Subplate (SP) neurons are among the earliest generated neurons of the cerebral cortex, and are present only during the time when cortical organization is highly susceptible to altered neural activity (the critical period). SP neurons have been implicated in visual cortical development because their removal before the critical period leads to disruption of thalamocortical connections and ocular dominance columns in visual cortex. SP removal also increases cortical expression of activity-regulated genes (such as BDNF, trbK and GAD). By controlling cortical activity levels, SP neurons may play a role in cortical development and the critical period. The basic physiology of the subplate and its influence on the cortical circuitry is unknown. The proposed research will investigate in vitro the developmental role of the SP. We will test the hypothesis that SP neurons control or modulate the balance of excitation and inhibition of developing cortex and by that manner influence the critical period. This work will investigate the cortical targets of SP innervation and how the SP modulates thalamocortical activity. Since SP ablation disrupts cortical development and affects cortical gene expression, studies proposed here will test if synaptic efficacy and plasticity are altered. Because inhibition has been shown to be crucial for development, we will also examine if SP ablation affects the maturation cortical inhibition. These studies should further our understanding of SP physiology, and also elucidate how the subplate influences cortical excitability. Thus, this study will provide crucial insight into the function of this transient neuronal population during development and its possible role in regulating the onset and duration of the critical period.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32EY013526-01
Application #
6338505
Study Section
Visual Sciences B Study Section (VISB)
Program Officer
Oberdorfer, Michael
Project Start
2001-07-01
Project End
Budget Start
2001-07-01
Budget End
2002-06-30
Support Year
1
Fiscal Year
2001
Total Cost
$34,832
Indirect Cost
Name
Harvard University
Department
Biology
Type
Schools of Medicine
DUNS #
082359691
City
Boston
State
MA
Country
United States
Zip Code
02115
Kanold, Patrick O; Kim, Yoon A; GrandPre, Tadzia et al. (2009) Co-regulation of ocular dominance plasticity and NMDA receptor subunit expression in glutamic acid decarboxylase-65 knock-out mice. J Physiol 587:2857-67
Datwani, Akash; McConnell, Michael J; Kanold, Patrick O et al. (2009) Classical MHCI molecules regulate retinogeniculate refinement and limit ocular dominance plasticity. Neuron 64:463-70
Butts, Daniel A; Kanold, Patrick O; Shatz, Carla J (2007) A burst-based ""Hebbian"" learning rule at retinogeniculate synapses links retinal waves to activity-dependent refinement. PLoS Biol 5:e61