NR2C in the Thalamic Reticular Nucleus; Effects of the NR2C Knockout

NMDAR antagonists can evoke delta frequency bursting in the nucleus reticularis of the thalamus (nRT). The mechanism of
this oscillation was determined; antagonist blocks an NR2C-like conductance that has low Mg block at resting potential and
thus can contribute a resting inward current in response to ambient glutamate. Block of this current hyperpolarizes the cell,
deinactivating T-type Ca channels and thus triggering delta frequency bursting. The basis for assuming a NR2C-like
conductance was that (1) transcripts for NR2C are abundant in the thalamus and (2) the current-voltage curve of the
synaptically evoked NMDAR current has the low rectification characteristic of NR2C. In the current study, we have sought to
determine whether the channels that generate the NMDAR current are NR2C-like or are actually comprised of receptors
containing NR2C. We studied the current-voltage curve of synaptically evoked NMDAR current in the nRT of NR2C knockout
mice. In wild-type mice, the current was weakly voltage dependent, as previously observed in rats. This weak rectification
was absent in NR2C KO mice. In contrast, NR2C KO had no effect on the strongly rectifying NMDAR current in pyramidal cells
of the prefrontal cortex. These results demonstrate that the low rectification normally observed in the nRT is due to NR2C.