DENDRITIC SPINE MOTILITY IN VISUAL CORTEX IS REGULATED BY BRIEF MONOCULAR
DEPRIVATION AND EXTRACELLULAR MATRIX DEGRADATION

S. Oray*; A. Majewska; M. Sur
Brain & Cognitive Sci, MIT, Cambridge, MA, USA

Remodeling of the primary visual cortex during ocular dominance plasticity is thought to progress from functional alterations in the response properties of single neurons to large anatomical shifts in axonal arborizations. Moreover, it has been suggested that the functional changes are a direct result of altered synaptic efficacy which is first apparent in the extragranular layers of the cortex (layers II/III, V and VI). We have examined the structural correlates of this functional modification at the level of single synapses by using two-photon microscopy to visualize the dynamic properties of dendritic spines in V1 both in vivo and in acute slices. In transgenic mice expressing GFP in a subset of their layer 5 pyramidal neurons, spine dynamics were elevated in extragranular layers following brief (2-3 day) monocular lid suture during the critical period. This increase in spine dynamics was not accompanied by other morphological changes in average spine length, head diameter or neck diameter. In order to explore potential mechanisms that might promote structural dynamics, we examined the effects of extracellular matrix degradation through the tissue plasminogen activator (tPA) / plasmin proteolytic cascade. In acute slices, both tPA and plasmin significantly upregulated spine dynamics in normal, non-deprived visual cortex. Further, brief monocular deprivation occluded any subsequent effects of the tPA/plasmin cascade in a lamina-specific manner, indicating that these processes share common mechanisms. These data are consistent with the hypothesis that rapid changes in synaptic efficacy following monocular deprivation are accompanied by increased extracellular matrix degradation, which can then promote structural remodeling and may potentially lead to significant anatomical reorganization.
Support Contributed By: Grants from the NIH (MS) and a Whiteman Fellowship (AM).