Eb. Roberts et As. Ramoa, Enhanced NR2A subunit expression and decreased NMDA receptor decay time atthe onset of ocular dominance plasticity in the ferret, J NEUROPHYS, 81(5), 1999, pp. 2587-2591
Enhanced NR2A subunit expression and decreased NMDA receptor decay time at
the onset of ocular dominance plasticity in the ferret. J. Neurophysiol. 81
: 2587-2591, 1999. The NMDA subtype of glutamate receptor is known to exhib
it marked changes in subunit composition and functional properties during n
eural development. The prevailing idea is that NMDA receptor-mediated synap
tic responses decrease in duration after the peak of cortical plasticity in
rodents. Accordingly, it is believed that shortening of the NMDA receptor-
mediated current underlies the developmental reduction of ocular dominance
plasticity. However, some previous evidence actually suggests that the dura
tion of NMDA receptor currents decreases before the peak of plasticity. In
the present study, we have examined the time course of NMDA receptor change
s and how they correlate with the critical period of ocular dominance plast
icity in the visual cortex of a highly binocular animal, the ferret. The ex
pression of NMDA receptor subunits NR1, NR2A, and NR2B was examined in anim
als ranging in age from postnatal day 16 to adult using Western blotting. F
unctional properties of NMDA receptors in layer IV cortical neurons were st
udied using whole cell patch-clamp techniques in an in vitro slice preparat
ion of ferret primary visual cortex. We observed a remarkable increase in N
R1 and NR2A, but not NR2B, expression after eye opening. The NMDA receptor-
mediated synaptic currents showed an abrupt decrease in decay time concurre
nt with the increase in NR2A subunit expression. Importantly, these changes
occurred in parallel with increased ocular dominance plasticity reported i
n the ferret. In conclusion, molecular changes leading to decreased duratio
n of the NMDA receptor excitatory postsynaptic current may be a requirement
for the onset, rather than the end, of the critical period of ocular domin
ance plasticity.