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Co‐regulation of ocular dominance plasticity and NMDA receptor subunit expression in glutamic acid decarboxylase‐65 knock‐out mice
Author(s) -
Kanold Patrick O.,
Kim Yoon A.,
GrandPre Tadzia,
Shatz Carla J.
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.171215
Subject(s) - nmda receptor , neuroscience , ocular dominance , synaptic plasticity , neuroplasticity , metaplasticity , plasticity , glutamate receptor , excitatory postsynaptic potential , homeostatic plasticity , developmental plasticity , biology , inhibitory postsynaptic potential , gabaergic , nonsynaptic plasticity , synaptic scaling , visual cortex , receptor , biochemistry , physics , thermodynamics
Experience can shape cortical circuits, especially during critical periods for plasticity. In visual cortex, imbalance of activity from the two eyes during the critical period shifts ocular dominance (OD) towards the more active eye. Inhibitory circuits are crucial in this process: OD plasticity is absent in GAD65KO mice that show diminished inhibition. This defect can be rescued by application of benzodiazepines, which increase GABAergic signalling. However, it is unknown how such changes in inhibition might disrupt and then restore OD plasticity. Since NMDA dependent synaptic plasticity mechanisms are also known to contribute to OD plasticity, we investigated whether NMDA receptor levels and function are also altered in GAD65KO. There are reduced NR2A levels and slower NMDA currents in visual cortex of GAD65KO mice. Application of benzodiazepines, which rescues OD plasticity, also increases NR2A levels. Thus it appears as if OD plasticity can be restored by adding a critical amount of excitatory transmission through NR2A‐containing NMDA receptors. Together, these observations can unify competing ideas of how OD plasticity is regulated: changes in either inhibition or excitation would engage homeostatic mechanisms that converge to regulate NMDA receptors, thereby enabling plasticity mechanisms and also ensuring circuit stability.