title: Synaptic density in geniculocortical afferents remains constant after monocular deprivation in the cat.
abstract: Monocular eyelid closure in cats during a critical period in development produces both physiological plasticity, as indicated by a loss of responsiveness of primary visual cortical neurons to deprived eye stimulation, and morphological 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 deprivation (MD), the shrinkage of deprived-eye geniculocortical arbors is less than half-maximal at 4 d and is not maximal until 7 d of deprivation, at which time the deprived arbors are approximately half their previous size. To study this form of plasticity at the level of individual thalamocortical synapses rather than arbors, we developed a new double-label colocalization technique. First, geniculocortical afferent arbors serving either the deprived or nondeprived eye were labeled by injection of the anterograde tracer Phaseolus vulgaris leucoagglutinin into lamina A of the lateral geniculate nucleus. 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 sites 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 afferents, 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 deprived-eye geniculocortical presynaptic sites is responsible for the prompt physiological effects of MD.
authors.affiliation: W.M. Keck Center for Integrative Neuroscience, Department of Physiology, University of California, San Francisco, California 94143-0444, USA.
authors.forename: M A
authors.initials: MA
authors.lastname: Silver
authors.forename: M P
authors.initials: MP
authors.lastname: Stryker
mesh_terms: D000375:Aging / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development / Q000502:physiology; D002415:Cats; D007839:Functional Laterality / Q000502:physiology; D005829:Geniculate Bodies / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D005968:Glutamate Decarboxylase / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology* / Q000648:ultrastructure; D009799:Ocular Physiological Phenomena; D012683:Sensory Deprivation / Q000502:physiology*; D013569:Synapses / Q000502:physiology* / Q000648:ultrastructure; D013572:Synaptic Vesicles / Q000378:metabolism; D013997:Time Factors; D014018:Tissue Distribution; D015349:Vision, Monocular / Q000502:physiology*
chemical_list: D007527:Isoenzymes; D009419:Nerve Tissue Proteins; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2