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J Neurophysiol 99: 629-643, 2008. First published November 21, 2007; doi:10.1152/jn.01171.2007
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Different Roles for AMPA and NMDA Receptors in Transmission at the Immature Retinogeniculate Synapse

Xiaojin Liu and Chinfei Chen

Neurobiology Program, Division in Neuroscience, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts

Submitted 22 October 2007; accepted in final form 15 November 2007

The relay of information at the retinogeniculate synapse, the connection between retina and visual thalamus, begins days before eye opening and is thought to play an important role in the maturation of neural circuits in the thalamus and visual cortex. Remarkably, during this period of development, the retinogeniculate synapse is immature, with single retinal ganglion cell inputs evoking an average peak excitatory postsynaptic current (EPSC) of only about 40 pA compared with 800 pA in mature synapses. Yet, at the mature synapse, EPSCs >400 pA are needed to drive relay neuron firing. This raises the question of how small-amplitude EPSCs can drive transmission at the immature retinogeniculate synapse. Here we find that several features of the immature synapse, compared with the mature synapse, contribute to synaptic transmission. First, although the peak amplitude of EPSC is small, the decay time course of both {alpha}-amino-3-hydroxy-5-methyl-4isoxazolepropionic acid receptor (AMPAR) and N-methyl-D-aspartate receptor (NMDAR) currents is significantly slower. The prolonged time course of NMDAR currents is a result of the presence of both NR2B and NR2C/D subunits. In addition, the extended presence of neurotransmitter released prolongs the synaptic current time course. Second, reduced sensitivity to magnesium block results in significantly greater synaptic charge transfer through NMDAR. Third, AMPAR currents contribute to the spike latency, but not to temporal precision, at the immature synapse. Furthermore, intrinsic excitability is greater. These properties enable immature synapses with predominantly NMDARs and little or no AMPARs to contribute to the relay of information from retina to visual cortex.


Address for reprint requests and other correspondence: C. Chen, The Children's Hospital, Neurobiology Program, Division in Neuroscience, 300 Longwood Avenue, Boston, MA 02115 (E-mail: chinfei.chen{at}childrens.harvard.edu)







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