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* To whom correspondence should be addressed. E-mail: yan.rao{at}yale.edu.
In vitro long-term depression (LTD) is thought to be a model for the loss of cortical responsiveness to an eye deprived of vision during the critical period. Using whole-cell recording, the present study investigates the mechanisms of LTD in vitro across layers in developing rat visual cortex. LTD was induced in layer II/III, layer V and layer VI but not layer IV with 10 min 1 Hz stimulation paired with postsynaptic depolarization. LTD in layer II/III and layer V could be blocked by the NMDA receptor antagonist D-AP5, but not by 100 µM LY341495, a metabotropic glutamate receptor inhibitor. In contrast, LTD in layer VI was blocked by 100 µM LY341495 and AIDA but not D-AP5, and partially blocked by application of GDP-
-S in patch pipette, suggesting an involvement of postsynaptic group I mGluRs. These results indicate that LTD in developing rat visual cortex varies with layer: LTD was absent in layer IV, suggesting a unique plasticity mechanism at geniculocortical synapses; LTD in layer II/III and V depends on NMDA receptors but not mGluRs; and LTD in layer VI requires mGluRs but not NMDA receptors.
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