Art - Bear (S)

The neuronal response to glutamate released at excitatory synapses depends on the complement of glutamate receptors in the postsynaptic membrane. Changes in receptor number, type and molecular composition can substantially alter the properties of synaptic transmission. During postnatal development, excitatory synaptic transmission is readily modified by sensory experience. Thus, it has been suggested that some forms of experience-dependent synaptic plasticity are associated with rapid changes in the complement of postsynaptic glutamate receptors. Most attention has focused on changes in the synaptic expression of AMPA receptors. However, NMDA receptors (NMDARs) are critical in triggering experience-dependent synaptic modifications, and changes in synaptic expression of these receptors could have a large effect on the properties of synaptic plasticity during development. In the present study, we addressed the possibility that experience rapidly regulates the synaptic expression of NMDARs in visual cortex in vivo. NMDARs in vivo are heteromeric ion channels composed of NR1 and NR2 subunits. The subtype (A–D) of the NR2 subunit confers distinct functional properties to the receptor1–7. Receptors containing NR2B predominate in the neonatal forebrain, and over the course of development, these are replaced or supplemented with NR2A-containing receptors2,8. This subunit switch alters the channel properties such that the synaptic NMDARmediated currents shorten in duration2,9. The developmental shortening of NMDAR currents in visual cortical neurons is postponed when animals are deprived of vision10, suggesting that the NR2A/B subunit composition of synaptic NMDARs differs between dark-reared animals and light-reared controls. We tested this hypothesis and then examined the effects of brief light exposure in dark-reared animals. Our results show that new Rapid, experience-dependent expression of synaptic NMDA receptors in visual cortex in vivo