Developmental visual cortex plasticity, the susceptibility of the brain to be modified by the environmental changes during postnatal development, is deemed representative of many life-sustaining neural functions such as learning, memory, sensory plasticity and aging. Furthermore, this process underlies the formation of normal neural connections, which is assailed by conditions that prevent normal sensory stimulation, including strabismus and childhood cataract. A research plan is proposed to study the ultastructural basis of developmental plasticity, combining tract-tracing, immunocytochemistry and electron microscopy techniques for qualitative and quantitative ultrastructural analysis. The long term objective of this research is to understand the roles of the glutamate and the cholinergic receptors in activity dependent synaptic modifications that underlie the critical period of visual plasticity. A newly developed technique will be used to dually identify developing thalamocortical(TC) axons and the chemically specified target sites to determine afferent-target relationships between thalamic terminals and the neurotransmitter receptors. Specifically, 1) the morphological properties of sites contacted by thalamocortical axons, and the GABA content of the targets, 2) the connection pattern of TC axons on NMDA, metabotropic and AMPA type glutamate receptors, and 3) the relationships between TC axons and the muscarinic receptors, will be examined in visual cortex layer IV and the subplate, before, during and after the critical period of visual plasticity. The specific goals of the proposed research address the identification of transient cellular mechanisms that lead to refinement and segregation of thalamic axons into ocular dominance columns, and to termination of early cortical plasticity by synaptic consolidation. The knowledge on how the neural proteins that are implicated in plasticity are structurally utilized by neural circuitry may provide insights in understanding the mechanisms of normal brain function as well as the conditions result from the sensory deprivation.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
5R01EY012138-04
Application #
6402633
Study Section
Visual Sciences B Study Section (VISB)
Program Officer
Hunter, Chyren
Project Start
1999-05-01
Project End
2003-07-31
Budget Start
2001-08-01
Budget End
2003-07-31
Support Year
4
Fiscal Year
2001
Total Cost
$127,945
Indirect Cost
Name
University of Virginia
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
001910777
City
Charlottesville
State
VA
Country
United States
Zip Code
22904
Owe, S G; Erisir, A; Heggelund, P (2013) Terminals of the major thalamic input to visual cortex are devoid of synapsin proteins. Neuroscience 243:115-25
Li, Jianli; Erisir, Alev; Cline, Hollis (2011) In vivo time-lapse imaging and serial section electron microscopy reveal developmental synaptic rearrangements. Neuron 69:273-86
Lillard, Angeline S; Erisir, Alev (2011) Old Dogs Learning New Tricks: Neuroplasticity Beyond the Juvenile Period. Dev Rev 31:207-239
Coleman, Jason E; Nahmani, Marc; Gavornik, Jeffrey P et al. (2010) Rapid structural remodeling of thalamocortical synapses parallels experience-dependent functional plasticity in mouse primary visual cortex. J Neurosci 30:9670-82
Corson, J; Nahmani, M; Lubarsky, K et al. (2009) Sensory activity differentially modulates N-methyl-D-aspartate receptor subunits 2A and 2B in cortical layers. Neuroscience 163:920-32
Goehler, L E; Erisir, A; Gaykema, R P A (2006) Neural-immune interface in the rat area postrema. Neuroscience 140:1415-34
Erisir, Alev; Dreusicke, Mark (2005) Quantitative morphology and postsynaptic targets of thalamocortical axons in critical period and adult ferret visual cortex. J Comp Neurol 485:11-31
Nahmani, Marc; Erisir, Alev (2005) VGluT2 immunochemistry identifies thalamocortical terminals in layer 4 of adult and developing visual cortex. J Comp Neurol 484:458-73
Aoki, Chiye; Fujisawa, Sho; Mahadomrongkul, Veera et al. (2003) NMDA receptor blockade in intact adult cortex increases trafficking of NR2A subunits into spines, postsynaptic densities, and axon terminals. Brain Res 963:139-49
Erisir, Alev; Harris, Janna L (2003) Decline of the critical period of visual plasticity is concurrent with the reduction of NR2B subunit of the synaptic NMDA receptor in layer 4. J Neurosci 23:5208-18

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